You searched for subject:(Neoplasms pathology).
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University of Western Ontario
1.
Aldhafeeri, Hamad.
CRISPR Screen for Identification of Kinases that Mediate Prostate Cancer Cell Invasion.
Degree: 2017, University of Western Ontario
URL: https://ir.lib.uwo.ca/etd/5205 
► Metastasis is the primary cause of mortality in cancer patients. Inhibition of proteins that are involved in the regulation of metastasis are expected to suppress…
(more)
▼ Metastasis is the primary cause of mortality in cancer patients. Inhibition of proteins that are involved in the regulation of metastasis are expected to suppress metastasis and represent treatment targets. Our focus is on prostate cancer metastasis and we have developed a novel high-throughput means of performing in vitro screens for regulators of prostate cancer metastasis. We propose to use a focused CRISPR library screen that will “knock out” all human kinases to determine which ones are responsible for prostate cancer metastasis. CRISPR is a potent genetic editing tool and was used to silence all kinases in prostate cells (BPH cells). These cells form spheroid colonies in 3D culture and were subjected to a CRISPR kinase screen. We observed a morphological change in some colonies to a stellate morphology, which represents aggressive behavior. These stellate colonies were then isolated to identify the responsible kinase. We identified Glycogen synthase kinase 3 beta (GSK3ß) as a potential regulator for prostate cancer cell morphology and possible, metastasis.
Subjects/Keywords: Medical Pathology; Neoplasms
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APA (6th Edition):
Aldhafeeri, H. (2017). CRISPR Screen for Identification of Kinases that Mediate Prostate Cancer Cell Invasion. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/5205
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Aldhafeeri, Hamad. “CRISPR Screen for Identification of Kinases that Mediate Prostate Cancer Cell Invasion.” 2017. Thesis, University of Western Ontario. Accessed March 06, 2021.
https://ir.lib.uwo.ca/etd/5205.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Aldhafeeri, Hamad. “CRISPR Screen for Identification of Kinases that Mediate Prostate Cancer Cell Invasion.” 2017. Web. 06 Mar 2021.
Vancouver:
Aldhafeeri H. CRISPR Screen for Identification of Kinases that Mediate Prostate Cancer Cell Invasion. [Internet] [Thesis]. University of Western Ontario; 2017. [cited 2021 Mar 06].
Available from: https://ir.lib.uwo.ca/etd/5205.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Aldhafeeri H. CRISPR Screen for Identification of Kinases that Mediate Prostate Cancer Cell Invasion. [Thesis]. University of Western Ontario; 2017. Available from: https://ir.lib.uwo.ca/etd/5205
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Southern California
2.
Azhar, Raed A.
Histological analysis of the kidney tumor-parenchyma
interface.
Degree: MS, Clinical, Biomedical and Translational
Investigations, 2014, University of Southern California
URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/512074/rec/3195
► Purpose: During enucleative partial nephrectomy (PN), excision is performed adjacent to the tumor edge. To better inform the oncological propriety of enucleative PN, we histologically…
(more)
▼ Purpose: During enucleative partial nephrectomy (PN),
excision is performed adjacent to the tumor edge. To better inform
the oncological propriety of enucleative PN, we histologically
examined the tumor-parenchyma interface. ❧ Materials and Methods:
Archived hematoxylin-eosin slides from 124 nephrectomy specimens
were re-reviewed. Representative sections of tumor abutting the
renal parenchyma and overlying pseudo-capsule(PC)/peri-renal fat
were selected 4 mm² sectors apportioned at 1, 2, 3, 4 and from
tumor edge were evaluated. ❧ Results: Median tumor size was 3.5 cm.
111 tumors were malignant (90%) and 119 (96%) possessed a PC with
median thickness 0.6 mm. 82% of malignant and 31% of benign tumors
possessed intra-renal PCs (p
Advisors/Committee Members: Gill, Inderbir S.Azen, Stanley P. (Committee Chair), Desai, Mihir (Committee Member).
Subjects/Keywords: renal neoplasms; pathology; capsule; nephrectomy
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APA (6th Edition):
Azhar, R. A. (2014). Histological analysis of the kidney tumor-parenchyma
interface. (Masters Thesis). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/512074/rec/3195
Chicago Manual of Style (16th Edition):
Azhar, Raed A. “Histological analysis of the kidney tumor-parenchyma
interface.” 2014. Masters Thesis, University of Southern California. Accessed March 06, 2021.
http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/512074/rec/3195.
MLA Handbook (7th Edition):
Azhar, Raed A. “Histological analysis of the kidney tumor-parenchyma
interface.” 2014. Web. 06 Mar 2021.
Vancouver:
Azhar RA. Histological analysis of the kidney tumor-parenchyma
interface. [Internet] [Masters thesis]. University of Southern California; 2014. [cited 2021 Mar 06].
Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/512074/rec/3195.
Council of Science Editors:
Azhar RA. Histological analysis of the kidney tumor-parenchyma
interface. [Masters Thesis]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/512074/rec/3195
East Carolina University
3.
Corbin, Joshua Moses.
TMEFF2 is an epigenetic modulator that promotes androgen independent growth in castration-resistant prostate cancer cells.
Degree: MS, Biomedical Sciences, 2014, East Carolina University
URL: http://hdl.handle.net/10342/4662
► While the ability to detect PCa has improved significantly due to PSA screenings, the survival rate for men diagnosed with PCa has remained stagnant, and…
(more)
▼ While the ability to detect PCa has improved significantly due to PSA screenings, the survival rate for men diagnosed with PCa has remained stagnant, and the disease remains the second leading cause of cancer related deaths in men. Most patients initially respond to androgen deprivation treatment; however, a significant percentage of patients relapse with currently untreatable castration resistant prostate cancer (CRPC), during which the PCa cells develop the ability to grow in androgen depleted conditions. The androgen receptor (AR) plays a vital role in prostate development and homeostasis, and the deregulation of AR drives PCa tumorigenesis and progression to CRPC. Delineating molecular mechanisms that contribute to AR activity and/or PCa cell growth in androgen-depleted conditions may aid in the development of future CRPC therapies Epigenetic alterations play a critical role in differentiation during development, and aberrations in epigenetic regulation are associated with tumorigenesis and cancer progression. Two types of epigenetic modifications, DNA methylation and the methylation of multiple histone lysines, play significant roles in prostate cancer (PCa). Many histone methyltransferases (HMT) and demethylases (HDM), including the JMJD2 family of histone demethyalses, act as coregulators of AR, and many of these enzymes are implicated in CRPC. Because of this, HDMSs and HMTs have proven as attractive targets for therapeutic intervention. We have been studying TMEFF2, a protein that is regulated transcriptionally and translationally by the AR, and is overexpressed in PCa and CRPC suggesting a role in this disease. Data presented here demonstrate that TMEFF2 modulates JMJD2 controlled methyl histone marks and increases growth in androgen depleted conditions in CRPC cells. In correlation with its effect on histone methylation and growth, TMEFF2 overexpression increases resistance to the anti-growth effects of the pan-jumonji demethylase inhibitor, JIB-04, suggesting that TMEFF2 modulates growth, at least in part, by increasing jumonji demethylase activity. Additionally, TMEFF2 positively regulates PSA expression without altering AR levels in CRPC cells, indicating that TMEFF2 is a novel activator of AR. All together this data suggests a model in which TMEFF2, by modulating the activity of AR and JMJD2 enzymes, increases CRPC cell growth. Because CRPC remains to be a significant obstacle in the successful treatment of metastatic PCa, the results presented have the potential to be of therapeutic value.
Advisors/Committee Members: Ruiz-Echevarria, Maria (advisor).
Subjects/Keywords: Oncology;
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APA (6th Edition):
Corbin, J. M. (2014). TMEFF2 is an epigenetic modulator that promotes androgen independent growth in castration-resistant prostate cancer cells. (Masters Thesis). East Carolina University. Retrieved from http://hdl.handle.net/10342/4662
Chicago Manual of Style (16th Edition):
Corbin, Joshua Moses. “TMEFF2 is an epigenetic modulator that promotes androgen independent growth in castration-resistant prostate cancer cells.” 2014. Masters Thesis, East Carolina University. Accessed March 06, 2021.
http://hdl.handle.net/10342/4662.
MLA Handbook (7th Edition):
Corbin, Joshua Moses. “TMEFF2 is an epigenetic modulator that promotes androgen independent growth in castration-resistant prostate cancer cells.” 2014. Web. 06 Mar 2021.
Vancouver:
Corbin JM. TMEFF2 is an epigenetic modulator that promotes androgen independent growth in castration-resistant prostate cancer cells. [Internet] [Masters thesis]. East Carolina University; 2014. [cited 2021 Mar 06].
Available from: http://hdl.handle.net/10342/4662.
Council of Science Editors:
Corbin JM. TMEFF2 is an epigenetic modulator that promotes androgen independent growth in castration-resistant prostate cancer cells. [Masters Thesis]. East Carolina University; 2014. Available from: http://hdl.handle.net/10342/4662
University of Cape Town
4.
Tiltman, Andrew John.
The histogenesis of experimental bladder cancer.
Degree: Image, Division of Chemical Pathology, 1972, University of Cape Town
URL: http://hdl.handle.net/11427/26458
Subjects/Keywords: Neoplasms; Experimental - Pathology
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APA (6th Edition):
Tiltman, A. J. (1972). The histogenesis of experimental bladder cancer. (Thesis). University of Cape Town. Retrieved from http://hdl.handle.net/11427/26458
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Tiltman, Andrew John. “The histogenesis of experimental bladder cancer.” 1972. Thesis, University of Cape Town. Accessed March 06, 2021.
http://hdl.handle.net/11427/26458.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Tiltman, Andrew John. “The histogenesis of experimental bladder cancer.” 1972. Web. 06 Mar 2021.
Vancouver:
Tiltman AJ. The histogenesis of experimental bladder cancer. [Internet] [Thesis]. University of Cape Town; 1972. [cited 2021 Mar 06].
Available from: http://hdl.handle.net/11427/26458.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Tiltman AJ. The histogenesis of experimental bladder cancer. [Thesis]. University of Cape Town; 1972. Available from: http://hdl.handle.net/11427/26458
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Universidade Federal de Mato Grosso do Sul
5.
Braz, Paulo Henrique.
Comparação entre a citopatologia por biopsia aspirativa com agulha fina e a histopatologia no diagnóstico das neoplasias cutâneas e subcutâneas de cães
.
Degree: 2015, Universidade Federal de Mato Grosso do Sul
URL: http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2291
► Os neoplasmas cutâneos estão entre as mais diagnosticadas em medicina veterinária, diante disso busca-se que o diagnóstico desses tumores sejam rápido e eficaz. Em medicina…
(more)
▼ Os neoplasmas cutâneos estão entre as mais diagnosticadas em medicina veterinária,
diante disso busca-se que o diagnóstico desses tumores sejam rápido e eficaz. Em medicina
veterinária a citopatologia como método para diagnóstico tornou-se crescente. Diante disso, é
necessário que estudos comprovem a eficiência da técnica para que a mesma possa ser usada
de maneira isolada. Este trabalho teve como objetivo comparar o diagnóstico obtido pelas
técnicas citopatológica e histopatológica de tumores cutâneos e subcutâneos de cães,
determinar qual o tipo neoplásico mais facilmente diagnosticado pela citopatologia e o
neoplasma mais prevalente nesses animais, atendidos em dois hospitais veterinários de
Campo Grande/MS, no período de março de 2012 a dezembro de 2013. Foram coletadas
amostras celulares de tumores, através de punção aspirativa por biópsia com agulha fina e
punch cirúrgico, de 91 cães. Os resultados citopatológicos demonstraram uma eficácia de
69,69%, em relação à histopatologia. Para a diferenciação entre tumores neoplásicos e não
neoplásicos, a eficiência aumenta, com resultados iguais em 91,91%. Para diferenciar tumores
benignos de malignos, foi possível chegar a uma concordância na ordem de 68,13%. Os
tumores mais prevalentes foram o mastocitoma, seguido do lipoma, fibrossarcoma e tumor de
célula basal.
Advisors/Committee Members: Brum, Karine Bonucielli (advisor).
Subjects/Keywords: Neoplasias Cutâneas - diagnóstico;
Cães;
Patologia - métodos;
Neoplasias;
Skin Neoplasms - diagnosis;
Dogs;
Pathology - methods;
Neoplasms
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APA (6th Edition):
Braz, P. H. (2015). Comparação entre a citopatologia por biopsia aspirativa com agulha fina e a histopatologia no diagnóstico das neoplasias cutâneas e subcutâneas de cães
. (Thesis). Universidade Federal de Mato Grosso do Sul. Retrieved from http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2291
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Braz, Paulo Henrique. “Comparação entre a citopatologia por biopsia aspirativa com agulha fina e a histopatologia no diagnóstico das neoplasias cutâneas e subcutâneas de cães
.” 2015. Thesis, Universidade Federal de Mato Grosso do Sul. Accessed March 06, 2021.
http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2291.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Braz, Paulo Henrique. “Comparação entre a citopatologia por biopsia aspirativa com agulha fina e a histopatologia no diagnóstico das neoplasias cutâneas e subcutâneas de cães
.” 2015. Web. 06 Mar 2021.
Vancouver:
Braz PH. Comparação entre a citopatologia por biopsia aspirativa com agulha fina e a histopatologia no diagnóstico das neoplasias cutâneas e subcutâneas de cães
. [Internet] [Thesis]. Universidade Federal de Mato Grosso do Sul; 2015. [cited 2021 Mar 06].
Available from: http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2291.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Braz PH. Comparação entre a citopatologia por biopsia aspirativa com agulha fina e a histopatologia no diagnóstico das neoplasias cutâneas e subcutâneas de cães
. [Thesis]. Universidade Federal de Mato Grosso do Sul; 2015. Available from: http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2291
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Universidade Nova
6.
Fradique, António Amável Caldeira.
Mecanismos biopatológicos da metastização ganglionar no carcinoma gástrico. Implicações para a cirurgia radical.
Degree: 2009, Universidade Nova
URL: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/5100
► RESUMO A constatação de que o carcinoma gástrico continua a ser a segunda causa de morte por doença oncológica no mundo em geral e em…
(more)
▼ RESUMO
A constatação de que o carcinoma gástrico continua a ser a segunda causa de morte por doença oncológica no mundo em geral e em particular em Portugal, assim como a verificação da elevada incidência e letalidade no nosso país, justifica uma particular atenção a esta doença.
Apesar de avanços recentes na acção adjuvante e neo-adjuvante de terapêuticas não cirúrgicas, com algumas referências a melhorias na sobrevivência, estas terapêuticas não têm eficácia curativa. Sendo assim, a cirurgia continua a constituir a única esperança de cura no carcinoma gástrico. Em consequência, a correcta selecção da técnica a aplicar, assim como a sua correcta execução, vão ter influência marcante na sobrevivência do doente.
