subject:(Cancer progression)

1. Bougnoux, Anne-Claire. Identification et caractérisation de biomarqueurs associés à la progression tumorale du mélanome malin cutané : implication de TRAP1 et PDIA4 : Identification and characterization of biomarkers associated with tumor progression of cutaneous malignant melanoma : involvement of TRAP1 and PDIA4.

Degree: Docteur es, Biologie Santé, 2014, Université Montpellier I

URL: http://www.theses.fr/2014MON1T014

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Bien que le mélanome malin cutané (MMC) ne représente que 10% des cancers cutanés, il en est la forme la plus agressive et est responsable… (more)

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Bien que le mélanome malin cutané (MMC) ne représente que 10% des cancers cutanés, il en est la forme la plus agressive et est responsable de 90% des décès dus aux cancers de la peau. Son incidence ne cesse d'augmenter ces dernières années et atteint 10.8 cas pour 100 000 habitants chez les hommes et 11 chez les femmes. La survie médiane des patients atteint de mélanome à un stade avancé est de 6.2 mois et seulement 1 patient sur 4 est encore en vie à 1an. Le diagnostic du mélanome est uniquement histopathologique et seul l'examen de la biopsie permet de le poser définitivement. De la même façon, il n'existe pas de marqueurs pronostiques associés au mélanome malin cutané. Seuls des facteurs histologiques tels que l'épaisseur de la tumeur, le degré d'invasion ou encore l'envahissement ganglionnaire ont été validés par l'American Joint Committee on Cancer et servent de facteurs pronostiques. Cependant, bien qu'ils permettent d'évaluer le risque métastatique, leur valeur pronostique est encore très insuffisante. L'objectif de ma thèse est d'identifier et de caractériser les protéines associées à la progression tumorale du MMC. Grâce à une approche protéomique quantitative de type iTRAQ par nanoLC MS/MS, j'ai pu identifier et caractériser 2242 protéines dans un modèle cellulaire de progression tumorale du mélanome. La surexpression de huit de ces protéines dans les lignées tumorales par rapport à la lignée normale a été validée par western blot. Deux d'entre elles, TRAP1 et PDIA4 ont ensuite été validées en immunohistochimie comme marqueurs associés à la progression tumorale dans le MMC. Dans un second temps, l'implication de ces deux protéines dans les mécanismes de carcinogénèse du mélanome a été étudiée. L'inhibition de TRAP1 et de PDIA4 induit une diminution de la migration et de la viabilité de la lignée cellulaire métastatique de mélanome 1676. Enfin, la sous-expression dePDIA4 induit une inhibition du complexe Cycline D/CDK4 provoquant un blocage des cellules en phase G0/G1. Ce blocage passerait par la voie PERK liées au stress du réticulum endoplasmique.

Although cutaneous malignant melanoma (CMM) represents only 10% of skin cancers, it is the most aggressive form with 90% of deaths from skin cancer. The Incidence rate is increasing in recent years to 10.8 cases and 11 cases per 100000, in men and women respectively. The prognosis of metastatic melanoma is poor, with a median survival of only 6.2 months. Histopathologic examination remains the gold standard for melanoma diagnosis. There are no prognostic markers associated with CMM. Only histological factors such as tumor thickness, level of invasion, or lymph node involvement have been validated by the American Joint Committee on Cancer and are currently used as prognostic factors. However, although these histological factors are used to assess the risk of metastasis development, their prognostic value is still very low. The aim of my PhD work is to identify and characterize biomarkers associated with tumor progression of CMM. Using a quantitative proteomics…

Advisors/Committee Members: Solassol, Jérôme (thesis director).

Subjects/Keywords: Cancer; Biomarqueurs; Mélanome; Progression tumorale; Cancer; Biomarkers; Melanoma; Tumor progression

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bougnoux, A. (2014). Identification et caractérisation de biomarqueurs associés à la progression tumorale du mélanome malin cutané : implication de TRAP1 et PDIA4 : Identification and characterization of biomarkers associated with tumor progression of cutaneous malignant melanoma : involvement of TRAP1 and PDIA4. (Doctoral Dissertation). Université Montpellier I. Retrieved from http://www.theses.fr/2014MON1T014

Chicago Manual of Style (16^th Edition):

Bougnoux, Anne-Claire. “Identification et caractérisation de biomarqueurs associés à la progression tumorale du mélanome malin cutané : implication de TRAP1 et PDIA4 : Identification and characterization of biomarkers associated with tumor progression of cutaneous malignant melanoma : involvement of TRAP1 and PDIA4.” 2014. Doctoral Dissertation, Université Montpellier I. Accessed March 06, 2021. http://www.theses.fr/2014MON1T014.

MLA Handbook (7^th Edition):

Bougnoux, Anne-Claire. “Identification et caractérisation de biomarqueurs associés à la progression tumorale du mélanome malin cutané : implication de TRAP1 et PDIA4 : Identification and characterization of biomarkers associated with tumor progression of cutaneous malignant melanoma : involvement of TRAP1 and PDIA4.” 2014. Web. 06 Mar 2021.

Vancouver:

Bougnoux A. Identification et caractérisation de biomarqueurs associés à la progression tumorale du mélanome malin cutané : implication de TRAP1 et PDIA4 : Identification and characterization of biomarkers associated with tumor progression of cutaneous malignant melanoma : involvement of TRAP1 and PDIA4. [Internet] [Doctoral dissertation]. Université Montpellier I; 2014. [cited 2021 Mar 06]. Available from: http://www.theses.fr/2014MON1T014.

Council of Science Editors:

Bougnoux A. Identification et caractérisation de biomarqueurs associés à la progression tumorale du mélanome malin cutané : implication de TRAP1 et PDIA4 : Identification and characterization of biomarkers associated with tumor progression of cutaneous malignant melanoma : involvement of TRAP1 and PDIA4. [Doctoral Dissertation]. Université Montpellier I; 2014. Available from: http://www.theses.fr/2014MON1T014

2. Jouida, Amina. Contrôle de la progression tumorale broncho-pulmonaire par FHIT : Implication du récepteur HER2 : Control of lung tumor progression by FHIT : Involvement of HER2 receptor.

Degree: Docteur es, Biochimie, biologie cellulaire et moléculaire, physiologie et nutrition, 2017, Reims

URL: http://www.theses.fr/2017REIMS008

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Dans les cancers du poumon, une des altérations les plus souvent observées est la perte ou l’atténuation de l’expression du gène FHIT (Fragile Histidine Triad).… (more)

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Dans les cancers du poumon, une des altérations les plus souvent observées est la perte ou l’atténuation de l’expression du gène FHIT (Fragile Histidine Triad). Nous avons précédemment montré que FHIT est un suppresseur d’invasion tumorale. En effet, FHIT contrôle l’invasion des cellules tumorales bronchiques en régulant négativement l'expression de gènes associés à la transition épithélio-mésenchymateuse (TEM), en particulier la vimentine et la MMP-9 via l’inhibition d’une voie orchestrée par l’EGFR. Un intérêt particulier a donc été porté aux relations entre FHIT et un autre membre de la famille de l’EGFR : HER2. Nous avons non seulement mis en évidence, in vivo et in vitro, une corrélation inverse entre les taux de FHIT et l’activité du récepteur HER2 dans les CBNPC mais également montré que FHIT est capable de réguler l’activité du récepteur HER2 dans les cellules tumorales pulmonaires et ce grâce à sa dimérisation avec HER3. De plus, l’utilisation de deux inhibiteurs spécifiques d’HER2, le Trastuzumab et l’Irbinitinib, nous a permis de mettre en évidence, que l’activation du récepteur HER2 lors de l’inhibition de FHIT, participe à l’acquisition par les cellules tumorales bronchiques de caractéristiques invasives via la régulation de certaines cibles de la TEM, telles la vimentine, la MMP-14 ou encore le facteur de transcription TWIST-1. Ces résultats montrent que FHIT régule l’activité d’HER2 dans les cellules tumorales pulmonaires et que les inhibiteurs d’HER2 sont capables de limiter l’invasion induite par l’inhibition de FHIT. Cette étude laisse envisager de nouvelles perspectives thérapeutiques pour le cancer du poumon.

The lack or decrease of FHIT (fragile histidine triad) expression is a common event in lung cancer. We recently showed that FHIT acts as a suppressor of tumor invasion. Indeed, FHIT controls the invasive phenotype of lung tumor cells by regulating the expression of genes associated with epithelial-mesenchymal transition (EMT) such as vimentin or MMP-9 through an EGFR signaling pathway. Accordingly, we focused on the relationships between FHIT and another member of this tyrosine kinase receptor family: HER2. First, we observed in vivo and in vitro a negative correlation between FHIT expression and the activated form of HER2 in lung tumor cells. Moreover, FHIT controls HER2 activation through its dimerization with HER3. The use of HER2 specific inhibitors, Trastuzumab and Irbinitinib, allowed to demonstrate that the in vitro invasion induced by FHIT inhibition is HER2-dependent. Furthermore, FHIT controls the HER2-dependent invasion by regulating genes associated with EMT such as vimentin, MMP-14 or TWIST-1. In conclusion, we showed that FHIT regulates HER2 activity in lung tumor cells and that HER2 inhibitors reduce invasion induced by FHIT inhibition. This study would allow for the identification of new therapeutic leads for lung cancer.

Advisors/Committee Members: Nawrocki, Béatrice (thesis director).

Subjects/Keywords: Cancer broncho-Pulmonaire; Fhit; Her2; Progression tumorale; Tem; Lung cancer; Fhit; Her2; Cancer progression; Emt

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Jouida, A. (2017). Contrôle de la progression tumorale broncho-pulmonaire par FHIT : Implication du récepteur HER2 : Control of lung tumor progression by FHIT : Involvement of HER2 receptor. (Doctoral Dissertation). Reims. Retrieved from http://www.theses.fr/2017REIMS008

Chicago Manual of Style (16^th Edition):

Jouida, Amina. “Contrôle de la progression tumorale broncho-pulmonaire par FHIT : Implication du récepteur HER2 : Control of lung tumor progression by FHIT : Involvement of HER2 receptor.” 2017. Doctoral Dissertation, Reims. Accessed March 06, 2021. http://www.theses.fr/2017REIMS008.

MLA Handbook (7^th Edition):

Jouida, Amina. “Contrôle de la progression tumorale broncho-pulmonaire par FHIT : Implication du récepteur HER2 : Control of lung tumor progression by FHIT : Involvement of HER2 receptor.” 2017. Web. 06 Mar 2021.

Vancouver:

Jouida A. Contrôle de la progression tumorale broncho-pulmonaire par FHIT : Implication du récepteur HER2 : Control of lung tumor progression by FHIT : Involvement of HER2 receptor. [Internet] [Doctoral dissertation]. Reims; 2017. [cited 2021 Mar 06]. Available from: http://www.theses.fr/2017REIMS008.

Council of Science Editors:

Jouida A. Contrôle de la progression tumorale broncho-pulmonaire par FHIT : Implication du récepteur HER2 : Control of lung tumor progression by FHIT : Involvement of HER2 receptor. [Doctoral Dissertation]. Reims; 2017. Available from: http://www.theses.fr/2017REIMS008

3. Sugie, Satoru; Mukai, Shoichiro; Yamasaki, Koji; Kamibeppu, Toyoharu; Tukino, Hiromasa. Significant association of caveolin-1 and caveolin-2 with prostate cancer progression.

Degree: 博士(医学), 2015, University of Miyazaki / 宮崎大学

URL: http://hdl.handle.net/10458/5828

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学位論文の一部を構成しているため、http://hdl.handle.net/10458/5829に本文を掲載。

Background/Aim: Up-regulation of caveolin (CAV)-1 is associated with aggressive prostate cancer. Recently, it has been inferred that CAV2, a co-factor sub-type of CAV1, cross-talks… (more)

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学位論文の一部を構成しているため、http://hdl.handle.net/10458/5829に本文を掲載。

Background/Aim: Up-regulation of caveolin (CAV)-1 is associated with aggressive prostate cancer. Recently, it has been inferred that CAV2, a co-factor sub-type of CAV1, cross-talks with CAV1 and promotes tumor growth. We previously reported that plasma CAV1 levels are elevated in patients with castration-resistant prostate cancer (CRPC), but not in hormone-sensitive prostate cancer (non-CRPC), implying that CAV1 may be a therapeutic target for CRPC. However, a correlation of CAV1 and CAV2 expression in PC has not yet been reported. Herein, we analyzed associations between PC progression and plasma CAV1 and -2 in Japanese men, and expression of CAV1 and -2 in PC3 (CRPC) and LNCaP (non-CRPC) cell lines. Materials and Methods: We investigated plasma samples from 36 patients with CRPC and 22 with non-CRPC. We used enzyme-linked immunosorbent assay (ELISA) to determine plasma levels of CAV1 and -2, and examined correlations with clinicopathological characteristics such as Gleason grade and clinical T stage. Real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was used to evaluate CAV1 and CAV2 mRNA in PC cell lines. We also introduced CAV1- and CAV2-specific small interfering (siRNA) into PC3 cells to knock-down (KD) both molecules, and examined its influence on the expression of these genes between PC3 CAV1 and -2 KD cells and control cells. Results: Plasma CAV1 and -2 levels in patients with CRPC were significantly higher than in those with non-CRPC (CAV1, p=0.003; CAV2, p<0.001). Plasma levels of CAV1 and -2 were significantly correlated (p<0.001). However, we did not find any significant relationship between CAV1 or CAV2 expression and clinicopathological factors. ELISA and real-time qRT-PCR showed that both proteins and mRNAs in PC3 cells were significantly over-expressed compared to LNCaP cells (p<0.001). In PC3 CAV1 KD cells, expression of CAV2 was suppressed and confirmed the linkage of CAV2 KD and suppression of CAV1 expression. Conclusion: There was a significant correlation between plasma CAV-1 and -2 levels and progression of PC. CAV1 and -2 were highly expressed in the PC3 compared to the LNCaP cell line. Our findings support the potential of these molecules as therapeutic targets for CRPC. Prostate cancer (PC) is the sixth leading cause of cancerrelated death among Japanese men (1), usually from metastatic disease. Understanding the mechanisms that underlie the progression of PC will facilitate the development of biomarkers and novel therapeutic strategies to control this devastating malignancy. Caveolin (CAV)-1 and CAV2, encoded by their respective genes, are major structural components of the caveolae that are co-expressed and form a hetero-oligomeric complex in many cell types, with particularly high levels in adipocytes (2). CAV1 expression is increased in cancer of the prostate (3-5), pancreas (6, 7), colon (8, 9), breast (10) and esophagus (11, 12), thus suggesting it plays a positive role in tumor progression.…