Os estudos dos centros oncológicos diferenciados em várias zonas geográficas demonstram que a cirurgia radical, com adequada extensão da gastrectomia e com linfadenectomia alargada permite obter as melhores sobrevivências.
O tipo de cirurgia mais praticado nos referidos centros oncológicos diferenciados é a gastrectomia com linfadenectomia D2, ou seja, com excisão da segunda estação ganglionar. Este tipo de cirurgia não aumenta a mortalidade, mas aumenta a morbilidade.
No entanto, verifica-se que muitos doentes não desenvolvem metastização que atinja a estação ganglionar de nível 2 e, por outro lado, muitos outros ultrapassam esta estação ganglionar. Ou seja, a linfadenectomia D2 é exagerada para alguns doentes, é necessária e suficiente para muitos, mas pelo contrário, é insuficiente para outros.
A questão radica na necessidade de equilíbrio em oferecer a cada doente a cirurgia necessária para obter a melhor sobrevivência, ainda que à custa de maior morbilidade e, por outro lado, conseguir identificar os factores que determinam que alguns doentes não necessitem de ser submetidos a uma terapêutica tão agressiva.
Se a primeira questão é eminentemente fisiopatológica e consiste em compreender os mecanismos da metastização ganglionar no carcinoma gástrico, de modo a poder prever a incidência e extensão da metastização ganglionar em cada doente em particular e, assim, adequar a terapêutica.
No estudo de 50 doentes, que elaborámos, a interpretação fisiopatológica apoia-se na avaliação de parâmetros aceites como convencionais e de parâmetros oncológicos.
Dentro dos parâmetros convencionais estudámos a localização do tumor, a sua dimensão, a classificação de Borrmann, as alterações metabólicas, a gastrina sérica, a citologia peritoneal, a infecção pelo Helicobacter pylori (Hp), a metaplasia intestinal, a classificação de Ming, a classificação de Lauren, a invasão em profundidade da parede gástrica (T), a metastização no “early gastric câncer”, a classificação TNM, o CEA 19.9 e o CA 72.4 séricos.
Para identificar quais os marcadores oncobiológicos mais adequados, efectuámos uma revisão da literatura relativamente a: Ki-67, p53, caderina-E, ERBB2, Instabilidade de Microssatélites, MUC 1, Sialil Tn e Sialil Lewis X.
De acordo com os resultados referidos na literatura, seleccionámos para estudo os seguintes…
Advisors/Committee Members: Rendas, António Bensabat.
Subjects/Keywords: Stomach Neoplasms - pathology; Adenocarcinome; Case Studies; Stomach Neoplasms - surgery; Portugal; Cirurgia Geral
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APA ·
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APA (6th Edition):
Fradique, A. A. C. (2009). Mecanismos biopatológicos da metastização ganglionar no carcinoma gástrico. Implicações para a cirurgia radical. (Thesis). Universidade Nova. Retrieved from http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/5100
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Fradique, António Amável Caldeira. “Mecanismos biopatológicos da metastização ganglionar no carcinoma gástrico. Implicações para a cirurgia radical.” 2009. Thesis, Universidade Nova. Accessed March 06, 2021.
http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/5100.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Fradique, António Amável Caldeira. “Mecanismos biopatológicos da metastização ganglionar no carcinoma gástrico. Implicações para a cirurgia radical.” 2009. Web. 06 Mar 2021.
Vancouver:
Fradique AAC. Mecanismos biopatológicos da metastização ganglionar no carcinoma gástrico. Implicações para a cirurgia radical. [Internet] [Thesis]. Universidade Nova; 2009. [cited 2021 Mar 06].
Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/5100.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Fradique AAC. Mecanismos biopatológicos da metastização ganglionar no carcinoma gástrico. Implicações para a cirurgia radical. [Thesis]. Universidade Nova; 2009. Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/5100
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
East Carolina University
7.
Nutter, Jennifer Makenzie.
Interrelated role of Notch signaling and mTORC pathways in prostate cancer cell survival and growth.
Degree: MS, Biomedical Sciences, 2014, East Carolina University
URL: http://hdl.handle.net/10342/4564
► Prostate cancer is currently the second highest leading cause of cancer death in men. Notch is a transmembrane receptor protein that is part of a…
(more)
▼ Prostate cancer is currently the second highest leading cause of
cancer death in men. Notch is a transmembrane receptor protein that
is part of a signaling pathway necessary in the normal development of
the prostate. Notch1 signaling has been shown to be lost in prostate
adenocarcinoma. One of prostate cancer's biggest risk factors is age
and mTOR has been shown to be linked to longevity and age related
diseases. mTOR exists as two complexes, mTORC 1/2, whose key
functions are to control cell survival, metabolism, and growth.
mTORC1/2 are often overexpressed in cancer. It was also reported that the mTORC1 pathway became inactivated when Notch1 signaling was inhibited in prostate cancer cell line PC-3. Herein, we suggest a link between Notch1 signaling and mTOR pathway activity which led to experiments with DU145 cells manipulated to have decreased Notch1 expression. The data shows that loss of Notch1 signaling causes decreased expression of the mTORC1 component Raptor as well as decreased phosphorylation of mTORC1 downstream target 4E-BP1 in conditions of cell stress. The mTORC2 pathway exhibited decreased phospho-mTOR (Ser2481) in normal conditions and decreased Rictor signaling in both normal and serum starved conditions when Notch1 expression was lost. The data also suggests there is less G[bata]L in conditions of stress in Notch1 knockdown cells. We hypothesize that downregulation of Notch1 signaling leads to the dysfunction of both mTOR pathways.
Advisors/Committee Members: Bertrand, Fred E. (advisor).
Subjects/Keywords: Oncology;
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APA (6th Edition):
Nutter, J. M. (2014). Interrelated role of Notch signaling and mTORC pathways in prostate cancer cell survival and growth. (Masters Thesis). East Carolina University. Retrieved from http://hdl.handle.net/10342/4564
Chicago Manual of Style (16th Edition):
Nutter, Jennifer Makenzie. “Interrelated role of Notch signaling and mTORC pathways in prostate cancer cell survival and growth.” 2014. Masters Thesis, East Carolina University. Accessed March 06, 2021.
http://hdl.handle.net/10342/4564.
MLA Handbook (7th Edition):
Nutter, Jennifer Makenzie. “Interrelated role of Notch signaling and mTORC pathways in prostate cancer cell survival and growth.” 2014. Web. 06 Mar 2021.
Vancouver:
Nutter JM. Interrelated role of Notch signaling and mTORC pathways in prostate cancer cell survival and growth. [Internet] [Masters thesis]. East Carolina University; 2014. [cited 2021 Mar 06].
Available from: http://hdl.handle.net/10342/4564.
Council of Science Editors:
Nutter JM. Interrelated role of Notch signaling and mTORC pathways in prostate cancer cell survival and growth. [Masters Thesis]. East Carolina University; 2014. Available from: http://hdl.handle.net/10342/4564
Universidade Estadual de Campinas
8.
Jales, Rodrigo Menezes, 1975-.
Importância da ultrassonografia na predição de malignidade e sua correlação com os fenótipos Luminal, Her 2 overexpression e Triplo Negativo nos nódulos de mama classificados na categoria BI-RADS® US 4: Importance of ultrasonography in predicting malignancy and its correlation with the phenotypes Luminal, Her 2 overexpression and Triple Negative in breast masses classified as category BI-RADS® US 4.
Degree: 2012, Universidade Estadual de Campinas
URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/309768
► Abstract: Objective: To evaluate the importance of ultrasound in predicting malignancy and its correlation with the phenotypes Luminal, Her 2 overexpression and Triple Negative in…
(more)
▼ Abstract: Objective: To evaluate the importance of ultrasound in predicting malignancy and its correlation with the phenotypes Luminal, Her 2 overexpression and Triple Negative in breast masses classified as BI-RADS 'TRADE MARK' -US 4. Article 1: To assess whether cyst diameter might contribute to the prediction of malignancy in complex breast masses. Article 2: To assess the sonographic characteristics of BI-RADS 'TRADEMARK'-US 4 breast masses in the Luminal, Triple Negative and HER2 phenotypes. Methods: In the first article, in a cross-sectional study, we identified 48 breast masses that had sonographic features suggestive of benignity, but presenting at least one cystic component. All breast masses were biopsied (25 core-needle; 23 core-needle and excision). Subsequent histologic analysis was performed and 12/48 (25%) malignancies were identified. Different sonographic measurements (largest diameter of the mass and cyst, vascular pattern) were assessed for the detection of malignancy. In the second article, in a cross-sectional study, we selected 327 masses classified in subcategories BI-RADS 'TRADEMARK' -US 4a, 4b and 4c. All masses were biopsied. The pathologic results were classified as benign 195 (60%) or malignant 132 (40%). The malignant masses were further grouped into three phenotypic subtypes: Luminal, Her 2 overexpression and Triple Negative. We then compared the sonographic features of the malignant lesions according to the phenotypic status of the masses. Results: In the first article, among sonographic features, vascular pattern [(present in the lesion (p=1.0) or present immediately adjacent to the lesion (p=0.46)] was not associated with malignancy, whereas the largest mass and cyst dimension had a significantly positive correlation (p=0.02 and p<0.001, respectively) with tumor malignancy. In the second article, the subcategories BI-RADS 'TRADEMARK' -US 4a, 4b and 4c were not clearly related to the phenotypes Luminal, Her2 overexpression or Triple Negative. However, spiculated margins, indistinct margins, echogenic halo, and posterior acoustic shadowing were significantly correlated with the Luminal phenotype. Moreover, circumscribed margins and attenuation were positively related to the Triple Negative phenotype. No sonographic variable was associated with Her2 overexpression phenotype. Conclusions: The first article presents the new concept that cyst diameter is a good predictor of malignancy in complex breast tumors which, except for the presence of the anechoic formation, would otherwise be rendered as probably benign (BI-RADS 'TRADEMARK' 3). The second article is in agreement with current knowledge that there is an association between ultrasound features as margins, posterior acoustic features and lesion boundary and phenotypic subtypes Luminal and Triple Negative. In our sample, this association was not clearly expressed in the subcategorization BI-RADS 'TRADEMARK' -US 4a, 4b and 4c
Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Derchain, Sophie Françoise Mauricette, 1959- (advisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Tocoginecologia (nameofprogram), Filho, Francisco Mauad (committee member), Elias, Simone (committee member), Pinto-Neto, Aarão Mendes (committee member), Juliato, Cássia Raquel Teatin (committee member).
Subjects/Keywords: Neoplasias da mama; Diagnóstico; Patologia; Breast neoplasms; Diagnosis; Pathology
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APA (6th Edition):
Jales, Rodrigo Menezes, 1. (2012). Importância da ultrassonografia na predição de malignidade e sua correlação com os fenótipos Luminal, Her 2 overexpression e Triplo Negativo nos nódulos de mama classificados na categoria BI-RADS® US 4: Importance of ultrasonography in predicting malignancy and its correlation with the phenotypes Luminal, Her 2 overexpression and Triple Negative in breast masses classified as category BI-RADS® US 4. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/309768
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Jales, Rodrigo Menezes, 1975-. “Importância da ultrassonografia na predição de malignidade e sua correlação com os fenótipos Luminal, Her 2 overexpression e Triplo Negativo nos nódulos de mama classificados na categoria BI-RADS® US 4: Importance of ultrasonography in predicting malignancy and its correlation with the phenotypes Luminal, Her 2 overexpression and Triple Negative in breast masses classified as category BI-RADS® US 4.” 2012. Thesis, Universidade Estadual de Campinas. Accessed March 06, 2021.
http://repositorio.unicamp.br/jspui/handle/REPOSIP/309768.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Jales, Rodrigo Menezes, 1975-. “Importância da ultrassonografia na predição de malignidade e sua correlação com os fenótipos Luminal, Her 2 overexpression e Triplo Negativo nos nódulos de mama classificados na categoria BI-RADS® US 4: Importance of ultrasonography in predicting malignancy and its correlation with the phenotypes Luminal, Her 2 overexpression and Triple Negative in breast masses classified as category BI-RADS® US 4.” 2012. Web. 06 Mar 2021.
Vancouver:
Jales, Rodrigo Menezes 1. Importância da ultrassonografia na predição de malignidade e sua correlação com os fenótipos Luminal, Her 2 overexpression e Triplo Negativo nos nódulos de mama classificados na categoria BI-RADS® US 4: Importance of ultrasonography in predicting malignancy and its correlation with the phenotypes Luminal, Her 2 overexpression and Triple Negative in breast masses classified as category BI-RADS® US 4. [Internet] [Thesis]. Universidade Estadual de Campinas; 2012. [cited 2021 Mar 06].
Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/309768.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Jales, Rodrigo Menezes 1. Importância da ultrassonografia na predição de malignidade e sua correlação com os fenótipos Luminal, Her 2 overexpression e Triplo Negativo nos nódulos de mama classificados na categoria BI-RADS® US 4: Importance of ultrasonography in predicting malignancy and its correlation with the phenotypes Luminal, Her 2 overexpression and Triple Negative in breast masses classified as category BI-RADS® US 4. [Thesis]. Universidade Estadual de Campinas; 2012. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/309768
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Universidade Nova
9.
Severino, Paulo Filipe.
Thomsen-Friedenreich antigens in bladder cancer: evaluation of their prognostic value.
Degree: 2015, Universidade Nova
URL: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/14246
► RESUMO: Introdução. O cancro de bexiga é uma patologia comum que representa o 6° e o 5° cancro mais incidente em Portugal e na Itália,…
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▼ RESUMO: Introdução. O cancro de bexiga é uma patologia comum que representa o 6° e o 5°
cancro mais incidente em Portugal e na Itália, respetivamente. Em mais de metade dos
casos ocorre reincidência durante o primeiro ano, requerendo acompanhamento clínico ao
longo da vida. A instilação intravesical de Bacillus Calmette-Guérin (BCG)
(uma estirpe atenuada do Mycobacterium bovis) representa uma imunoterapia eficaz no
combate ao cancro de bexiga, no entanto, muitos aspetos da interação de BCG com as
células tumorais bem como com as células do sistema imunitário permanecem por
desvendar. As células tumorais de bexiga expressam frequentemente as formas sialiladas
dos antigénios de Thomsen-Friedenreich (TF), i.e., sialil-T (sT) e sialil-Tn (sTn).