Subjects/Keywords: caveolin-1; caveolin-2; prostate cancer progression

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Sugie, Satoru; Mukai, Shoichiro; Yamasaki, Koji; Kamibeppu, Toyoharu; Tukino, H. (2015). Significant association of caveolin-1 and caveolin-2 with prostate cancer progression. (Thesis). University of Miyazaki / 宮崎大学. Retrieved from http://hdl.handle.net/10458/5828

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sugie, Satoru; Mukai, Shoichiro; Yamasaki, Koji; Kamibeppu, Toyoharu; Tukino, Hiromasa. “Significant association of caveolin-1 and caveolin-2 with prostate cancer progression.” 2015. Thesis, University of Miyazaki / 宮崎大学. Accessed March 06, 2021. http://hdl.handle.net/10458/5828.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sugie, Satoru; Mukai, Shoichiro; Yamasaki, Koji; Kamibeppu, Toyoharu; Tukino, Hiromasa. “Significant association of caveolin-1 and caveolin-2 with prostate cancer progression.” 2015. Web. 06 Mar 2021.

Vancouver:

Sugie, Satoru; Mukai, Shoichiro; Yamasaki, Koji; Kamibeppu, Toyoharu; Tukino H. Significant association of caveolin-1 and caveolin-2 with prostate cancer progression. [Internet] [Thesis]. University of Miyazaki / 宮崎大学; 2015. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/10458/5828.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sugie, Satoru; Mukai, Shoichiro; Yamasaki, Koji; Kamibeppu, Toyoharu; Tukino H. Significant association of caveolin-1 and caveolin-2 with prostate cancer progression. [Thesis]. University of Miyazaki / 宮崎大学; 2015. Available from: http://hdl.handle.net/10458/5828

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Vermont

4. Ojemann, Alexandra. Understanding the Role of Runx2 in a Breast Cancer Progression Cell Model.

Degree: MS, Biochemistry, 2017, University of Vermont

URL: https://scholarworks.uvm.edu/graddis/741

► Runx2 is a transcription factor required for bone formation and osteoblastic differentiation during normal development and is implicated in metastatic disease during breast cancer… (more)

Subjects/Keywords: Breast; Cancer; MCF10AT1; MCF10CA1a; Progression; Runx2; Biochemistry

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ojemann, A. (2017). Understanding the Role of Runx2 in a Breast Cancer Progression Cell Model. (Thesis). University of Vermont. Retrieved from https://scholarworks.uvm.edu/graddis/741

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Ojemann, Alexandra. “Understanding the Role of Runx2 in a Breast Cancer Progression Cell Model.” 2017. Thesis, University of Vermont. Accessed March 06, 2021. https://scholarworks.uvm.edu/graddis/741.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Ojemann, Alexandra. “Understanding the Role of Runx2 in a Breast Cancer Progression Cell Model.” 2017. Web. 06 Mar 2021.

Vancouver:

Ojemann A. Understanding the Role of Runx2 in a Breast Cancer Progression Cell Model. [Internet] [Thesis]. University of Vermont; 2017. [cited 2021 Mar 06]. Available from: https://scholarworks.uvm.edu/graddis/741.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Ojemann A. Understanding the Role of Runx2 in a Breast Cancer Progression Cell Model. [Thesis]. University of Vermont; 2017. Available from: https://scholarworks.uvm.edu/graddis/741

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

5. Patel, Ketan Vinodbhai. The development of an automated, fluorescent, quantitative three-dimensional in vitro organotypic invasion assay.

Degree: PhD, 2017, Queen Mary, University of London

URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/31860 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.786332

► Tumour metastasis is a complex multi-step biological process, which involves dispersion of cancer cells to various organ sites within the body. The tumour-stroma interface plays… (more)

▼ Tumour metastasis is a complex multi-step biological process, which involves dispersion of cancer cells to various organ sites within the body. The tumour-stroma interface plays an important role within cancer progression and is a major area of focus within cancer research. It is imperative that we are able to understand what mechanisms the tumour cells use in order to achieve maximum invasive potential. Fibroblasts are one of the major host cell types that are usurped by the tumour cells to promote invasion. Thus, we must understand the molecular mechanisms by which fibroblasts are transformed by the tumours into tumour-promoting fibroblasts, thus enabling cancer progression. Over 10 years ago our laboratory developed a quantitative image analysis methodology for analysing tumour and stromal fibroblast-interactions using 1ml collagen type I based three-dimensional (3D) organotypic gels. The assay is expensive, slow and can take 3-4 weeks before results are available. In this study I have developed two smaller versions of this assay that enable drug/gene screening in 3D, that are quicker to analyse and affordable; mini-organotypics (100μl) and micro-organotypics (50μl). Using fluorescently labelled tumour (red) and fibroblast (green) populations, it is possible to view the invasive process live and in situ, using confocal microscopy. Analysis of fluorescent organotypic gels after 72 hours, showed that the fibroblasts are the principal invading cell type that commence invasion and are followed by the tumour cells. For a proof-of-principle study I transfected human dermal fibroblasts with a customised SMARTpool siRNA library targeting proteases. Data collection was automated, thus allowing results within three days instead of three weeks. Relative to siRNA control treated fibroblasts, 16 out of 60 targeted proteases significantly reduced fibroblast and tumour cell invasion. Moreover, re-analysis of five lead proteases using individual siRNA for each gene identified that fibroblast MMP-17 and TMPRSS-13 is required by dermal fibroblasts to support invasion of cancer cells within this 3D assay. I believe this novel 24-well 3D fluorescent mini-organotypic invasion assay will allow drug/gene screens to be conducted affordably on multiple different tumour-stroma cell combinations. Moreover, the 96-well 3D fluorescent micro-organotypic invasion assay is almost ready for use in high-throughput screening and thus will be of great value in both academia and industry.

Subjects/Keywords: Tumour Biology; Tumour metastasis; cancer progression

10 more images…

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Patel, K. V. (2017). The development of an automated, fluorescent, quantitative three-dimensional in vitro organotypic invasion assay. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/31860 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.786332

Chicago Manual of Style (16^th Edition):

Patel, Ketan Vinodbhai. “The development of an automated, fluorescent, quantitative three-dimensional in vitro organotypic invasion assay.” 2017. Doctoral Dissertation, Queen Mary, University of London. Accessed March 06, 2021. http://qmro.qmul.ac.uk/xmlui/handle/123456789/31860 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.786332.

MLA Handbook (7^th Edition):

Patel, Ketan Vinodbhai. “The development of an automated, fluorescent, quantitative three-dimensional in vitro organotypic invasion assay.” 2017. Web. 06 Mar 2021.

Vancouver:

Patel KV. The development of an automated, fluorescent, quantitative three-dimensional in vitro organotypic invasion assay. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2017. [cited 2021 Mar 06]. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/31860 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.786332.

Council of Science Editors:

Patel KV. The development of an automated, fluorescent, quantitative three-dimensional in vitro organotypic invasion assay. [Doctoral Dissertation]. Queen Mary, University of London; 2017. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/31860 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.786332

University of Southern California

6. Oghamian, Shirley. The role of DNA methylation in early detection and progression of pancreatic cancer.

Degree: PhD, Biochemistry & Molecular Biology, 2011, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/242078/rec/7214

► Cancer is the second leading cause of death in the United States and each year nearly half a million Americans die of the disease. The… (more)

Subjects/Keywords: DNA methylation; pancreatic cancer; progression; early detection

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Oghamian, S. (2011). The role of DNA methylation in early detection and progression of pancreatic cancer. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/242078/rec/7214

Chicago Manual of Style (16^th Edition):

Oghamian, Shirley. “The role of DNA methylation in early detection and progression of pancreatic cancer.” 2011. Doctoral Dissertation, University of Southern California. Accessed March 06, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/242078/rec/7214.

MLA Handbook (7^th Edition):

Oghamian, Shirley. “The role of DNA methylation in early detection and progression of pancreatic cancer.” 2011. Web. 06 Mar 2021.

Vancouver:

Oghamian S. The role of DNA methylation in early detection and progression of pancreatic cancer. [Internet] [Doctoral dissertation]. University of Southern California; 2011. [cited 2021 Mar 06]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/242078/rec/7214.

Council of Science Editors:

Oghamian S. The role of DNA methylation in early detection and progression of pancreatic cancer. [Doctoral Dissertation]. University of Southern California; 2011. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll127/id/242078/rec/7214

7. I. Forno. EXPRESSION ANALYSIS OF MICRORNA IN PROSTATE CANCER AND IDENTIFICATION OF NOVEL DIAGNOSTIC BIOMARKER.

Degree: 2014, Università degli Studi di Milano

URL: http://hdl.handle.net/2434/231097

► Introduzione: Il tumore alla prostata (PCa) è una delle neoplasie più comuni tra gli uomini nel mondo occidentale e, globalmente, rappresenta la sesta causa di… (more)

▼ Introduzione: Il tumore alla prostata (PCa) è una delle neoplasie più comuni tra gli uomini nel mondo occidentale e, globalmente, rappresenta la sesta causa di morte dovuta a cancro. L'approccio diagnostico attuale si basa sulla misurazione dei livelli sierici dell’antigene prostatico PSA (prostate specific antigen), nonostante recenti studi clinici abbiano dimostrato che questo marcatore non riduce significativamente la mortalità associata a PCa. In questo scenario abbiamo ipotizzato che i microRNA possano essere nuovi potenziali biomarcatori di PCa. Scopo del lavoro: L'identificazione di microRNA, coinvolti nella progressione neoplastica del tumore prostatico come nuovi biomarcatori diagnostici aggiuntivi al PSA, prognostici e predittivi di aggressività tumorale. La nostra strategia sperimentale ha previsto l’uso di linee cellulari di prostata non tumorigeniche e a diverso grado di malignità, modelli murini di carcinoma prostatico e casistiche di pazienti affetti da PCa. Materiali e metodi: Linee cellulari commerciali: analisi dell'espressione globale dei miRNA tramite piattaforma low-density array nelle linee di PCa (LNCap, PC3, DU145), normali o iperplastiche (RWPE-1 e BPH-1). Casistiche cliniche: analisi di miRNA selezionati, in un set di pazienti (n=58) nei tessuti di parenchima normale, pre-neoplastico (prostatic intraepithelial neoplasia, PIN) e tumorale. I risultati ottenuti sono stati correlati a parametri clinicopatologici dei pazienti. I potenziali target proteici dei miRNA selezionati sono stati valutati in una casistica più ampia mediante tissue micro-array (TMA). Modello murino transgenico TRAMP: analisi globale di espressione dei miRNA in ghiandole di PIN e tumorali, e nello stroma associato. Linee cellulari primarie: ottenimento di linee di fibroblasti derivate da resezioni chirurgiche di PCa (n=10). Risultati: Dallo screening nelle linee cellulari abbiamo selezionato 23 miRNA poi valutati nei 58 pazienti. Tredici miRNA hanno mostrato differenze di espressione significative (p<0.05). In particolare, nove miRNA (miR-135b,-193a-5p,-205,-224,-22,-34b,-34c-5p,-452,miR-886-3p) sono risultati progressivamente diminuiti nella progressione neoplastica (N-PIN-PCa). Viceversa, i miR-130a, -218, -532, -542-5p, -489 e let-7c hanno mostrato una diminuzione di espressione nel PIN rispetto al tessuto normale. È noto che i miR-205, miR-218, miR-224 abbiano come bersaglio proteico RUNX2 (Runt-related transcription factor 2), un fattore di trascrizione coinvolto nel tropismo osseo di cellule metastatiche. La valutazione di RUNX2 nei TMA di prostata ha rivelato che la positività nucleare è specifica delle cellule tumorali (p<0.0001) e correla con l’estensione del tumore e con l'invasione capsulare. Inoltre il confronto tra l’espressione dei miRNA e RUNX2 ha mostrato correlazione inversa significativa. Dall’analisi del modello TRAMP abbiamo identificato un pannello di miRNA differenzialmente espressi tra le componenti epiteliali e stromali associate a PIN o PCa (n=52). Conclusioni: I nostri risultati mostrano una… Advisors/Committee Members: tutore: S. Bosari, direttore del dottorato: M. Clerici, BOSARI, SILVANO, CLERICI, MARIO SALVATORE.