Contudo ainda se desconhece o significado da sua expressão na malignidade tumoral e se
afeta a eficácia da terapêutica BCG. Objetivo do estudo. Investigar o papel dos
antigénios sT e sTn no fenótipo maligno de células de cancro de bexiga bem como na
resposta mediada pelo sistema imunitário à terapia com BCG. Metodologia. Para tal,
foram utilizadas as linhas celulares de cancro da bexiga HT1376 e MCR, geneticamente
modificadas por transdução com vetores codificantes para as sialiltransferases ST3GAL1
ou ST6GALNAC1, de forma a expressar homogeneamente os antigénios sT ou sTn
respetivamente. Estes modelos celulares foram estudados após confronto com BCG.
O nível de BCG internalizado foi avaliado por citometria de fluxo. O perfil global de
expressão genética dos modelos celulares antes e após incubação com BCG foi analisado
pela tecnologia de microarray. O perfil de citocinas secretadas pelos modelos celulares
após incubação com BCG, bem como de macrófagos estimulados pelo secretoma de
células de cancro de bexiga que por sua vez foram estimuladas previamente por BCG,
foi estudado pelo sistema multiplex de “imuno-esferas”. Resultados. A análise do
transcritoma dos modelos celulares revelou que grupos de genes envolvidos em funções
específicas foram modulados em paralelo nos dois modelos celulares, após transdução,
independentemente da sialiltransferase expressa. Ou seja, em células que expressavam a sialiltransferase ST3GAL1 ou ST6GALNAC1, os genes envolvidos na regulação da segregação cromossómica e na reparação do DNA foram consistentemente regulados
negativamente. Genes descritos na literatura como marcadores para o cancro de bexiga
foram também modulados. A incubação com BCG resultou numa tendência ao aumento
da expressão de genes relevantes na preservação e estabilidade genómica e menor
malignidade, no entanto, apenas em células que expressavam sT ou sTn. Entre as dez
citocinas testadas, apenas a IL-6 e IL-8 foram expressas pelas linhas celulares de cancro
da bexiga, com indução destas após estimulação com BCG, e principalmente em células
que expressavam ST3GAL1 ou ST6GALNAC1. Em macrófagos, citocinas inflamatórias,
tais como IL-1β, IL-6 e TNFα, e a citocina anti-inflamatória IL-10, foram induzidas
apenas pelo secretoma de células de cancro da bexiga confrontadas com BCG, com…
Advisors/Committee Members: Videira, Paula, dall'Olio, Fabio.
Subjects/Keywords: Urinary Bladder Neoplasms - pathology; Immunotherapy; BCG Vaccine - therapeutic use; Imunologia
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APA ·
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APA (6th Edition):
Severino, P. F. (2015). Thomsen-Friedenreich antigens in bladder cancer: evaluation of their prognostic value. (Thesis). Universidade Nova. Retrieved from http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/14246
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Severino, Paulo Filipe. “Thomsen-Friedenreich antigens in bladder cancer: evaluation of their prognostic value.” 2015. Thesis, Universidade Nova. Accessed March 06, 2021.
http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/14246.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Severino, Paulo Filipe. “Thomsen-Friedenreich antigens in bladder cancer: evaluation of their prognostic value.” 2015. Web. 06 Mar 2021.
Vancouver:
Severino PF. Thomsen-Friedenreich antigens in bladder cancer: evaluation of their prognostic value. [Internet] [Thesis]. Universidade Nova; 2015. [cited 2021 Mar 06].
Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/14246.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Severino PF. Thomsen-Friedenreich antigens in bladder cancer: evaluation of their prognostic value. [Thesis]. Universidade Nova; 2015. Available from: http://www.rcaap.pt/detail.jsp?id=oai:run.unl.pt:10362/14246
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Birmingham
10.
Ploumakis, Athanasios.
Characterisation of the cellular response to defective translational termination.
Degree: PhD, 2018, University of Birmingham
URL: http://etheses.bham.ac.uk//id/eprint/8081/
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742597
► Enzymatic hydroxylation of varied cellular substrates is catalyzed by the 2-oxoglutarate and Fe(II) dependent 2-oxoglutrate (OG) oxygenase group of proteins. These enzymes control gene expression,…
(more)
▼ Enzymatic hydroxylation of varied cellular substrates is catalyzed by the 2-oxoglutarate and Fe(II) dependent 2-oxoglutrate (OG) oxygenase group of proteins. These enzymes control gene expression, from epigenetics to splicing and translation. The 2OG oxygenase JMJD4 has been shown to catalyse the hydroxylation of the eukaryotic omnipotent termination factor 1 (eRF1), and is essential for optimal translational termination. In this thesis, we expand on previous work by examining two further potential binding partners of JMJD4, GTF2I and TCP1-γ. Subsequently, we find that depletion of JMJD4 and eRF1 is associated with growth reduction in cancer cell lines in 2D and 3D. The transcriptomic changes in response to eRF1 depletion are then assessed by RNA-Seq. Among the potential pathways identified, downstream targets of the transcription factor ATF4 were most prominent. Upregulation of ATF4 and its downstream targets was validated in an eRF1 rescue system and the contribution of specific subdomains of eRF1 to the transcriptional response assessed, indicating multiple arms of the unfolded protein response being upregulated downstream of defective translational termination. The implications of our findings and their relevance in wider biological and disease contexts, including cancer, is finally discussed.
Subjects/Keywords: 616.99; RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer)
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APA ·
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Export
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APA (6th Edition):
Ploumakis, A. (2018). Characterisation of the cellular response to defective translational termination. (Doctoral Dissertation). University of Birmingham. Retrieved from http://etheses.bham.ac.uk//id/eprint/8081/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742597
Chicago Manual of Style (16th Edition):
Ploumakis, Athanasios. “Characterisation of the cellular response to defective translational termination.” 2018. Doctoral Dissertation, University of Birmingham. Accessed March 06, 2021.
http://etheses.bham.ac.uk//id/eprint/8081/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742597.
MLA Handbook (7th Edition):
Ploumakis, Athanasios. “Characterisation of the cellular response to defective translational termination.” 2018. Web. 06 Mar 2021.
Vancouver:
Ploumakis A. Characterisation of the cellular response to defective translational termination. [Internet] [Doctoral dissertation]. University of Birmingham; 2018. [cited 2021 Mar 06].
Available from: http://etheses.bham.ac.uk//id/eprint/8081/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742597.
Council of Science Editors:
Ploumakis A. Characterisation of the cellular response to defective translational termination. [Doctoral Dissertation]. University of Birmingham; 2018. Available from: http://etheses.bham.ac.uk//id/eprint/8081/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.742597
11.
이, 국빈.
Comparative Analysis of Radiologically Measured Size and True Size of Renal Tumors.
Degree: 2013, Ajou University
URL: http://repository.ajou.ac.kr/handle/201003/8647
;
http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000014696
► PURPOSE: We evaluated the effects of different tumor conditions on discrepancy between radiologically measured size and true size of renal tumors. MATERIALS AND METHODS: The…
(more)
▼ PURPOSE: We evaluated the effects of different tumor conditions on discrepancy between radiologically measured size and true size of renal tumors.
MATERIALS AND METHODS: The data from 238 patients who underwent radical or partial nephrectomy for a renal tumor at our institution were reviewed. Radiologic tumor size defined as the largest diameter on a CT scan was compared to pathologic tumor size defined as the largest diameter on gross pathologic examination.
RESULTS: There was no significant difference between the mean radiologic and pathologic size for all tumors (p=0.078). When stratified according to radiologic size range, mean radiologic size was significantly larger than mean pathologic size for tumors <4 cm (p=0.001), but there was no significant difference between them for tumors 4-7 cm, and >7 cm. When classified according to histologic subtype, mean radiologic size was significantly larger than pathologic size only in clear cell renal cell carcinoma (p=0.005). When classified according to tumor location, mean radiologic size was larger than pathologic size in endophytic tumors (p=0.050), but not in exophytic tumors. When endophytic tumors were stratified according to radiologic size range, there was a significant difference between the radiologic and pathologic size for tumors <4 cm (p<0.001) and 4-7 cm (p=0.007), but not for tumors >7 cm.
CONCLUSIONS: Radiologic tumor size seems to correlate well with pathologic tumor size. However, there was a tendency to overestimate tumor size in smaller tumors. Endophytic renal tumors are more likely to have size overestimated by CT scan than exophytic tumors.
목적: 신종양의 수술적 치료방법 결정에서 중요한 인자 중 하나가 종양의 크기인데, 이전 연구들에서 술 전 영상의학적 크기와 술 후 병리학적 크기 사이에 유의한 차이가 있다는 결과가 보고되었으나 아직 논란의 여지가 있다. 본 연구에서는 신종양으로 부분 혹은 근치적 신절제술을 시행 받은 환자들에서 영상의학적으로 측정된 크기와 병리학적으로 측정된 실제크기사이의 차이에 대한 비교 분석을 하고자 하였다.
대상 및 방법: 2002년 3월부터 2011년 2월까지 신세포암이 의심되어 본원에서 부분 혹은 근치적 신절제술을 시행 받은 환자들 중 본원에서 술 전에 복부전산화단층촬영을 시행하여 분석이 가능하였던 238명 (남자 167명, 여자 71명, 평균연령 54.8세)을 대상으로 하였다. 술 전 영상의학적 크기는 복부전산화단층촬영을 재검토하여 종양의 가장 긴 길이로 정의하였고, 술 후 병리학적 크기는 의무기록을 재검토하여 검체에서 가장 긴 길이로 정의하였다.
결과: 30개월의 전체 238명의 환자 중 신세포암이 225례 (94.5%)였으며, 양성종양은 13례 (5.5%)로 호산성과립세포종 6례 (2.5%), 혈관근육지방종 5례 (2.1%), 고립섬유종양 1례 (0.4%), 혼합형 상피성 간질성 종양 1례 (0.4%)였다. 전체 크기 비교에서는 영상의학적 크기는 5.01±2.74 cm, 병리학적 크기는 4.92±2.83 cm으로 통계학적으로 유의한 차이가 없었다 (p=0.078). 임상적 T병기 기준으로 분류한 결과 T1a 군에서 (p=0.001), 조직학적 유형을 기준으로 분류하였을 때 투명세포암에서 영상의학적 크기가 병리학적 크기보다 통계학적으로 크다는 유의한 결과를 보였다 (p=0.005), 종양의 신장에서 위치를 기준으로 분류하였을 때 내장성(endophytic) 종양에서 영상의학적 크기가 병리학적 크기보다 통계학적으로 크다는 유의한 결과를 보였느나 (p=0.050), 외장성(exophytic) 종양에서는 유의한 차이가 없었다. 내장성 종양을 크기에 따른 분류를 하였을 때 4cm 미만(p<0.001), 4cm이상 7cm이하(p=0.007)에서는 영상의학적 크기가 병리학적크기보다 통계적으로 크다는 결과를 보였고, 7cm 초과에서는 통계적으로 유의한 차이가 없었다.
결론: 본 연구 결과 영상의학적으로 측정된 신종양의 크기와 병리학적으로 측정된 실제 크기는 대체적으로 잘 맞는 결과를 보였다. 하지만, 크기가 작을수록 영상의학적 크기가 과평가되는 성향을 보였다. 또한 내장성 종양이 외장성종양보다는 영상의학적으로 과평가되는 성향을 보였다.
ABSTRACT i
TABLE OF CONTENTS ii
LIST OF TABLES iii
I. INTRODUCTION 1
II. MATERIALS AND METHODS 2
III. RES ULTS 3
IV. DISCUSSION 8
V. CONCLUSIONS 11
RE FERE…
Advisors/Committee Members: 대학원 의학과, 201124128, 이, 국빈.
Subjects/Keywords: Kidney; Neoplasms; Pathology; Radiology; 신장; 종양; 병리학; 영상의학; 방사선학
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APA ·
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APA (6th Edition):
이, . (2013). Comparative Analysis of Radiologically Measured Size and True Size of Renal Tumors. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/8647 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000014696
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
이, 국빈. “Comparative Analysis of Radiologically Measured Size and True Size of Renal Tumors.” 2013. Thesis, Ajou University. Accessed March 06, 2021.
http://repository.ajou.ac.kr/handle/201003/8647 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000014696.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
이, 국빈. “Comparative Analysis of Radiologically Measured Size and True Size of Renal Tumors.” 2013. Web. 06 Mar 2021.
Vancouver:
이 . Comparative Analysis of Radiologically Measured Size and True Size of Renal Tumors. [Internet] [Thesis]. Ajou University; 2013. [cited 2021 Mar 06].
Available from: http://repository.ajou.ac.kr/handle/201003/8647 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000014696.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
이 . Comparative Analysis of Radiologically Measured Size and True Size of Renal Tumors. [Thesis]. Ajou University; 2013. Available from: http://repository.ajou.ac.kr/handle/201003/8647 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000014696
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Glasgow
12.
Willder, Jennifer Mary.
Androgen receptor phosphorylation in prostate diseases.
Degree: PhD, 2014, University of Glasgow
URL: http://theses.gla.ac.uk/5797/
;
http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.646715
► Prostatic diseases are common; benign prostate hyperplasia (BPH) is almost ubiquitous in elderly men and 899,000 men were diagnosed with prostate cancer worldwide in 2008.…
(more)
▼ Prostatic diseases are common; benign prostate hyperplasia (BPH) is almost ubiquitous in elderly men and 899,000 men were diagnosed with prostate cancer worldwide in 2008. The incidence of both is increasing and expected to continue to rise. Therefore, prostatic diseases represent a considerable economic burden, but there are currently no reliable markers available to accurately differentiate indolent from aggressive disease nor to predict who will benefit from treatment for either BPH or prostate cancer. This results in over and under-treatment of both diseases with consequent patient related morbidity and mortality. The molecular mechanisms underlying the natural history of prostatic diseases remain elusive. It is accepted that prostate cell growth and survival are exquisitely dependent upon activation of the androgen receptor (AR) by androgens. Following ligand binding, AR undergoes further phosphorylation at serine residues, which inhibit proteolytic degradation, stabilise AR and influence AR transactivation. It is therefore plausible that alterations in AR phosphorylation may drive prostatic disease progression. However, few studies have explored the significance of AR phosphorylation, or the kinases driving AR serine phosphorylation in the clinical setting. The over-riding objective of this study was to establish the clinical relevance of AR serine phosphorylation status in prostate tissue in both BPH and prostate cancer. The specific aims of the current study were: • To firstly establish and validate a panel of AR phosphospecific antibodies. • To evaluate site specific AR serine phosphorylation expression levels in prostate cancer and BPH patient cohorts, with full clinical data and follow-up. • To investigate the expression of candidate kinases mediating such phosphorylation. This involved establishing tissue banks with linked comprehensive clinical databases, and utilising this tissue to establish AR phosphorylation expression profiles for each patient. Six AR phosphospecific antibodies (pARS81, pARS94, pARS213, pARS515, pARS578, pARS650) were verified using peptide competition assays and western blotting. Cdk1, ERK1/2, Akt and PKC were identified as putative kinases mediating AR phosphorylation using the online kinase search tool Scansite 2.0. Immunohistochemistry was performed on hormone naïve diagnostic prostate cancer tissue relating to 90 patients. High expression levels of AR phosphorylation at serine sites 81, 515 and 578 were each associated with a poorer clinical outcome. Following cox regression analysis, cytoplasmic pARS515 expression (p=0.038, HR 4.5 (95% CI 1.1–20.6)) and pARS81 nuclear expression (p=0.030, HR 0.033 95% CI 0.002-0.721) were independently associated with shorter time to biochemical relapse and shorter disease specific survival respectively. Cdk1 and/or pCdk1161 were significantly associated with pARS81 and pARS515 as predicted by Scansite 2.0. Similarly, nuclear PKC expression was significantly associated with pARS578 expression both in the cytoplasm and the nucleus. In patients…
Subjects/Keywords: 362.109678; RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer); RD Surgery
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Willder, J. M. (2014). Androgen receptor phosphorylation in prostate diseases. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/5797/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.646715
Chicago Manual of Style (16th Edition):
Willder, Jennifer Mary. “Androgen receptor phosphorylation in prostate diseases.” 2014. Doctoral Dissertation, University of Glasgow. Accessed March 06, 2021.
http://theses.gla.ac.uk/5797/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.646715.