Subjects/Keywords: prostate cancer; microRNA; PIN; cancer progression; Settore MED/08 - Anatomia Patologica

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APA (6^th Edition):

Forno, I. (2014). EXPRESSION ANALYSIS OF MICRORNA IN PROSTATE CANCER AND IDENTIFICATION OF NOVEL DIAGNOSTIC BIOMARKER. (Thesis). Università degli Studi di Milano. Retrieved from http://hdl.handle.net/2434/231097

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Forno, I.. “EXPRESSION ANALYSIS OF MICRORNA IN PROSTATE CANCER AND IDENTIFICATION OF NOVEL DIAGNOSTIC BIOMARKER.” 2014. Thesis, Università degli Studi di Milano. Accessed March 06, 2021. http://hdl.handle.net/2434/231097.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Forno, I.. “EXPRESSION ANALYSIS OF MICRORNA IN PROSTATE CANCER AND IDENTIFICATION OF NOVEL DIAGNOSTIC BIOMARKER.” 2014. Web. 06 Mar 2021.

Vancouver:

Forno I. EXPRESSION ANALYSIS OF MICRORNA IN PROSTATE CANCER AND IDENTIFICATION OF NOVEL DIAGNOSTIC BIOMARKER. [Internet] [Thesis]. Università degli Studi di Milano; 2014. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/2434/231097.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Forno I. EXPRESSION ANALYSIS OF MICRORNA IN PROSTATE CANCER AND IDENTIFICATION OF NOVEL DIAGNOSTIC BIOMARKER. [Thesis]. Università degli Studi di Milano; 2014. Available from: http://hdl.handle.net/2434/231097

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Deakin University

8. Liem-Weits, Marije. Tumour microenvironment interactions in breast cancer and the role of caveolin-1.

Degree: School of Life and Environmental Sciences, 2017, Deakin University

URL: http://hdl.handle.net/10536/DRO/DU:30105453

This study contributes to knowledge about the role of caveolin-1 in the microenvironment of breast cancer tumours. An important findings is that differentiated monocytes contribute to the regulation of caveolin-1 levels in co-cultures of fibroblasts and breast cancer cells. Advisors/Committee Members: Ackland M. Leigh, Michalczyk, Agnes.

Subjects/Keywords: caveolin-1 (CAV1); breast cancer; tumour progression; cancer cell physiology

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APA (6^th Edition):

Liem-Weits, M. (2017). Tumour microenvironment interactions in breast cancer and the role of caveolin-1. (Thesis). Deakin University. Retrieved from http://hdl.handle.net/10536/DRO/DU:30105453

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Liem-Weits, Marije. “Tumour microenvironment interactions in breast cancer and the role of caveolin-1.” 2017. Thesis, Deakin University. Accessed March 06, 2021. http://hdl.handle.net/10536/DRO/DU:30105453.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Liem-Weits, Marije. “Tumour microenvironment interactions in breast cancer and the role of caveolin-1.” 2017. Web. 06 Mar 2021.

Vancouver:

Liem-Weits M. Tumour microenvironment interactions in breast cancer and the role of caveolin-1. [Internet] [Thesis]. Deakin University; 2017. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/10536/DRO/DU:30105453.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Liem-Weits M. Tumour microenvironment interactions in breast cancer and the role of caveolin-1. [Thesis]. Deakin University; 2017. Available from: http://hdl.handle.net/10536/DRO/DU:30105453

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

9. Musrap, Natasha. Proteomic Identification of Mediators Implicated in the Metastatic Progression of Ovarian Cancer.

Degree: PhD, 2015, University of Toronto

URL: http://hdl.handle.net/1807/71578

► Ovarian cancer (OvCa) is the leading cause of death among gynecological malignancies, and is characterized by peritoneal metastasis and increased resistance to chemotherapy. Acquired drug… (more)

▼ Ovarian cancer (OvCa) is the leading cause of death among gynecological malignancies, and is characterized by peritoneal metastasis and increased resistance to chemotherapy. Acquired drug resistance is often attributed to the formation of multicellular aggregates (MCAs) in the peritoneal cavity, which seed abdominal surfaces, particularly, the mesothelial lining of the peritoneum. Given that the presence of metastatic implants is a predictor of poor survival, a better understanding of the underlying biology surrounding OvCa metastasis may lead to the identification of key molecules that are integral to the progression of the disease, which therefore, may serve as practicable therapeutic targets. To that end, in vitro cell line models of cancer-peritoneal interaction and aggregate formation were used to identify proteins that are differentially expressed during cancer progression, using mass spectrometry-based approaches. First, we performed a proteomics analysis of a co-culture model of ovarian cancer and mesothelial cells, in which we identified numerous proteins that were differentially regulated during cancer-peritoneal interaction. We further validated one protein, MUC5AC, and confirmed its expression at the cancer-peritoneal interface. Next, we conducted a quantitative proteomics analysis of a cell line grown as a monolayer and as MCAs. After identifying a subset of overexpressed proteins, we determined that CLCA1 plays a role in MCA formation. Additional studies using a CLCA1 blocker, as well as siRNA knockdown of CLCA1 in OvCa cells, resulted in a decreased ability of cancer cells to aggregate, a reduced ability to adhere to extracellular matrix components, and decreased cell viability. Moreover, we demonstrated that CLCA1 is able to regulate MUC5AC expression, as CLCA1-knockdown cells exhibited reduced expression of MUC5AC. In summary, the research presented in this thesis adds to our current understanding about ovarian cancer progression, and identifies two proteins that play a role in OvCa progression, which may serve as novel therapeutic targets. Advisors/Committee Members: Diamandis, Eleftherios P, Laboratory Medicine and Pathobiology.

Subjects/Keywords: Cancer Progression; Mass Spectrometry; Metastasis; Ovarian Cancer; Proteomics; 0992

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APA (6^th Edition):

Musrap, N. (2015). Proteomic Identification of Mediators Implicated in the Metastatic Progression of Ovarian Cancer. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/71578

Chicago Manual of Style (16^th Edition):

Musrap, Natasha. “Proteomic Identification of Mediators Implicated in the Metastatic Progression of Ovarian Cancer.” 2015. Doctoral Dissertation, University of Toronto. Accessed March 06, 2021. http://hdl.handle.net/1807/71578.

MLA Handbook (7^th Edition):

Musrap, Natasha. “Proteomic Identification of Mediators Implicated in the Metastatic Progression of Ovarian Cancer.” 2015. Web. 06 Mar 2021.

Vancouver:

Musrap N. Proteomic Identification of Mediators Implicated in the Metastatic Progression of Ovarian Cancer. [Internet] [Doctoral dissertation]. University of Toronto; 2015. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/1807/71578.

Council of Science Editors:

Musrap N. Proteomic Identification of Mediators Implicated in the Metastatic Progression of Ovarian Cancer. [Doctoral Dissertation]. University of Toronto; 2015. Available from: http://hdl.handle.net/1807/71578

10. VanderVeen, Brandon N. The Regulation of Skeletal Muscle Fatigue During the Progression of Cancer Cachexia.

Degree: PhD, Exercise Science, 2019, University of South Carolina

URL: https://scholarcommons.sc.edu/etd/5249

► Cachexia is the unintentional loss of body weight secondary to chronic disease and is prevalent is roughly 50% of cancer patients. The loss of… (more)

▼ Cachexia is the unintentional loss of body weight secondary to chronic disease and is prevalent is roughly 50% of cancer patients. The loss of body weight and skeletal muscle mass is reduced functional capacity associated with reduced life quality. The etiology of cachexia is multimodal and complex; however, cachexia has been linked to several systemic (e.g. chronic inflammation, hypogonadism, anemia, insulin resistance) and behavioral (e.g. anorexia, inactivity) changes that can compound to accelerate muscle mass and body weight loss. While several inflammatory cytokines are associated with cachexia’s disease progression, our laboratory has established that Interleukin-6 (IL-6) is a key regulator of skeletal muscle mass maintenance in tumor-bearing ApcMin/+ (MIN) mice. Additionally, we have shown that reduced volitional activity and increased skeletal muscle fatigue occurs prior to significant wasting and exercise training is able to prevent IL-6- induced cachexia in the MIN without affecting muscle inflammatory signaling. Furthermore, repeated muscle contractions were able to attenuate myofibrillar atrophy, and increase muscle oxidative metabolism without effecting the tumor environment. While the efficacy of exercise to improve skeletal muscle’s metabolic health during aging and disease has been well described, the effects of volitional activity on cancer-induced skeletal muscle fatigue, oxidative metabolism, and muscle inflammatory signaling is not well understood. The overall purpose of this study is to determine the regulation of skeletal muscle fatigue by activity and muscle inflammatory signaling during the progression of cachexia. Our central hypothesis is that cancer-induced skeletal muscle fatigue develops prior to significant weight loss concomitant with decreased muscle use and disrupted muscle oxidative metabolism which occurs through chronically activated muscle gp130 signaling. Our results suggest that the onset of skeletal muscle fatigue developed prior to significant weight loss in MIN mice. Furthermore, elevated circulating IL-6 accelerated skeletal muscle fatigue and reduced muscle oxidative metabolism through muscle gp130 signaling; however, loss of muscle gp130 signaling was unable to improve skeletal muscle fatigue in MIN mice. Last, we demonstrate that there is a direct relationship between activity and skeletal muscle fatigability in healthy and tumor-bearing mice. Together, these results suggest that fatigue develops independent of weight loss and while elevated IL-6 contributes to skeletal muscle fatigue, cancer-induced fatigue was not solely regulated by IL-6/muscle gp130 signaling. Advisors/Committee Members: James A. Carson.

Subjects/Keywords: Exercise Science; Public Health; cancer cachexia; fatigue; skeletal; muscle; cancer; progression

10 more images…

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APA (6^th Edition):

VanderVeen, B. N. (2019). The Regulation of Skeletal Muscle Fatigue During the Progression of Cancer Cachexia. (Doctoral Dissertation). University of South Carolina. Retrieved from https://scholarcommons.sc.edu/etd/5249

Chicago Manual of Style (16^th Edition):

VanderVeen, Brandon N. “The Regulation of Skeletal Muscle Fatigue During the Progression of Cancer Cachexia.” 2019. Doctoral Dissertation, University of South Carolina. Accessed March 06, 2021. https://scholarcommons.sc.edu/etd/5249.

MLA Handbook (7^th Edition):

VanderVeen, Brandon N. “The Regulation of Skeletal Muscle Fatigue During the Progression of Cancer Cachexia.” 2019. Web. 06 Mar 2021.

Vancouver:

VanderVeen BN. The Regulation of Skeletal Muscle Fatigue During the Progression of Cancer Cachexia. [Internet] [Doctoral dissertation]. University of South Carolina; 2019. [cited 2021 Mar 06]. Available from: https://scholarcommons.sc.edu/etd/5249.

Council of Science Editors:

VanderVeen BN. The Regulation of Skeletal Muscle Fatigue During the Progression of Cancer Cachexia. [Doctoral Dissertation]. University of South Carolina; 2019. Available from: https://scholarcommons.sc.edu/etd/5249

University of Louisville

11. Leggett, Carmine Simone. Role of human arylamine N-acetyltransferase in carcinogen metabolism and human breast cancer progression.

Degree: PhD, 2012, University of Louisville

URL: 10.18297/etd/812 ; https://ir.library.louisville.edu/etd/812

► Human arylamine N-acetyltransferase (NAT) is a phase II cytosolic enzyme that occurs as two isozymes, NAT1 and NAT2. This family of polymorphic enzymes catalyzes the… (more)

▼ Human arylamine N-acetyltransferase (NAT) is a phase II cytosolic enzyme that occurs as two isozymes, NAT1 and NAT2. This family of polymorphic enzymes catalyzes the detoxification and/or activation of many aromatic and heterocyclic amine drugs and carcinogens. These metabolism reactions can lead to detoxification of xenobiotics by N-acetylation, or bioactivation by O-acetylation which is preceded by cytochrome P450 (CYP) hydroxylation. This study evaluates the role of human arylamine N-acetyltransferase in carcinogen metabolism as it pertains to substrate selectivity, kinetic activity towards arylamine and alkylaniline substrates, and toxicological risk. Here we introduce the use of immortalized human fibroblasts (GM4429) to investigate the effects of combinations of human NAT1, human NAT2 haplotypes (NA T2*4, NA T2*S8, or NAT2*78), and varying CYP1 A2 enzymatic activity on carcinogen metabolism. We determined the apparent Michaelis-Menten constants of human NAT1 and human NAT2 for several well-characterized and putative environmental carcinogens. We utilized these data to investigate NAT substrate selectivity for these compounds of interest. NAT1 has been implicated in several cancers including urinary bladder, colorectal, lung, and breast cancer. Studies suggest that NAT1 plays an important role in cell growth and survival, as well as in cell proliferation and cell invasion, which are hallmarks of metastatic cancer. Here we describe the use of computational screening to identify effective, novel small molecule inhibitors of the molecular target NAT1. Our lead compound, Compound 10, suppressed carcinogen metabolism and 4-aminobiphenyl (ASP) -induced DNA adducts. The results in this study show that upon NAT1 inhibition there is a significant decrease in ASP activation, cell invasion, and cell proliferation in human breast adenocarcinoma cells. We also show that NAT1 inhibition in human breast cancer cells resulted in mitotic arrest, which supports findings suggesting that NAT1 plays an important role in human breast cancer progression. Our results indicate that human NAT1 is a molecular target for cancer therapy. Advisors/Committee Members: Hein, David W..

Subjects/Keywords: Arylamine N-acetyltransferase; cancer; environmental carcinogens; cancer progression; carcinogen metabolism

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APA (6^th Edition):

Leggett, C. S. (2012). Role of human arylamine N-acetyltransferase in carcinogen metabolism and human breast cancer progression. (Doctoral Dissertation). University of Louisville. Retrieved from 10.18297/etd/812 ; https://ir.library.louisville.edu/etd/812

Chicago Manual of Style (16^th Edition):

Leggett, Carmine Simone. “Role of human arylamine N-acetyltransferase in carcinogen metabolism and human breast cancer progression.” 2012. Doctoral Dissertation, University of Louisville. Accessed March 06, 2021. 10.18297/etd/812 ; https://ir.library.louisville.edu/etd/812.