MLA Handbook (7th Edition):
Willder, Jennifer Mary. “Androgen receptor phosphorylation in prostate diseases.” 2014. Web. 06 Mar 2021.
Vancouver:
Willder JM. Androgen receptor phosphorylation in prostate diseases. [Internet] [Doctoral dissertation]. University of Glasgow; 2014. [cited 2021 Mar 06].
Available from: http://theses.gla.ac.uk/5797/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.646715.
Council of Science Editors:
Willder JM. Androgen receptor phosphorylation in prostate diseases. [Doctoral Dissertation]. University of Glasgow; 2014. Available from: http://theses.gla.ac.uk/5797/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.646715
University of Glasgow
13.
Powell, Arfon Gethyn Morgan Tregellis.
The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer.
Degree: PhD, 2016, University of Glasgow
URL: http://theses.gla.ac.uk/7652/
;
http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.700320
► Colorectal cancer (CRC) is the third most common cancer in the UK with 41,000 new cases diagnosed in 2011. Despite undergoing potentially curative resection, a…
(more)
▼ Colorectal cancer (CRC) is the third most common cancer in the UK with 41,000 new cases diagnosed in 2011. Despite undergoing potentially curative resection, a significant amount of patients develop recurrence. Biomarkers that aid prognostication or identify patients who are suitable for adjuvant treatments are needed. The TNM staging system does a reasonably good job at offering prognostic information to the treating clinician, but it could be better and identifying methods of improving its accuracy are needed. Tumour progression is based on a complex relationship between tumour behaviour and the hosts’ inflammatory responses. Sustained tumour cell proliferation, evading growth suppressors, resisting apoptosis, replicative immortality, sustained angiogenesis, invasion & metastasis, avoiding immune destruction, deregulated cellular energetics, tumour promoting inflammation and genomic instability & mutation have been identified as hallmarks. These hallmarks are malignant behaviors are what makes the cell cancerous and the more extreme the behaviour the more aggressive the cancer the more likely the risk of a poor outcome. There are two primary genomic instability pathways: Microsatellite Instability (MSI) and Chromosomal Instability (CI) also referred to as Microsatellite Stability (MSS). Tumours arising by these pathways have a predilection for specific anatomical, histological and molecular biological features. It is possible that aberrant molecular expression of genes/proteins that promote malignant behaviors may also act as prognostic and predictive biomarkers, which may offer superior prognostic information to classical prognostic features. Cancer related inflammation has been described as a 7th hallmark of cancer. Despite the systemic inflammatory response (SIR) being associated with more aggressive malignant disease, infiltration by immune cells, particularly CD8+ lymphocytes, at the advancing edge of the tumour have been associated with improved outcome and tumour MSI. It remains unknown if the SIR is associated with tumour MSI and this requires further study. The mechanisms by which colorectal cancer cells locally invade through the bowel remain uncertain, but connective tissue degradation by matrix metalloproteinases (MMPs) such as MMP-9 have been implicated. MMP-9 has been found in the cancer cells, stromal cells and patient circulation. Although tumoural MMP-9 has been associated with poor survival, reports are conflicting and contain relatively small sample sizes. Furthermore, the influence of high serum MMP-9 on survival remains unknown. Src family kinases (SFKs) have been implicated in many adverse cancer cell behaviors. SFKs comprise 9 family members BLK, C-SRC, FGR, FYN, HCK, LCK, LYN, YES, YRK. C-SRC has been the most investigated of all SFKs, but the role of other SFKs in cellular behaviors and their prognostic value remains largely unknown. The development of Src inhibitors, such as Dasatinib, has identified SFKs as a potential therapeutic target for patients at higher risk of poor survival.…
Subjects/Keywords: 616.99; RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer); RD Surgery
Record Details
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Record Details
Similar Records
Cite
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Powell, A. G. M. T. (2016). The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/7652/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.700320
Chicago Manual of Style (16th Edition):
Powell, Arfon Gethyn Morgan Tregellis. “The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer.” 2016. Doctoral Dissertation, University of Glasgow. Accessed March 06, 2021.
http://theses.gla.ac.uk/7652/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.700320.
MLA Handbook (7th Edition):
Powell, Arfon Gethyn Morgan Tregellis. “The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer.” 2016. Web. 06 Mar 2021.
Vancouver:
Powell AGMT. The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer. [Internet] [Doctoral dissertation]. University of Glasgow; 2016. [cited 2021 Mar 06].
Available from: http://theses.gla.ac.uk/7652/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.700320.
Council of Science Editors:
Powell AGMT. The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer. [Doctoral Dissertation]. University of Glasgow; 2016. Available from: http://theses.gla.ac.uk/7652/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.700320
University of Glasgow
14.
Patek, Samantha Clare.
Androgen receptor phosphorylation in prostate cancer.
Degree: PhD, 2018, University of Glasgow
URL: http://theses.gla.ac.uk/38914/
► Prostate cancer is the most common male cancer in the UK. Although incidence is increasing, prostate cancer mortality is decreasing, mainly owing to the over…
(more)
▼ Prostate cancer is the most common male cancer in the UK. Although incidence is increasing, prostate cancer mortality is decreasing, mainly owing to the over diagnosis of disease that would not have become clinically apparent during the patient’s lifetime. The gold-standard for prostate cancer diagnosis is transrectal ultrasound guided biopsy of the prostate. Whilst prostate biopsy can inform on diagnosis, it’s prognostic ultiltiy is poor. Currently clinicians lack pathological biomarkers to differentiate between patients with prostate cancer who have indolent disease that can be safely managed with surveillance strategies, and those who will go onto develop aggressive disease which requires early radical curative treatment.
Phosphorylation of the androgen receptor has been extensively investigated in relation to prostate cancer development and progression. Androgen receptor phosphorylation has been shown to regulate cellular localisation, transcriptional activity, cell growth and sensitivity to androgens in prostate cancer. However, only a small number of studies have investigated the prognostic significance of androgen receptor phosphorylation, and only consider a limited number of serine residues in clinical specimens.
The research presented in this thesis sought to investigate the prognostic and predictive significance of AR phosphorylation at serine 578 in hormone-naïve prostate cancer. It was hypothesised that pARS578 would be associated with poor outcomes in prostate cancer and may be utilised as a prognostic marker at diagnosis in prostate cancer and predict response to drug treatment with a PKC inhibitor. It was also hypothesised that PKC, the putative kinase for phosphorylation at serine 578, would be associated with poor outcomes and may offer a potential therapeutic target in prostate cancer.
In the current study, the phosphorylation site of primary interest was serine 578. Scansite 2.0, an online kinase search tool, predicted that PKC is the putative kinase mediating phosphorylation at serine 578 on the androgen receptor. Phosphorylation of the androgen receptor at serine 578 has been linked with increased AR transcriptional activity, cell growth, nuclear cytoplasmic shuttling, modulation of other AR phosphorylation sites and DNA-repair mechanisms. The prognostic significance of androgen receptor phosphorylation at serine 81 was also investigated in this study. Serine 81 is phosphorylated in response to DHT via an alternative pathway to that of serine 578. Serine 81 phosphorylation is associated with increased androgen receptor transcriptional activity and increased cell growth in prostate cancer. It was therefore hypothesised that androgen receptor phosphorylation at serine 578 and serine 81 would be associated with poor outcome measures in prostate cancer.
Immunohistochemical analysis was performed in a cohort of 105 hormone-naïve prostate cancer patients undergoing active surveillance, representing a cohort of patients with low-risk disease, as defined by current clinical markers…
Subjects/Keywords: RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer); RD Surgery
Record Details
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Share »
Record Details
Similar Records
Cite
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Patek, S. C. (2018). Androgen receptor phosphorylation in prostate cancer. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/38914/
Chicago Manual of Style (16th Edition):
Patek, Samantha Clare. “Androgen receptor phosphorylation in prostate cancer.” 2018. Doctoral Dissertation, University of Glasgow. Accessed March 06, 2021.
http://theses.gla.ac.uk/38914/.
MLA Handbook (7th Edition):
Patek, Samantha Clare. “Androgen receptor phosphorylation in prostate cancer.” 2018. Web. 06 Mar 2021.
Vancouver:
Patek SC. Androgen receptor phosphorylation in prostate cancer. [Internet] [Doctoral dissertation]. University of Glasgow; 2018. [cited 2021 Mar 06].
Available from: http://theses.gla.ac.uk/38914/.
Council of Science Editors:
Patek SC. Androgen receptor phosphorylation in prostate cancer. [Doctoral Dissertation]. University of Glasgow; 2018. Available from: http://theses.gla.ac.uk/38914/
University of Glasgow
15.
Powell, Arfon Gethyn Morgan Tregellis.
The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer.
Degree: PhD, 2016, University of Glasgow
URL: http://theses.gla.ac.uk/7652/
► Colorectal cancer (CRC) is the third most common cancer in the UK with 41,000 new cases diagnosed in 2011. Despite undergoing potentially curative resection, a…
(more)
▼ Colorectal cancer (CRC) is the third most common cancer in the UK with 41,000 new cases diagnosed in 2011. Despite undergoing potentially curative resection, a significant amount of patients develop recurrence. Biomarkers that aid prognostication or identify patients who are suitable for adjuvant treatments are needed. The TNM staging system does a reasonably good job at offering prognostic information to the treating clinician, but it could be better and identifying methods of improving its accuracy are needed.
Tumour progression is based on a complex relationship between tumour behaviour and the hosts’ inflammatory responses. Sustained tumour cell proliferation, evading growth suppressors, resisting apoptosis, replicative immortality, sustained angiogenesis, invasion & metastasis, avoiding immune destruction, deregulated cellular energetics, tumour promoting inflammation and genomic instability & mutation have been identified as hallmarks. These hallmarks are malignant behaviors are what makes the cell cancerous and the more extreme the behaviour the more aggressive the cancer the more likely the risk of a poor outcome.
There are two primary genomic instability pathways: Microsatellite Instability (MSI) and Chromosomal Instability (CI) also referred to as Microsatellite Stability (MSS). Tumours arising by these pathways have a predilection for specific anatomical, histological and molecular biological features. It is possible that aberrant molecular expression of genes/proteins that promote malignant behaviors may also act as prognostic and predictive biomarkers, which may offer superior prognostic information to classical prognostic features.
Cancer related inflammation has been described as a 7th hallmark of cancer. Despite the systemic inflammatory response (SIR) being associated with more aggressive malignant disease, infiltration by immune cells, particularly CD8+ lymphocytes, at the advancing edge of the tumour have been associated with improved outcome and tumour MSI. It remains unknown if the SIR is associated with tumour MSI and this requires further study.
The mechanisms by which colorectal cancer cells locally invade through the bowel remain uncertain, but connective tissue degradation by matrix metalloproteinases (MMPs) such as MMP-9 have been implicated. MMP-9 has been found in the cancer cells, stromal cells and patient circulation. Although tumoural MMP-9 has been associated with poor survival, reports are conflicting and contain relatively small sample sizes. Furthermore, the influence of high serum MMP-9 on survival remains unknown.
Src family kinases (SFKs) have been implicated in many adverse cancer cell behaviors. SFKs comprise 9 family members BLK, C-SRC, FGR, FYN, HCK, LCK, LYN, YES, YRK. C-SRC has been the most investigated of all SFKs, but the role of other SFKs in cellular behaviors and their prognostic value remains largely unknown. The development of Src inhibitors, such as Dasatinib, has identified SFKs as a potential therapeutic target for patients at higher risk of…
Subjects/Keywords: RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer); RD Surgery
Record Details
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Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Powell, A. G. M. T. (2016). The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/7652/
Chicago Manual of Style (16th Edition):
Powell, Arfon Gethyn Morgan Tregellis. “The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer.” 2016. Doctoral Dissertation, University of Glasgow. Accessed March 06, 2021.
http://theses.gla.ac.uk/7652/.
MLA Handbook (7th Edition):
Powell, Arfon Gethyn Morgan Tregellis. “The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer.” 2016. Web. 06 Mar 2021.
Vancouver:
Powell AGMT. The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer. [Internet] [Doctoral dissertation]. University of Glasgow; 2016. [cited 2021 Mar 06].
Available from: http://theses.gla.ac.uk/7652/.
Council of Science Editors:
Powell AGMT. The role of cancer related inflammation, Src family kinases and matrix metalloproteinase 9 in colorectal cancer. [Doctoral Dissertation]. University of Glasgow; 2016. Available from: http://theses.gla.ac.uk/7652/
East Carolina University
16.
Yu, Zhou.
THE EFFECTS OF ACIDIC TUMOR MICROENVIRONMENT ON LYMPHOMA CELL RESPONSES TO CHEMOTHERAPEUTICS.