MLA Handbook (7^th Edition):

Leggett, Carmine Simone. “Role of human arylamine N-acetyltransferase in carcinogen metabolism and human breast cancer progression.” 2012. Web. 06 Mar 2021.

Vancouver:

Leggett CS. Role of human arylamine N-acetyltransferase in carcinogen metabolism and human breast cancer progression. [Internet] [Doctoral dissertation]. University of Louisville; 2012. [cited 2021 Mar 06]. Available from: 10.18297/etd/812 ; https://ir.library.louisville.edu/etd/812.

Council of Science Editors:

Leggett CS. Role of human arylamine N-acetyltransferase in carcinogen metabolism and human breast cancer progression. [Doctoral Dissertation]. University of Louisville; 2012. Available from: 10.18297/etd/812 ; https://ir.library.louisville.edu/etd/812

Université de Lorraine

12. Chamard-Jovenin, Clémence. Impact d’une surexpression d’ERα36 et/ou d’une exposition aux alkylphénols sur la physiopathologie de la glande mammaire : Consequences of of ERα36 overexpression and/or alkylphenols exposure on mammary gland physiopathology.

Degree: Docteur es, Sciences de la vie et de la santé, 2016, Université de Lorraine

URL: http://www.theses.fr/2016LORR0232

►

Durant ma thèse, j’ai étudié l’implication d’un variant du récepteur aux œstrogènes α, ERα36, dans l’initiation et la progression du cancer du sein. Au laboratoire,… (more)

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Durant ma thèse, j’ai étudié l’implication d’un variant du récepteur aux œstrogènes α, ERα36, dans l’initiation et la progression du cancer du sein. Au laboratoire, son expression dans les cancers testiculaires avait été montrée comme étant inductrice de la prolifération cellulaire in vitro et in vivo après une exposition à un mélange de polluants environnementaux, considérés comme perturbateurs endocriniens oestrogéno-mimétique : les alkylphénols. Une analyse rétrospective d’échantillons de tumeurs mammaires a montré, par la modélisation de réseaux d’interactions géniques, que l’expression d’ERα36 était corrélée avec l’expression de marqueurs de migration cellulaire, caractéristiques de la progression tumorale. La surexpression d’ERα36 par transfection in vitro et dans un modèle unique de souris Knocked In exprimant ERalpha36 dans la glande mammaire ont montré qu’ERα36 est suffisant pour altérer le phénotype épithélial des cellules mammaires saines. Une exposition aux alkylphénols qui stimulent son expression endogène accentue les altérations cellulaires observées et contribue à l’acquisition transgénérationnelle de propriétés relatives à une transformation tumorale. Les analyses de ce projet pluridisciplinaire se sont appuyées sur des expertises biologiques, mathématiques et bioinformatiques et ont permis de mettre en évidence pour la première fois le rôle potentiel d’ERα36 dans l’initiation tumorale et de confirmer son implication dans la progression du cancer du sein. Enfin, nous avons montré que l’exposition à des doses environnementales d’alkylphénols lors de la période de périnatalité peut conduire à une modification transgénérationnelle de la différenciation de la glande mammaire sous le contrôle d’ERα36 et ainsi augmenter le risque de cancer mammaire

This work was dedicated to study how a variant of estrogen receptor α, ERα36, acts in initiation and progression of breast cancer. In the laboratory, his expression in testicular cancer was shown to stimulate cell proliferation in vitro and in vivo after environmental pollutant exposure. The compounds studied, the alkylphenols, are endocrine disruptors, interfering with normal estrogen signaling. Gene interaction network modelling from retrospective analysis of breast cancer samples showed that ERα36 expression was correlated with the expression of cell migration markers, typical of tumor progression. In vitro ERα36 overexpression and in a unique mouse Knocked In model, expressing ERα36 in the mammary gland, showed that ERα36 is sufficient to alter epithelial phenotype of normal breast cells. Alkylphenols exposure, that stimulated ERα36 endogenous expression, increased cellular alterations and contributed to transgenerational acquisition of properties related to neoplastic transformation. Analysis of this multidisciplinary project were based on biological expertise, mathematics and bioinformatic tools. These results enabled to highlight for the first time the potential role of ERα36 in tumor initiation and confirmed his involvement in breast cancer…

Advisors/Committee Members: Dumond, Hélène (thesis director), Boukhobza, Taha (thesis director).

Subjects/Keywords: Cancer du sein; Erα36; Initiation; Progression; Perturbateurs endocriniens; Effets transgénérationnels; Breast cancer; Erα36; Initiation; Progression; Endocrine disruptors; Transgenerational effects

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APA (6^th Edition):

Chamard-Jovenin, C. (2016). Impact d’une surexpression d’ERα36 et/ou d’une exposition aux alkylphénols sur la physiopathologie de la glande mammaire : Consequences of of ERα36 overexpression and/or alkylphenols exposure on mammary gland physiopathology. (Doctoral Dissertation). Université de Lorraine. Retrieved from http://www.theses.fr/2016LORR0232

Chicago Manual of Style (16^th Edition):

Chamard-Jovenin, Clémence. “Impact d’une surexpression d’ERα36 et/ou d’une exposition aux alkylphénols sur la physiopathologie de la glande mammaire : Consequences of of ERα36 overexpression and/or alkylphenols exposure on mammary gland physiopathology.” 2016. Doctoral Dissertation, Université de Lorraine. Accessed March 06, 2021. http://www.theses.fr/2016LORR0232.

MLA Handbook (7^th Edition):

Chamard-Jovenin, Clémence. “Impact d’une surexpression d’ERα36 et/ou d’une exposition aux alkylphénols sur la physiopathologie de la glande mammaire : Consequences of of ERα36 overexpression and/or alkylphenols exposure on mammary gland physiopathology.” 2016. Web. 06 Mar 2021.

Vancouver:

Chamard-Jovenin C. Impact d’une surexpression d’ERα36 et/ou d’une exposition aux alkylphénols sur la physiopathologie de la glande mammaire : Consequences of of ERα36 overexpression and/or alkylphenols exposure on mammary gland physiopathology. [Internet] [Doctoral dissertation]. Université de Lorraine; 2016. [cited 2021 Mar 06]. Available from: http://www.theses.fr/2016LORR0232.

Council of Science Editors:

Chamard-Jovenin C. Impact d’une surexpression d’ERα36 et/ou d’une exposition aux alkylphénols sur la physiopathologie de la glande mammaire : Consequences of of ERα36 overexpression and/or alkylphenols exposure on mammary gland physiopathology. [Doctoral Dissertation]. Université de Lorraine; 2016. Available from: http://www.theses.fr/2016LORR0232

13. Toulet, Aurélie. Dissémination du cancer de la prostate : un chemin pavé de gras : Dissemination of prostate cancer : a way paved of fat.