Degree: MS, Biomedical Sciences, 2014, East Carolina University
URL: http://hdl.handle.net/10342/4734
► Acidic tumor microenvironment exists in many types of cancer. Altered glycolytic metabolism of tumor cells and deficient blood supply in tissues are major causes for…
(more)
▼ Acidic tumor microenvironment exists in many types of cancer. Altered glycolytic metabolism of tumor cells and deficient blood supply in tissues are major causes for this phenomenon. Lymphoma cells may have different responses to chemotherapeutics when they are exposed to acidic tumor microenvironment. Bortezomib (BTZ) is a chemotherapeutic drug already approved by FDA for treating multiple myeloma and mantle cell lymphoma, which can inhibit the 26S proteasome and block the protein degradation process. Ramos parental cells (Human Burkitt's lymphoma cell line) and BTZ-resistant Ramos cells (obtained after chronic selection using low concentration of BTZ) were used in the study. Cells were treated from 2h to 24h with RPMI culture media buffered to pH 7.4 and pH 6.4, with or without chemical therapeutics. Cancer therapeutics tested in this study were BTZ, Cyclophosphamide, Doxorubicin, and ABT-737. MTT assay was utilized to detect cell viability under each treatment condition. Flow cytometry was used to examine changes on apoptosis and cell cycle. Western blots were performed to measure the changes of cellular protein levels. The MTT assays showed the acidic microenvironment could decrease cell proliferation rate, and if combined with BTZ treatment it could notably increase the cytotoxic efficacy of BTZ. After chronic selection under low concentration of BTZ, BTZ-resistant Ramos cells were obtained and were able to survive and grow in the presence of BTZ. However, acidic pH with BTZ could sensitize the BTZ-Resistant Ramos cells to BTZ again. Apoptosis assays demonstrated that acidic pH itself did not significantly induce cell apoptosis within 24h. But the combination of acidic pH with BTZ treatment caused much more apoptosis than BTZ alone. Cell cycle analysis showed that acidic pH could block the cell cycle, which led to cell cycle arrest and reduced percentage of cells in the G2/M phase. Western blots illustrated that acidic pH alone could upregulate the level of p53, Phospho-p53 at Ser15, Phospho-CHK1, Phospho-CHK2, pro-apoptotic proteins of the mitochondrial Bcl-2 family, and the pro-apoptotic Caspase family. In addition, if combined with BTZ treatment, acidosis could further increase phosphorylation of p53 at Ser15, expression of the Bcl-2 family proteins, and level of cleaved caspases. In conclusion, the combination of acidosis and BTZ treatment induce higher level of apoptosis and decrease Ramos cell proliferation. Our study demonstrates that arrested cell proliferation and increased apoptosis occur by the inhibition of cell cycle regulators and the activation of p53-mitochondria-caspase apoptosis pathways respectively. Â
Advisors/Committee Members: Yang, Li (advisor).
Subjects/Keywords: Biology; Oncology; Acidosis; Chemotherapeutics; Lymphoma; Tumor microenvironment; Neoplasms – physiopathology; Lymphoma – pathology
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Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Yu, Z. (2014). THE EFFECTS OF ACIDIC TUMOR MICROENVIRONMENT ON LYMPHOMA CELL RESPONSES TO CHEMOTHERAPEUTICS. (Masters Thesis). East Carolina University. Retrieved from http://hdl.handle.net/10342/4734
Chicago Manual of Style (16th Edition):
Yu, Zhou. “THE EFFECTS OF ACIDIC TUMOR MICROENVIRONMENT ON LYMPHOMA CELL RESPONSES TO CHEMOTHERAPEUTICS.” 2014. Masters Thesis, East Carolina University. Accessed March 06, 2021.
http://hdl.handle.net/10342/4734.
MLA Handbook (7th Edition):
Yu, Zhou. “THE EFFECTS OF ACIDIC TUMOR MICROENVIRONMENT ON LYMPHOMA CELL RESPONSES TO CHEMOTHERAPEUTICS.” 2014. Web. 06 Mar 2021.
Vancouver:
Yu Z. THE EFFECTS OF ACIDIC TUMOR MICROENVIRONMENT ON LYMPHOMA CELL RESPONSES TO CHEMOTHERAPEUTICS. [Internet] [Masters thesis]. East Carolina University; 2014. [cited 2021 Mar 06].
Available from: http://hdl.handle.net/10342/4734.
Council of Science Editors:
Yu Z. THE EFFECTS OF ACIDIC TUMOR MICROENVIRONMENT ON LYMPHOMA CELL RESPONSES TO CHEMOTHERAPEUTICS. [Masters Thesis]. East Carolina University; 2014. Available from: http://hdl.handle.net/10342/4734
University of Glasgow
17.
Willder, Jennifer Mary.
Androgen receptor phosphorylation in prostate diseases.
Degree: PhD, 2014, University of Glasgow
URL: http://theses.gla.ac.uk/5797/
► Prostatic diseases are common; benign prostate hyperplasia (BPH) is almost ubiquitous in elderly men and 899,000 men were diagnosed with prostate cancer worldwide in 2008.…
(more)
▼ Prostatic diseases are common; benign prostate hyperplasia (BPH) is almost ubiquitous in elderly men and 899,000 men were diagnosed with prostate cancer worldwide in 2008. The incidence of both is increasing and expected to continue to rise. Therefore, prostatic diseases represent a considerable economic burden, but there are currently no reliable markers available to accurately differentiate indolent from aggressive disease nor to predict who will benefit from treatment for either BPH or prostate cancer. This results in over and under-treatment of both diseases with consequent patient related morbidity and mortality.
The molecular mechanisms underlying the natural history of prostatic diseases remain elusive. It is accepted that prostate cell growth and survival are exquisitely dependent upon activation of the androgen receptor (AR) by androgens. Following ligand binding, AR undergoes further phosphorylation at serine residues, which inhibit proteolytic degradation, stabilise AR and influence AR transactivation. It is therefore plausible that alterations in AR phosphorylation may drive prostatic disease progression. However, few studies have explored the significance of AR phosphorylation, or the kinases driving AR serine phosphorylation in the clinical setting.
The over-riding objective of this study was to establish the clinical relevance of AR serine phosphorylation status in prostate tissue in both BPH and prostate cancer. The specific aims of the current study were:
• To firstly establish and validate a panel of AR phosphospecific antibodies.
• To evaluate site specific AR serine phosphorylation expression levels in prostate cancer and BPH patient cohorts, with full clinical data and follow-up.
• To investigate the expression of candidate kinases mediating such phosphorylation.
This involved establishing tissue banks with linked comprehensive clinical databases, and utilising this tissue to establish AR phosphorylation expression profiles for each patient.
Six AR phosphospecific antibodies (pARS81, pARS94, pARS213, pARS515, pARS578, pARS650) were verified using peptide competition assays and western blotting. Cdk1, ERK1/2, Akt and PKC were identified as putative kinases mediating AR phosphorylation using the online kinase search tool Scansite 2.0.
Immunohistochemistry was performed on hormone naïve diagnostic prostate cancer tissue relating to 90 patients. High expression levels of AR phosphorylation at serine sites 81, 515 and 578 were each associated with a poorer clinical outcome. Following cox regression analysis, cytoplasmic pARS515 expression (p=0.038, HR 4.5 (95% CI 1.1–20.6)) and pARS81 nuclear expression (p=0.030, HR 0.033 95% CI 0.002-0.721) were independently associated with shorter time to biochemical relapse and shorter disease specific survival respectively. Cdk1 and/or pCdk1161 were significantly associated with pARS81 and pARS515 as predicted by Scansite 2.0. Similarly, nuclear PKC expression was significantly associated with pARS578 expression both in the cytoplasm and the…
Subjects/Keywords: RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer); RD Surgery
Record Details
Similar Records
Cite
Share »
Record Details
Similar Records
Cite
« Share
❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Willder, J. M. (2014). Androgen receptor phosphorylation in prostate diseases. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/5797/
Chicago Manual of Style (16th Edition):
Willder, Jennifer Mary. “Androgen receptor phosphorylation in prostate diseases.” 2014. Doctoral Dissertation, University of Glasgow. Accessed March 06, 2021.
http://theses.gla.ac.uk/5797/.
MLA Handbook (7th Edition):
Willder, Jennifer Mary. “Androgen receptor phosphorylation in prostate diseases.” 2014. Web. 06 Mar 2021.
Vancouver:
Willder JM. Androgen receptor phosphorylation in prostate diseases. [Internet] [Doctoral dissertation]. University of Glasgow; 2014. [cited 2021 Mar 06].
Available from: http://theses.gla.ac.uk/5797/.
Council of Science Editors:
Willder JM. Androgen receptor phosphorylation in prostate diseases. [Doctoral Dissertation]. University of Glasgow; 2014. Available from: http://theses.gla.ac.uk/5797/
University of Birmingham
18.
Ploumakis, Athanasios.
Characterisation of the cellular response to defective translational termination.
Degree: d_ph, College of Medical & Dental Sciences, 2018, University of Birmingham
URL: http://etheses.bham.ac.uk//id/eprint/8081/
► Enzymatic hydroxylation of varied cellular substrates is catalyzed by the 2-oxoglutarate and Fe(II) dependent 2-oxoglutrate (OG) oxygenase group of proteins. These enzymes control gene expression,…
(more)
▼ Enzymatic hydroxylation of varied cellular substrates is catalyzed by the 2-oxoglutarate and Fe(II) dependent 2-oxoglutrate (OG) oxygenase group of proteins. These enzymes control gene expression, from epigenetics to splicing and translation. The 2OG oxygenase JMJD4 has been shown to catalyse the hydroxylation of the eukaryotic omnipotent termination factor 1 (eRF1), and is essential for optimal translational termination. In this thesis, we expand on previous work by examining two further potential binding partners of JMJD4, GTF2I and TCP1-γ. Subsequently, we find that depletion of JMJD4 and eRF1 is associated with growth reduction in cancer cell lines in 2D and 3D. The transcriptomic changes in response to eRF1 depletion are then assessed by RNA-Seq. Among the potential pathways identified, downstream targets of the transcription factor ATF4 were most prominent. Upregulation of ATF4 and its downstream targets was validated in an eRF1 rescue system and the contribution of specific subdomains of eRF1 to the transcriptional response assessed, indicating multiple arms of the unfolded protein response being upregulated downstream of defective translational termination. The implications of our findings and their relevance in wider biological and disease contexts, including cancer, is finally discussed.
Subjects/Keywords: RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer)
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Record Details
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ploumakis, A. (2018). Characterisation of the cellular response to defective translational termination. (Thesis). University of Birmingham. Retrieved from http://etheses.bham.ac.uk//id/eprint/8081/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Ploumakis, Athanasios. “Characterisation of the cellular response to defective translational termination.” 2018. Thesis, University of Birmingham. Accessed March 06, 2021.
http://etheses.bham.ac.uk//id/eprint/8081/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Ploumakis, Athanasios. “Characterisation of the cellular response to defective translational termination.” 2018. Web. 06 Mar 2021.
Vancouver:
Ploumakis A. Characterisation of the cellular response to defective translational termination. [Internet] [Thesis]. University of Birmingham; 2018. [cited 2021 Mar 06].
Available from: http://etheses.bham.ac.uk//id/eprint/8081/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Ploumakis A. Characterisation of the cellular response to defective translational termination. [Thesis]. University of Birmingham; 2018. Available from: http://etheses.bham.ac.uk//id/eprint/8081/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Nottingham
19.
Alhazmi, Safiah.
Assessing the relationship between DNA methylation and gene expression in germ cell tumours.
Degree: PhD, 2016, University of Nottingham
URL: http://eprints.nottingham.ac.uk/31981/
;
http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698011
► Germ cell tumours (GCTs) are a class of tumours classified histologically into two main types: seminoma and non-seminoma. Prior studies revealed that there is a…
(more)
▼ Germ cell tumours (GCTs) are a class of tumours classified histologically into two main types: seminoma and non-seminoma. Prior studies revealed that there is a significant difference in global DNA methylation between those two types, where non-seminomas represent more differentiated cells and exhibit a high level of methylation compared with seminomas that resemble the precursor cells of GCTs. A number of studies have reported that silencing of genes by DNA methylation is a common phenomenon in many types of cancer. However, the silenced genes and the genomic targets that are methylated in GCTs have not yet been systematically identified. Furthermore, many methylation studies in GCTs do not include the level of gene expression in their investigation. We hypothesized that the methylation of genes might play an important role in gene silencing in GCTs, so the main focus of this thesis was studying the relationship between the gene methylation and gene expression in GCT cell lines representing seminoma and non-seminoma. We analysed genome methylation and gene expression of these cell lines using the Illumina infinium Human Methylome 450 bead chip system and Affymetrix Gene Chip Human Genome U133 Plus 2.0 arrays, respectively. We also compared our results with gene expression data from primary tumours in order to identify which events were shared in primary GCTs tumour. qPCR analysis was carried out after treatment of cells with the demethylation agent, 5-aza-2-deoxycytidine, to confirm that expression of identified genes was regulated by methylation. These analyses showed that differential methylation of CpG islands between seminoma and non-seminoma cell lines correlated well with differential gene expression and revealed that hypermethylation of CpG islands near the transcriptional start site was more strongly correlated with low gene expression than was methylation of other regions. Meanwhile, methylation analysis identified uniquely methylated genes and features for each cell line, which may imply an underlying mechanism of their development. One-hundred and forty-seven silenced genes which exhibited a difference in methylation and expression between seminoma and non-seminoma cell lines were identified, some of these genes were also differentially expressed in primary tumours. Re-expression of selected silenced genes in non-seminoma cells after treatment with 5-aza-2-deoxycytidine confirmed that methylation played a role in gene silencing. Some of the genes identified are closely associated with pluripotency and implicated in chemosensitivity (PRDM14, KLF4, TDRD12, DDX43, MNS1, and RBMXL2). Silencing of these genes could therefore account for the progression process from seminoma to non-seminoma. PRDM14 was given special attention as it plays an important role in germ cell development and maintenance of germ cell pluripotency. The role of PRDM14 in GCT biology was studied, revealing that high expression of PRDM14 in combination with 5-aza-2-deoxycytidine treatment increased the response of cells to chemotherapy…
Subjects/Keywords: 616.99; QZ Pathology; RC 254 Neoplasms. Tumors. Oncology (including Cancer)
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APA (6th Edition):
Alhazmi, S. (2016). Assessing the relationship between DNA methylation and gene expression in germ cell tumours. (Doctoral Dissertation). University of Nottingham. Retrieved from http://eprints.nottingham.ac.uk/31981/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698011
Chicago Manual of Style (16th Edition):
Alhazmi, Safiah. “Assessing the relationship between DNA methylation and gene expression in germ cell tumours.” 2016. Doctoral Dissertation, University of Nottingham. Accessed March 06, 2021.
http://eprints.nottingham.ac.uk/31981/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698011.
MLA Handbook (7th Edition):
Alhazmi, Safiah. “Assessing the relationship between DNA methylation and gene expression in germ cell tumours.” 2016. Web. 06 Mar 2021.
Vancouver:
Alhazmi S. Assessing the relationship between DNA methylation and gene expression in germ cell tumours. [Internet] [Doctoral dissertation]. University of Nottingham; 2016. [cited 2021 Mar 06].
Available from: http://eprints.nottingham.ac.uk/31981/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698011.
Council of Science Editors:
Alhazmi S. Assessing the relationship between DNA methylation and gene expression in germ cell tumours. [Doctoral Dissertation]. University of Nottingham; 2016. Available from: http://eprints.nottingham.ac.uk/31981/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.698011
University of Glasgow
20.
Leach, Joshua.
Investigating right-sided colon cancer and the involvement of inflammation, the microbiome, and foetal stem cell-like plasticity.
Degree: PhD, 2021, University of Glasgow
URL: http://theses.gla.ac.uk/81917/
► Human right-sided colorectal cancer (CRC) has a poor prognosis and distinct mutational profile compared with left-sided CRC. Indeed right-sided CRCs are associated with BRAF mutations…
(more)
▼ Human right-sided colorectal cancer (CRC) has a poor prognosis and distinct mutational profile compared with left-sided CRC. Indeed right-sided CRCs are associated with BRAF mutations and aberrations in both the mismatch repair and TGF signalling pathways, whilst left-sided CRCs are associated with APC and TP53 mutations.
In chapter III I establish a mouse model of right-sided colon cancer driven by activation of BRAF and loss of TGF-receptor signalling. Furthermore I confirm that this model reproduces a number of the key stereotypical clinicopathological behaviours observed in right-sided tumours in patients, particularly the lack of Wnt pathway activation.
In chapter IV I show that these tumours, though lacking Wnt pathway activation, exhibit a foetal-like phenotype (Ly6a+). This phenotype, also recently recognised in the context of colitis associated intestinal regeneration, had initially been identified in the foetal intestine and characterised by the absence of Lgr5 expression and expression of markers including Ly6a. Following the identification of this epithelial differentiation status in the murine right-sided tumours, I also showed that this phenotype is present in patient derived right-sided CRCs and that the gene expression pattern associated with these murine tumours is predictive of the key clinicopathological features of right-sided disease.
In chapter V and VI I show that this foetal-like phenotype is due to the direct activation of YAP1 by MAPK signalling, and that the phenotype is further amplified by microenvironmentally driven inflammation. Importantly I also confirm that the tumorigenic potential of this foetal-like epithelial population, whether driven by MAPK-dependent or independent mechanisms, is uniquely suppressed by epithelial TGF signalling. Finally I also confirm that YAP1 activation is vital for the ongoing viability of these foetal-like epithelial populations and that they have unique growth requirements (e.g. prostaglandin E2) that potentially provide the possibility for novel targeted therapeutic strategies in patients with right-sided disease.
Subjects/Keywords: RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer)
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APA (6th Edition):
Leach, J. (2021). Investigating right-sided colon cancer and the involvement of inflammation, the microbiome, and foetal stem cell-like plasticity. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/81917/
Chicago Manual of Style (16th Edition):
Leach, Joshua. “Investigating right-sided colon cancer and the involvement of inflammation, the microbiome, and foetal stem cell-like plasticity.” 2021. Doctoral Dissertation, University of Glasgow. Accessed March 06, 2021.
http://theses.gla.ac.uk/81917/.
MLA Handbook (7th Edition):
Leach, Joshua. “Investigating right-sided colon cancer and the involvement of inflammation, the microbiome, and foetal stem cell-like plasticity.” 2021. Web. 06 Mar 2021.
Vancouver:
Leach J. Investigating right-sided colon cancer and the involvement of inflammation, the microbiome, and foetal stem cell-like plasticity. [Internet] [Doctoral dissertation]. University of Glasgow; 2021. [cited 2021 Mar 06].
Available from: http://theses.gla.ac.uk/81917/.
Council of Science Editors:
Leach J. Investigating right-sided colon cancer and the involvement of inflammation, the microbiome, and foetal stem cell-like plasticity. [Doctoral Dissertation]. University of Glasgow; 2021. Available from: http://theses.gla.ac.uk/81917/
University of Glasgow
21.
Patek, Samantha Clare.
Androgen receptor phosphorylation in prostate cancer.
Degree: PhD, 2018, University of Glasgow
URL: http://theses.gla.ac.uk/38914/
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.761935
► Prostate cancer is the most common male cancer in the UK. Although incidence is increasing, prostate cancer mortality is decreasing, mainly owing to the over…
(more)
▼ Prostate cancer is the most common male cancer in the UK. Although incidence is increasing, prostate cancer mortality is decreasing, mainly owing to the over diagnosis of disease that would not have become clinically apparent during the patient’s lifetime. The gold-standard for prostate cancer diagnosis is transrectal ultrasound guided biopsy of the prostate. Whilst prostate biopsy can inform on diagnosis, it’s prognostic ultiltiy is poor. Currently clinicians lack pathological biomarkers to differentiate between patients with prostate cancer who have indolent disease that can be safely managed with surveillance strategies, and those who will go onto develop aggressive disease which requires early radical curative treatment. Phosphorylation of the androgen receptor has been extensively investigated in relation to prostate cancer development and progression. Androgen receptor phosphorylation has been shown to regulate cellular localisation, transcriptional activity, cell growth and sensitivity to androgens in prostate cancer. However, only a small number of studies have investigated the prognostic significance of androgen receptor phosphorylation, and only consider a limited number of serine residues in clinical specimens. The research presented in this thesis sought to investigate the prognostic and predictive significance of AR phosphorylation at serine 578 in hormone-naïve prostate cancer. It was hypothesised that pARS578 would be associated with poor outcomes in prostate cancer and may be utilised as a prognostic marker at diagnosis in prostate cancer and predict response to drug treatment with a PKC inhibitor. It was also hypothesised that PKC, the putative kinase for phosphorylation at serine 578, would be associated with poor outcomes and may offer a potential therapeutic target in prostate cancer. In the current study, the phosphorylation site of primary interest was serine 578. Scansite 2.0, an online kinase search tool, predicted that PKC is the putative kinase mediating phosphorylation at serine 578 on the androgen receptor. Phosphorylation of the androgen receptor at serine 578 has been linked with increased AR transcriptional activity, cell growth, nuclear cytoplasmic shuttling, modulation of other AR phosphorylation sites and DNA-repair mechanisms. The prognostic significance of androgen receptor phosphorylation at serine 81 was also investigated in this study. Serine 81 is phosphorylated in response to DHT via an alternative pathway to that of serine 578. Serine 81 phosphorylation is associated with increased androgen receptor transcriptional activity and increased cell growth in prostate cancer. It was therefore hypothesised that androgen receptor phosphorylation at serine 578 and serine 81 would be associated with poor outcome measures in prostate cancer. Immunohistochemical analysis was performed in a cohort of 105 hormone-naïve prostate cancer patients undergoing active surveillance, representing a cohort of patients with low-risk disease, as defined by current clinical markers such as PSA and…
Subjects/Keywords: 616.99; RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer); RD Surgery
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APA (6th Edition):
Patek, S. C. (2018). Androgen receptor phosphorylation in prostate cancer. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/38914/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.761935
Chicago Manual of Style (16th Edition):
Patek, Samantha Clare. “Androgen receptor phosphorylation in prostate cancer.” 2018. Doctoral Dissertation, University of Glasgow. Accessed March 06, 2021.
http://theses.gla.ac.uk/38914/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.761935.
MLA Handbook (7th Edition):
Patek, Samantha Clare. “Androgen receptor phosphorylation in prostate cancer.” 2018. Web. 06 Mar 2021.
Vancouver:
Patek SC. Androgen receptor phosphorylation in prostate cancer. [Internet] [Doctoral dissertation]. University of Glasgow; 2018. [cited 2021 Mar 06].
Available from: http://theses.gla.ac.uk/38914/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.761935.
Council of Science Editors:
Patek SC. Androgen receptor phosphorylation in prostate cancer. [Doctoral Dissertation]. University of Glasgow; 2018. Available from: http://theses.gla.ac.uk/38914/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.761935
22.
Bispo Júnior, Rosalvo Zosimo.
Fatores prognósticos da sobrevida no osteossarcoma primário: grau I versus II de Huvos.
Degree: PhD, Ortopedia e Traumatologia, 2009, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/5/5140/tde-24022010-153548/
;
► O objetivo deste trabalho foi comparar o prognóstico de sobrevida da graduação histológica após efeito da quimioterapia (graus I versus II de Huvos), visando também…
(more)
▼ O objetivo deste trabalho foi comparar o prognóstico de sobrevida da graduação histológica após efeito da quimioterapia (graus I versus II de Huvos), visando também identificar fatores prognósticos no que diz respeito à sobrevida livre de recidiva local (SLRL), sobrevida livre de metástase (SLM) e sobrevida global (SG), em pacientes portadores de osteossarcoma primário não metastático ao diagnóstico. Vinte e quatro entre 45 pacientes admitidos no Instituto de Ortopedia e Traumatologia do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo IOT/HC/FMUSP, entre 2000 e 2004, foram eleitos para o estudo, segundo os critérios de inclusão e exclusão utilizados. As probabilidades de sobrevida acumuladas foram feitas pela técnica de Kaplan-Meier e os índices I e II de HUVOS comparados pelos testes de Log Rank. A análise multivariada foi feita pela técnica de regressão logística com modelo de risco proporcional de COX e a validade estatística estabelecida para valores de p<0,05. Os graus I e II de Huvos, quando comparados, não foram considerados de valor prognóstico em nenhuma das sobrevidas estudadas (SLRL, SLM e SG). Os fatores adversos que influenciaram o risco de recidiva local e a sobrevida global, na análise univariada foram: subtipo histológico diferente do osteoblástico (p=0,017) e o tamanho tumoral maior que 15 cm (p=0,048). Em relação à SLM o subtipo não osteoblástico (p=0,007) teve um pior prognóstico. O subtipo histológico manteve sua significância na análise multivariada em todas as sobrevidas estudadas
The purpose of this study was to compare the prognostic of survivor of histologic graduation post chemotherapy (Huvos´s grade I versus II), aiming to identify prognostic factors concerning to local recurrence free survival (LRFS), metastases free survival (MFS) and overall survival (OS) in patients with nonmetastatic primary osteosarcoma. This study included 24 patients registred in the Instituto de Ortopedia e Traumatologia do Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo - Brazil, from 2000 to 2004. Survivor rates were calculed using Kaplan-Meier method. Huvos´s grade (I e II) were compared using the Log Rank test. Cox proportional hazards model was used for multifatorial analysis. Statistical significance was defined as a p value less than 0, 05. The Huvos´s grade I versus II was not significant factor for LRFS, MFS or OS. The adverse factors for LRFS and OS in univariate analysis were nonosteoblastic histologic subtypes (p=0,017) and large tumor (p=0,048). For MFS nonosteoblastic histologic subtypes (p=0,007) had worse prognostic. The histologic subtypes maintained their significance in multivariate testing on all studied survivor
Advisors/Committee Members: Camargo, Olavo Pires de.
Subjects/Keywords: Bone neoplasms/drug therapy; Bone neoplasms/epidemiology; Bone neoplasms/pathology; Bone neoplasms/surgery; Neoplasias ósseas/cirurgia; Neoplasias ósseas/epidemiologia; Neoplasias ósseas/patologia; Neoplasias ósseas/quimioterapia
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APA ·
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APA (6th Edition):
Bispo Júnior, R. Z. (2009). Fatores prognósticos da sobrevida no osteossarcoma primário: grau I versus II de Huvos. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5140/tde-24022010-153548/ ;
Chicago Manual of Style (16th Edition):
Bispo Júnior, Rosalvo Zosimo. “Fatores prognósticos da sobrevida no osteossarcoma primário: grau I versus II de Huvos.” 2009. Doctoral Dissertation, University of São Paulo. Accessed March 06, 2021.
http://www.teses.usp.br/teses/disponiveis/5/5140/tde-24022010-153548/ ;.
MLA Handbook (7th Edition):
Bispo Júnior, Rosalvo Zosimo. “Fatores prognósticos da sobrevida no osteossarcoma primário: grau I versus II de Huvos.” 2009. Web. 06 Mar 2021.
Vancouver:
Bispo Júnior RZ. Fatores prognósticos da sobrevida no osteossarcoma primário: grau I versus II de Huvos. [Internet] [Doctoral dissertation]. University of São Paulo; 2009. [cited 2021 Mar 06].
Available from: http://www.teses.usp.br/teses/disponiveis/5/5140/tde-24022010-153548/ ;.
Council of Science Editors:
Bispo Júnior RZ. Fatores prognósticos da sobrevida no osteossarcoma primário: grau I versus II de Huvos. [Doctoral Dissertation]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/5/5140/tde-24022010-153548/ ;
23.
Agrawal, Anshu.
Expression of Leukemia/Lymphoma Related Factor (LRF) in Human Breast Carcinoma.
Degree: PhD, Biomedical Sciences (graduate program), 2008, Creighton University
URL: http://hdl.handle.net/10504/84
► The pox-virus zinc finger protein (POZ-ZF), also termed leukemia/lymphoma related factor (LRF) belongs to the POK family of transcriptional repressors, which is also known as…
(more)
▼ The pox-virus zinc finger protein (POZ-ZF), also termed leukemia/lymphoma related factor (LRF) belongs to the POK family of transcriptional repressors, which is also known as POK erythroid myeloid ontogenic factor (Pokemon), factor binding to short transcripts of HIV-1 (FBI-1), and TTF-1 interacting peptide (TIP21). Its oncogenic role is known only in lymphoma, non-small cell lung carcinoma, and malignant gliomas. The functional expression of LRF in human breast carcinoma has not been confirmed. The aim of this study was to investigate the expression of LRF and propose a mechanism for its function in human breast carcinoma. |The expression of LRF mRNA transcripts and protein in human breast biopsy tissues was quantified by RT-PCR and western blotting. All malignant breast tissues expressed significantly more LRF mRNA transcripts and total protein than the benign breast tissues. LRF expression was also observed in human colon, renal, lung, hepatocellular, mesothelioma, and thymoma carcinomas. In general, a significantly higher expression of LRF was seen in malignant tissue than in the corresponding benign or normal tissue. |LRF expression was high in four of five breast cell lines. Its expression was significantly increased in response to IGF-1, TGF-β1, and TGF-β2 but not EGF. Overexpressed LRF significantly increased TGF-βRII and Smad4 expression. It also activated and interacted with the active p65 subunit of NF-κB. Overexpressed LRF also upregulated the expression of the cyclin A, down- regulated p21CIP/WAF expression and induced cell cycle arrest in the G2 phase. Further studies are warranted to determine the malignant or proliferative role of LRF in human breast carcinoma.
Advisors/Committee Members: Murphy, Richard F. (advisor), Agrawal, Anshu (cuauthor).
Subjects/Keywords: DNA-Binding Proteins; Breast Neoplasms – genetics; Breast Neoplasms – pathology
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APA (6th Edition):
Agrawal, A. (2008). Expression of Leukemia/Lymphoma Related Factor (LRF) in Human Breast Carcinoma. (Doctoral Dissertation). Creighton University. Retrieved from http://hdl.handle.net/10504/84
Chicago Manual of Style (16th Edition):
Agrawal, Anshu. “Expression of Leukemia/Lymphoma Related Factor (LRF) in Human Breast Carcinoma.” 2008. Doctoral Dissertation, Creighton University. Accessed March 06, 2021.
http://hdl.handle.net/10504/84.
MLA Handbook (7th Edition):
Agrawal, Anshu. “Expression of Leukemia/Lymphoma Related Factor (LRF) in Human Breast Carcinoma.” 2008. Web. 06 Mar 2021.
Vancouver:
Agrawal A. Expression of Leukemia/Lymphoma Related Factor (LRF) in Human Breast Carcinoma. [Internet] [Doctoral dissertation]. Creighton University; 2008. [cited 2021 Mar 06].
Available from: http://hdl.handle.net/10504/84.
Council of Science Editors:
Agrawal A. Expression of Leukemia/Lymphoma Related Factor (LRF) in Human Breast Carcinoma. [Doctoral Dissertation]. Creighton University; 2008. Available from: http://hdl.handle.net/10504/84
24.
Steg, Adam.
Analysis of the hedgehog pathway in pancreatic adenocarcinoma.
Degree: PhD, 2008, University of Alabama – Birmingham
URL: http://contentdm.mhsl.uab.edu/u?/etd,290
► Pancreatic adenocarcinoma (PAC) is the fourth leading cause of cancer mortality in the United States. Despite the use of highly aggressive treatment regimens (surgery, chemotherapy…
(more)
▼ Pancreatic adenocarcinoma (PAC) is the fourth leading cause of cancer mortality in the United States. Despite the use of highly aggressive treatment regimens (surgery, chemotherapy and radiation), almost all patients succumb to metastatic disease within 6-10 months of diagnosis. The hedgehog (HH) signaling pathway was originally discov-ered to play a critical role in mammalian embryological development. Interestingly, re-cent studies have suggested that aberrant expression of this pathway is involved in the initiation and continued growth of PAC. Small molecules that antagonize the transmem-brane protein Smoothened (Smo), a critical signaling component of the HH pathway, have proven effective in decreasing PAC growth both in vitro and in vivo and show promise as a new therapeutic strategy. Data from our laboratory indicate the HH path-way is overexpressed in pancreatic cancers and Smo antagonism decreases pancreatic cancer cell growth in vitro. The major accomplishments of this dissertation research in-clude (1) the validation of a recently developed technique known as Taqman low-density array (TLDA) which can be used to analyze the expression of multiple genes in a single RNA sample, (2) the identification of novel, tumor-associated genes through an extensive characterization of the HH pathway and its transcriptional targets in PAC clinical speci-mens (both surgically resected tissues and fine-needle biopsies) and (3) the identification of genes associated with in vitro response to cyclopamine, a selective HH pathway inhibi-tor, in human pancreatic cancer cell lines. These findings contribute to the growing characterization of the HH pathway in pancreatic cancer etiology and may provide a basis for future clinical applications in which PAC patients most likely to respond to HH pathway antagonists could be identified based upon gene expression profiling, thereby maximizing the efficacy of this type of therapy.
xiii, 149 p. : ill., digital, PDF file
Pharmacology and Toxicology
Joint Health Sciences
Hedgehog
Pancreatic Cancer
GLI3
UNRESTRICTED
Advisors/Committee Members: Johnson, Martin R., Buchsbaum, Donald J.<br>, Frost, Andra R.<br>, Ruppert, J. Michael <br>, Smith, Jeffrey B..
Subjects/Keywords: Adenocarcinoma – metabolism <; br>;
Adenocarcinoma – pathology <; br>;
Hedgehog Proteins – metabolism <; br>;
Pancreatic Neoplasms – metabolism <; br>;
Pancreatic Neoplasms – pathology
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APA ·
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APA (6th Edition):
Steg, A. (2008). Analysis of the hedgehog pathway in pancreatic adenocarcinoma. (Doctoral Dissertation). University of Alabama – Birmingham. Retrieved from http://contentdm.mhsl.uab.edu/u?/etd,290
Chicago Manual of Style (16th Edition):
Steg, Adam. “Analysis of the hedgehog pathway in pancreatic adenocarcinoma.” 2008. Doctoral Dissertation, University of Alabama – Birmingham. Accessed March 06, 2021.
http://contentdm.mhsl.uab.edu/u?/etd,290.
MLA Handbook (7th Edition):
Steg, Adam. “Analysis of the hedgehog pathway in pancreatic adenocarcinoma.” 2008. Web. 06 Mar 2021.
Vancouver:
Steg A. Analysis of the hedgehog pathway in pancreatic adenocarcinoma. [Internet] [Doctoral dissertation]. University of Alabama – Birmingham; 2008. [cited 2021 Mar 06].
Available from: http://contentdm.mhsl.uab.edu/u?/etd,290.
Council of Science Editors:
Steg A. Analysis of the hedgehog pathway in pancreatic adenocarcinoma. [Doctoral Dissertation]. University of Alabama – Birmingham; 2008. Available from: http://contentdm.mhsl.uab.edu/u?/etd,290
Texas Medical Center
25.
Salazar, Katrina.
TAZ AS A REGULATOR OF MESENCHYMAL TRANSFORMATION AND CLINICAL AGGRESSIVENESS IN GLIOMAS.
Degree: PhD, 2012, Texas Medical Center
URL: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/229
► Glioblastoma multiforme (GBM) is an aggressive, high grade brain tumor. Microarray studies have shown a subset of GBMs with a mesenchymal gene signature. This…
(more)
▼ Glioblastoma multiforme (GBM) is an aggressive, high grade brain tumor. Microarray studies have shown a subset of GBMs with a mesenchymal gene signature. This subset is associated with poor clinical outcome and resistance to treatment. To establish the molecular drivers of this mesenchymal transition, we correlated transcription factor expression to the mesenchymal signature and identified transcriptional co-activator with PDZ-binding motif (TAZ) to be highly associated with the mesenchymal shift. High TAZ expression correlated with worse clinical outcome and higher grade. These data led to the hypothesis that TAZ is critical to the mesenchymal transition and aggressive clinical behavior seen in GBM.
We investigated the expression of TAZ, its binding partner TEAD, and the mesenchymal marker FN1 in human gliomas. Western analyses demonstrated increased expression of TAZ, TEAD4, and FN1 in GBM relative to lower grade gliomas. We also identified CpG islands in the TAZ promoter that are methylated in most lower grade gliomas, but not in GBMs. TAZ-methylated glioma stem cell (GSC) lines treated with a demethylation agent showed an increase in mRNA and protein TAZ expression; therefore, methylation may be another novel way TAZ is regulated since TAZ is epigenetically silenced in tumors with a better clinical outcome.
To further characterize the role of TAZ in gliomagenesis, we stably silenced or over-expressed TAZ in GSCs. Silencing of TAZ decreased invasion, self-renewal, mesenchymal protein expression, and tumor-initiating capacity. Over-expression of TAZ led to an increase in invasion, mesenchymal protein expression, mesenchymal differentiation, and tumor-initiating ability. These actions are dependent on TAZ interacting with TEAD since all these effects were abrogated with TAZ could not bind to TEAD. We also show that TAZ and TEAD directly bind to mesenchymal gene promoters. Thus, TAZ-TEAD interaction is critically important in the mesenchymal shift and in the aggressive clinical behavior of GBM.
We identified TAZ as a regulator of the mesenchymal transition in gliomas. TAZ could be used as a biomarker to both estimate prognosis and stratify patients into clinically relevant subgroups. Since mesenchymal transition is correlated to tumor aggressiveness, strategies to target and inhibit TAZ-TEAD and the downstream gene targets may be warranted in alternative treatment.
Advisors/Committee Members: Kenneth Aldape, M.D., Russell Broaddus, M.D./Ph.D., Daniel Cahill, M.D./Ph.D..
Subjects/Keywords: Glioblastoma; TAZ; TEAD; Hippo pathway; mesenchymal transition; proneural; Medical Molecular Biology; Medical Pathology; Medicine and Health Sciences; Neoplasms; Oncology; Pathology
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APA (6th Edition):
Salazar, K. (2012). TAZ AS A REGULATOR OF MESENCHYMAL TRANSFORMATION AND CLINICAL AGGRESSIVENESS IN GLIOMAS. (Doctoral Dissertation). Texas Medical Center. Retrieved from https://digitalcommons.library.tmc.edu/utgsbs_dissertations/229
Chicago Manual of Style (16th Edition):
Salazar, Katrina. “TAZ AS A REGULATOR OF MESENCHYMAL TRANSFORMATION AND CLINICAL AGGRESSIVENESS IN GLIOMAS.” 2012. Doctoral Dissertation, Texas Medical Center. Accessed March 06, 2021.
https://digitalcommons.library.tmc.edu/utgsbs_dissertations/229.
MLA Handbook (7th Edition):
Salazar, Katrina. “TAZ AS A REGULATOR OF MESENCHYMAL TRANSFORMATION AND CLINICAL AGGRESSIVENESS IN GLIOMAS.” 2012. Web. 06 Mar 2021.
Vancouver:
Salazar K. TAZ AS A REGULATOR OF MESENCHYMAL TRANSFORMATION AND CLINICAL AGGRESSIVENESS IN GLIOMAS. [Internet] [Doctoral dissertation]. Texas Medical Center; 2012. [cited 2021 Mar 06].
Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/229.
Council of Science Editors:
Salazar K. TAZ AS A REGULATOR OF MESENCHYMAL TRANSFORMATION AND CLINICAL AGGRESSIVENESS IN GLIOMAS. [Doctoral Dissertation]. Texas Medical Center; 2012. Available from: https://digitalcommons.library.tmc.edu/utgsbs_dissertations/229
26.
Patrícia Sayuri Suzuki.
Papel do torque Teno Vírus (TTV) e do polimorfismo do gene CCR5 no desenvolvimento do câncer cervical.
Degree: 2008, Universidade Estadual de Londrina
URL: http://www.bibliotecadigital.uel.br/document/?code=vtls000128854
► High-risk human papillomaviruses (HPVs) are a required factor for cervical uterine cancer development. However, only a small proportion of HPV-infected women will develop cervical cancer;…
(more)
▼ High-risk human papillomaviruses (HPVs) are a required factor for cervical uterine cancer development. However, only a small proportion of HPV-infected women will develop cervical cancer; several other cofactors may enhance persistent infection and oncogenesis. Torque Teno Virus (TTV) and genetic polymorphism for chemokine receptor 5 may act as cofactor for cervical carcinogenesis. TTV is an unenveloped, circular, single-strand DNA and its pathological role remains unclear. The aim of this work was to investigate the association of TTV in patients coinfected with HPV in the cervical cancer development. The presence of TTV was investigated in the peripheral blood of 117 Brazilian women by nested PCR, using a set of primers for the N22 region of the large ORF-1 and the analyze CCR5 polymorphism was using primers wich GenBank acession AF009962. TTV DNA presence was observed in 18.6% (08/43) of HPV negative individuals and in 24.32% (18/74) HPV suggestive patients. TTV presence was also investigated in the HPV suggestive patient group, for comparison of cancer and noncancer patients. TTV DNA was significantly more prevalent among HPV suggestive patients presenting cancer (57.14%; 08/14) compared to HPV suggestive noncancer patients (both 16.67%; 10/60). The wild type polymorphism of CCR5 gene was prevalent both in the HPV negative (38/43) and patients with oncotic colpocytology suggestive for HPV (70/74). In this work, was verified that the presence of TTV infection could be a risk factor for cancer development in patients with co-infection for HPV-TTV, and there was no association with CCR5 polymorphism. However, further studies are required to clarify the influence of TTV in the cervical cancer development.
Papilomavirus humano (HPV) de alto risco é um fator necessário para o desenvolvimento de câncer cervical uterino. Contudo, somente uma pequena proporção de mulheres infectadas pelo HPV desenvolverá câncer cervical; muitos outros co-fatores podem aumentar a persistência da infecção e sua oncogênese. O Torque Teno Vírus (TTV) e o polimorfismo do gene para o receptor de quimiocina 5 podem agir como co-fatores para carcinogênese cervical. TTV é um vírus não-envelopado, circular, DNA fita simples e seu papel patogênico ainda não foi elucidado. Este trabalho teve como objetivo investigar a relação do TTV em pacientes coinfectados com HPV no desenvolvimento do câncer cervical uterino. A presença do TTV foi investigada no sangue periférico de 117 indivíduos, por PCR nested utilizando um conjunto de oligos iniciadores para a região N22 da ORF-1 e para a análise do polimorfismo do gene CCR5 foram utilizados oligos inciadores sintetizados de acordo com a seqüência no GenBank AF009962. A presença do DNA do TTV foi observada em 18,6% (08/43) dos pacientes negativos para HPV, e em 24,32% (18/74) dos pacientes sugestivos para infecção por HPV. O TTV também foi investigado em pacientes sugestivos para infecção por HPV sem câncer e com câncer. O DNA do TTV foi significantemente mais prevalente em pacientes sugestivos para HPV com…
Advisors/Committee Members: Maria Angelica Ehara Watanabe ., Jeane Eliete Laguila Visentainer, Emerson José Venâncio.
Subjects/Keywords: Patologia experimental; Colo uterino - Câncer; Polimorfismo (Genética); Experimental pathology; Cervix Uteri - Neoplasms; Genetic polymorphisms
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APA (6th Edition):
Suzuki, P. S. (2008). Papel do torque Teno Vírus (TTV) e do polimorfismo do gene CCR5 no desenvolvimento do câncer cervical. (Thesis). Universidade Estadual de Londrina. Retrieved from http://www.bibliotecadigital.uel.br/document/?code=vtls000128854
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Suzuki, Patrícia Sayuri. “Papel do torque Teno Vírus (TTV) e do polimorfismo do gene CCR5 no desenvolvimento do câncer cervical.” 2008. Thesis, Universidade Estadual de Londrina. Accessed March 06, 2021.
http://www.bibliotecadigital.uel.br/document/?code=vtls000128854.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Suzuki, Patrícia Sayuri. “Papel do torque Teno Vírus (TTV) e do polimorfismo do gene CCR5 no desenvolvimento do câncer cervical.” 2008. Web. 06 Mar 2021.
Vancouver:
Suzuki PS. Papel do torque Teno Vírus (TTV) e do polimorfismo do gene CCR5 no desenvolvimento do câncer cervical. [Internet] [Thesis]. Universidade Estadual de Londrina; 2008. [cited 2021 Mar 06].
Available from: http://www.bibliotecadigital.uel.br/document/?code=vtls000128854.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Suzuki PS. Papel do torque Teno Vírus (TTV) e do polimorfismo do gene CCR5 no desenvolvimento do câncer cervical. [Thesis]. Universidade Estadual de Londrina; 2008. Available from: http://www.bibliotecadigital.uel.br/document/?code=vtls000128854
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Glasgow
27.
Hannay, Jonathan A. F.
Soft tissue sarcoma : biology and therapeutic correlates.
Degree: PhD, 2015, University of Glasgow
URL: http://theses.gla.ac.uk/6988/
;
http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.685837
► Soft tissue sarcomas (STS) comprise a heterogenenous group of greater than 50 malignancies of putative mesenchymal cell origin and as such they may arise in…
(more)
▼ Soft tissue sarcomas (STS) comprise a heterogenenous group of greater than 50 malignancies of putative mesenchymal cell origin and as such they may arise in diverse tissue types in various anatomical locations throughout the whole body. Collectively they account for approximately 1% of all human malignancies yet have a spectrum of aggressive behaviours amongst their subtypes. They thus pose a particular challenge to manage and remain an under investigated group of cancers with no generally applicable new therapies in the past 40 years and an overall 5-year survival rate that remains stagnant at around 50%. From September 2000 to July 2006 I undertook a full time post-doctoral level research fellowship at the MD Anderson Cancer Center, Houston, Texas, USA in the department of Surgical Oncology to investigate the biology of soft tissue sarcoma and test novel anti- sarcoma adenovirus-based therapy in the preclinical nude rat model of isolated limb perfusion against human sarcoma xenografts. This work, in collaboration with colleagues as indicated herein, led to a number of publications in the scientific literature furthering our understanding of the malignant phenotype of sarcoma and reported preclinical studies with wild-type p53, in a replication deficient adenovirus vector, and oncolytic adenoviruses administered by isolated limb perfusion. Additional collaborative and pioneering preclinical studies reported the molecular imaging of sarcoma response to systemically delivered therapeutic phage RGD-4c AAVP. Doxorubicin chemotherapy is the single most active broadly applicable anti-sarcoma chemotherapeutic yet only has an approximate 30% overall response rate with additional breakthrough tumour progression and recurrence after initial chemo-responsiveness further problematic features in STS management. Doxorubicin is a substrate for the multi- drug resistance (mdr) gene product p-glycoprotein drug efflux pump and exerts its main mode of action by induction of DNA double-strand breaks during the S-phase of the cell cycle. Two papers in my thesis characterise different aspects of chemoresistance in sarcoma. The first shows that wild-type p53 suppresses Protein Kinase Calpha (PKCα) phosphorylation (and activation) of p-glycoprotein by transcriptional repression of PKCα through a Sp-1 transcription factor binding site in its -244/-234 promoter region. The second paper demonstrates that Rad51 (a central mediator of homologous recombination repair of double strand breaks) has elevated levels in sarcoma and particularly in the S- G2 phase of the cell cycle. Suppression of Rad51 with small interfering RNA in sarcoma cell culture led to doxorubicin chemosensitisation. Reintroduction of wild-type p53 into STS cell lines resulted in decreased Rad51 protein and mRNA expression via transcriptional repression of the Rad51 promoter through increased AP-2 binding. In light of poor response rates to chemotherapy, escape from local control portends a poor prognosis for patients with sarcoma. Two papers in my thesis characterise aspects…
Subjects/Keywords: 616.99; RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer); RD Surgery; RM Therapeutics. Pharmacology
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APA ·
Chicago ·
MLA ·
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to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hannay, J. A. F. (2015). Soft tissue sarcoma : biology and therapeutic correlates. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/6988/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.685837
Chicago Manual of Style (16th Edition):
Hannay, Jonathan A F. “Soft tissue sarcoma : biology and therapeutic correlates.” 2015. Doctoral Dissertation, University of Glasgow. Accessed March 06, 2021.
http://theses.gla.ac.uk/6988/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.685837.
MLA Handbook (7th Edition):
Hannay, Jonathan A F. “Soft tissue sarcoma : biology and therapeutic correlates.” 2015. Web. 06 Mar 2021.
Vancouver:
Hannay JAF. Soft tissue sarcoma : biology and therapeutic correlates. [Internet] [Doctoral dissertation]. University of Glasgow; 2015. [cited 2021 Mar 06].
Available from: http://theses.gla.ac.uk/6988/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.685837.
Council of Science Editors:
Hannay JAF. Soft tissue sarcoma : biology and therapeutic correlates. [Doctoral Dissertation]. University of Glasgow; 2015. Available from: http://theses.gla.ac.uk/6988/ ; http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.685837
University of Glasgow
28.
Hannay, Jonathan A.F.
Soft tissue sarcoma: biology and therapeutic correlates.
Degree: PhD, 2015, University of Glasgow
URL: http://theses.gla.ac.uk/6988/
► Soft tissue sarcomas (STS) comprise a heterogenenous group of greater than 50 malignancies of putative mesenchymal cell origin and as such they may arise in…
(more)
▼ Soft tissue sarcomas (STS) comprise a heterogenenous group of greater than 50 malignancies of putative mesenchymal cell origin and as such they may arise in diverse tissue types in various anatomical locations throughout the whole body. Collectively they account for approximately 1% of all human malignancies yet have a spectrum of aggressive behaviours amongst their subtypes. They thus pose a particular challenge to manage and remain an under investigated group of cancers with no generally applicable new therapies in the past 40 years and an overall 5-year survival rate that remains stagnant at around 50%.
From September 2000 to July 2006 I undertook a full time post-doctoral level research fellowship at the MD Anderson Cancer Center, Houston, Texas, USA in the department of Surgical Oncology to investigate the biology of soft tissue sarcoma and test novel anti- sarcoma adenovirus-based therapy in the preclinical nude rat model of isolated limb perfusion against human sarcoma xenografts. This work, in collaboration with colleagues as indicated herein, led to a number of publications in the scientific literature furthering our understanding of the malignant phenotype of sarcoma and reported preclinical studies with wild-type p53, in a replication deficient adenovirus vector, and oncolytic adenoviruses administered by isolated limb perfusion. Additional collaborative and pioneering preclinical studies reported the molecular imaging of sarcoma response to systemically delivered therapeutic phage RGD-4c AAVP.
Doxorubicin chemotherapy is the single most active broadly applicable anti-sarcoma chemotherapeutic yet only has an approximate 30% overall response rate with additional breakthrough tumour progression and recurrence after initial chemo-responsiveness further problematic features in STS management. Doxorubicin is a substrate for the multi- drug resistance (mdr) gene product p-glycoprotein drug efflux pump and exerts its main mode of action by induction of DNA double-strand breaks during the S-phase of the cell cycle. Two papers in my thesis characterise different aspects of chemoresistance in sarcoma. The first shows that wild-type p53 suppresses Protein Kinase Calpha (PKCα) phosphorylation (and activation) of p-glycoprotein by transcriptional repression of PKCα through a Sp-1 transcription factor binding site in its -244/-234 promoter region. The second paper demonstrates that Rad51 (a central mediator of homologous recombination repair of double strand breaks) has elevated levels in sarcoma and particularly in the S- G2 phase of the cell cycle. Suppression of Rad51 with small interfering RNA in sarcoma cell culture led to doxorubicin chemosensitisation. Reintroduction of wild-type p53 into STS cell lines resulted in decreased Rad51 protein and mRNA expression via transcriptional repression of the Rad51 promoter through increased AP-2 binding.
In light of poor response rates to chemotherapy, escape from local control portends a poor prognosis for patients with sarcoma. Two papers in my thesis characterise…
Subjects/Keywords: RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer); RD Surgery; RM Therapeutics. Pharmacology
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Hannay, J. A. F. (2015). Soft tissue sarcoma: biology and therapeutic correlates. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/6988/
Chicago Manual of Style (16th Edition):
Hannay, Jonathan A F. “Soft tissue sarcoma: biology and therapeutic correlates.” 2015. Doctoral Dissertation, University of Glasgow. Accessed March 06, 2021.
http://theses.gla.ac.uk/6988/.
MLA Handbook (7th Edition):
Hannay, Jonathan A F. “Soft tissue sarcoma: biology and therapeutic correlates.” 2015. Web. 06 Mar 2021.
Vancouver:
Hannay JAF. Soft tissue sarcoma: biology and therapeutic correlates. [Internet] [Doctoral dissertation]. University of Glasgow; 2015. [cited 2021 Mar 06].
Available from: http://theses.gla.ac.uk/6988/.
Council of Science Editors:
Hannay JAF. Soft tissue sarcoma: biology and therapeutic correlates. [Doctoral Dissertation]. University of Glasgow; 2015. Available from: http://theses.gla.ac.uk/6988/
29.
Raymond, Daniel.
EVALUATING SOLUBLE AXL AS A BIOMARKER FOR GLIOBLASTOMA.
Degree: MS, Biology, 2020, Northen Michigan University
URL: https://commons.nmu.edu/theses/635
► AXL, a receptor tyrosine kinase, is known to promote malignant phenotypes in various types of cancer. AXL overexpression is commonly observed in glioblastoma and…
(more)
▼ AXL, a receptor tyrosine kinase, is known to promote malignant phenotypes in various types of cancer. AXL overexpression is commonly observed in glioblastoma and correlates with a worse prognosis. Detectable in most biological fluids, the extracellular domain of AXL, sAXL, is the product of enzymatic cleavage by ADAM10/17. Here we used ELISA, BCA and BCG assays to characterize blood serum from 23 newly diagnosed GBM patients which was collected roughly 24 hours before and after surgery as well as every three months post-surgery, corresponding to follow-up treatment visits. Immunoblotting was used to determine relative AXL expression in 13 patient tumor tissue samples. Additionally, T-1 weighted MRI scans were used to interpolate pre-operative tumor volume in all participating patients. Here we report that sAXL was elevated in the 84 GBM samples compared to the 40 control samples (
p = 0.013). Normalizing sAXL values against corresponding serum albumin concentrations further defined the distinction between the two groups (<em>p < 0.0001)</em>. While in the 19 paired, pre- and post- operative samples, sAXL did not respond significantly to surgical intervention, normalizing the values against albumin showed a significant elevation in response to surgery (
p = 0.013). In patients whose pre-operative samples presented with sAXL elevated compared to the healthy control average (30.16 ng/mL), there was a strong positive correlation between sAXL and AXL found in the corresponding tumor tissue. Though sAXL shed from brain tumors is detectable in the serum of GBM patients, in this small series of patients, it does not correlate with tumor volume.
Advisors/Committee Members: Robert Winn.
Subjects/Keywords: Biomarker; Glioblastoma; Receptor; RTK; AXL; Serum; ADAM; ELISA; MRI; Medical Pathology; Neoplasms
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APA ·
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MLA ·
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Raymond, D. (2020). EVALUATING SOLUBLE AXL AS A BIOMARKER FOR GLIOBLASTOMA. (Thesis). Northen Michigan University. Retrieved from https://commons.nmu.edu/theses/635
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Raymond, Daniel. “EVALUATING SOLUBLE AXL AS A BIOMARKER FOR GLIOBLASTOMA.” 2020. Thesis, Northen Michigan University. Accessed March 06, 2021.
https://commons.nmu.edu/theses/635.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Raymond, Daniel. “EVALUATING SOLUBLE AXL AS A BIOMARKER FOR GLIOBLASTOMA.” 2020. Web. 06 Mar 2021.
Vancouver:
Raymond D. EVALUATING SOLUBLE AXL AS A BIOMARKER FOR GLIOBLASTOMA. [Internet] [Thesis]. Northen Michigan University; 2020. [cited 2021 Mar 06].
Available from: https://commons.nmu.edu/theses/635.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Raymond D. EVALUATING SOLUBLE AXL AS A BIOMARKER FOR GLIOBLASTOMA. [Thesis]. Northen Michigan University; 2020. Available from: https://commons.nmu.edu/theses/635
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Birmingham
30.
Nahorski, Michael Stefan.
Investigation into the molecular mechanisms of inherited renal cancer.
Degree: d_ph, College of Medical & Dental Sciences, 2012, University of Birmingham
URL: http://etheses.bham.ac.uk//id/eprint/3663/
► Birt Hogg Dubé (BHD) syndrome is an inherited cancer susceptibility syndrome characterised by the development of fibrofolliculomas on the face and upper torso, and increased…
(more)
▼ Birt Hogg Dubé (BHD) syndrome is an inherited cancer susceptibility syndrome characterised by the development of fibrofolliculomas on the face and upper torso, and increased risk of lung cysts, spontaneous pneumothorax and renal cancer. The findings presented in this thesis advance knowledge into how the mutations in the FLCN gene cause the phenotypes associated with BHD syndrome, and provides novel insights into the functions of folliculin within the cell. The results presented provide further evidence of the association between BHD syndrome and increased risk of colorectal cancer in a subset of BHD syndrome families, and suggest that this association appears restricted to those patients with an exon 11 mononucleotide tract mutation. Evolutionary conservation analysis across the FLCN sequence suggests that pathogenic mutations could be expected throughout the gene, and identifies a region between codons 100-230 of increased evolutionary significance. The experiments undertaken demonstrate a practical strategy for determining the pathogenicity of non-truncating folliculin variants in vitro, and indicate that loss of protein stability is the main mechanism of pathogenicity for the previously reported non-truncating mutations within FLCN. Finally, this thesis reports the first identification of p0071 as a folliculin interacting protein. Folliculin deficiency exerts a functional impact on previously reported p0071 functions inducing RhoA signalling upregulation, mitotic defects and disruption of cell junctions. These results demonstrate the potential efficacy of using inhibitors downstream of RhoA as therapeutic targets in BHD tumours with dyregulated RhoA signaling, and provide novel directions for research into BHD syndrome.
Subjects/Keywords: QH301 Biology; QH426 Genetics; RB Pathology; RC0254 Neoplasms. Tumors. Oncology (including Cancer)
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APA ·
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CSE |
Export
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Manager
APA (6th Edition):
Nahorski, M. S. (2012). Investigation into the molecular mechanisms of inherited renal cancer. (Thesis). University of Birmingham. Retrieved from http://etheses.bham.ac.uk//id/eprint/3663/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Nahorski, Michael Stefan. “Investigation into the molecular mechanisms of inherited renal cancer.” 2012. Thesis, University of Birmingham. Accessed March 06, 2021.
http://etheses.bham.ac.uk//id/eprint/3663/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Nahorski, Michael Stefan. “Investigation into the molecular mechanisms of inherited renal cancer.” 2012. Web. 06 Mar 2021.
Vancouver:
Nahorski MS. Investigation into the molecular mechanisms of inherited renal cancer. [Internet] [Thesis]. University of Birmingham; 2012. [cited 2021 Mar 06].
Available from: http://etheses.bham.ac.uk//id/eprint/3663/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Nahorski MS. Investigation into the molecular mechanisms of inherited renal cancer. [Thesis]. University of Birmingham; 2012. Available from: http://etheses.bham.ac.uk//id/eprint/3663/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
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Open Access Theses and Dissertations