Degree: Docteur es, Cancérologie, 2018, Université Toulouse III – Paul Sabatier

URL: http://www.theses.fr/2018TOU30237

►

Le cancer de la prostate (CaP) est la première cause de cancer chez l'homme dans les pays industrialisés. Il s'agit d'une maladie hétérogène pouvant être… (more)

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Le cancer de la prostate (CaP) est la première cause de cancer chez l'homme dans les pays industrialisés. Il s'agit d'une maladie hétérogène pouvant être indolente ou très agressive et mettant alors en jeu le pronostic des patients. Les mécanismes moléculaires impliqués dans cette progression tumorale sont mal connus. L'objectif de ma thèse était de caractériser le rôle d'un des composants majeurs du microenvironnement de ces tumeurs, le tissu adipeux périprostatique (TAPP), dépôt adipocytaire entourant la glande prostatique. En effet, l'invasion de ce TAPP par les cellules tumorales est reconnue comme un facteur de mauvais pronostic, suggérant que ce TAPP (en particulier les adipocytes) pourrait être un acteur clé de la progression tumorale. Dans un premier temps nous nous sommes intéressés au rôle paracrine de ce TAPP en condition d'obésité, qui est un facteur pronostique négatif dans le cancer de la prostate. Nous avons montré qu'une chimiokine adipocytaire (CCL7), en se liant à son récepteur CCR3 présent à la surface des cellules tumorales, attire ces dernières, favorisant ainsi la dissémination locale du cancer de la prostate, ce phénomène étant amplifié en conditions d'obésité. Une fois que les cellules tumorales ont franchi la capsule prostatique, elles entrent en contact direct avec les adipocytes du TAPP et un dialogue s'établit entre les deux types cellulaires. Nos résultats montrent que ce dialogue se manifeste par une lipolyse accrue dans les adipocytes qui relarguent des acides gras libres (AGL) qui sont ensuite captés par les cellules tumorales. Ces AGL activent une cascade de signalisation dans les cellules tumorales, en stimulant l'expression d'enzymes pro-oxydantes, et en particulier la NOX5 (NADPH-oxydase 5), qui va entraîner une augmentation des ROS (espèces réactives de l'oxygène) intracellulaires. Cette augmentation des ROS va entraîner une augmentation de certaines MMP (Matrix Metalloproteinases) impliquées dans l'invasion tumorale. Cette voie de signalisation est également amplifiée dans un contexte d'obésité. En dehors de l'obésité, des études récentes montrent que certains patients pourraient présenter une accumulation anormale de ce TAPP indépendamment de l'indice de masse corporelle (IMC), ces TAPP abondants étant associés à des cancers agressifs. Nous avons montré, en mesurant le volume de TAPP sur les IRM de 147 patients atteints de CaP, que l'abondance du TAPP est dissociée de l'IMC et des autres dépôts adipeux. [...]

Prostate cancer (PCa) is the most common cancer in men in Western countries. It is a heterogeneous disease ranging from indolent to very aggressive, life-threatening forms. The molecular mechanisms implicated in tumor progression have not been clearly identified yet. The aim of my thesis was to characterize the role of one of the main components of prostate cancer microenvironment, the periprostatic adipose tissue (PPAT), an adipose depot surrounding the prostate. Indeed, PPAT invasion by tumor cells is recognized as a poor prognosis factor in PCa, suggesting that PPAT…

Advisors/Committee Members: Muller, Catherine (thesis director), Milhas, Delphine (thesis director).

Subjects/Keywords: Cancer de la prostate; Microenvironnement tumoral; Adipocytes; Progression tumorale; Matrice extracellulaire; Prostate cancer; Tumor microenvironment; Adipocytes; Tumor progression; Extracellular matrix

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APA (6^th Edition):

Toulet, A. (2018). Dissémination du cancer de la prostate : un chemin pavé de gras : Dissemination of prostate cancer : a way paved of fat. (Doctoral Dissertation). Université Toulouse III – Paul Sabatier. Retrieved from http://www.theses.fr/2018TOU30237

Chicago Manual of Style (16^th Edition):

Toulet, Aurélie. “Dissémination du cancer de la prostate : un chemin pavé de gras : Dissemination of prostate cancer : a way paved of fat.” 2018. Doctoral Dissertation, Université Toulouse III – Paul Sabatier. Accessed March 06, 2021. http://www.theses.fr/2018TOU30237.

MLA Handbook (7^th Edition):

Toulet, Aurélie. “Dissémination du cancer de la prostate : un chemin pavé de gras : Dissemination of prostate cancer : a way paved of fat.” 2018. Web. 06 Mar 2021.

Vancouver:

Toulet A. Dissémination du cancer de la prostate : un chemin pavé de gras : Dissemination of prostate cancer : a way paved of fat. [Internet] [Doctoral dissertation]. Université Toulouse III – Paul Sabatier; 2018. [cited 2021 Mar 06]. Available from: http://www.theses.fr/2018TOU30237.

Council of Science Editors:

Toulet A. Dissémination du cancer de la prostate : un chemin pavé de gras : Dissemination of prostate cancer : a way paved of fat. [Doctoral Dissertation]. Université Toulouse III – Paul Sabatier; 2018. Available from: http://www.theses.fr/2018TOU30237

University of Windsor

14. Abedalrhman, Alkhateeb. Machine Learning Approaches for Cancer Analysis.

Degree: PhD, Computer Science, 2018, University of Windsor

URL: https://scholar.uwindsor.ca/etd/7597

► In addition, we propose many machine learning models that serve as contributions to solve a biological problem. First, we present Zseq, a linear time… (more)

▼ In addition, we propose many machine learning models that serve as contributions to solve a biological problem. First, we present Zseq, a linear time method that identifies the most informative genomic sequences and reduces the number of biased sequences, sequence duplications, and ambiguous nucleotides. Zseq finds the complexity of the sequences by counting the number of unique k-mers in each sequence as its corresponding score and also takes into the account other factors, such as ambiguous nucleotides or high GC-content percentage in k-mers. Based on a z-score threshold, Zseq sweeps through the sequences again and filters those with a z-score less than the user-defined threshold. Zseq is able to provide a better mapping rate; it reduces the number of ambiguous bases significantly in comparison with other methods. Evaluation of the filtered reads has been conducted by aligning the reads and assembling the transcripts using the reference genome as well as de novo assembly. The assembled transcripts show a better discriminative ability to separate cancer and normal samples in comparison with another state-of-the-art method. Studying the abundance of select mRNA species throughout prostate cancer progression may provide some insight into the molecular mechanisms that advance the disease. In the second contribution of this dissertation, we reveal that the combination of proper clustering, distance function and Index validation for clusters are suitable in identifying outlier transcripts, which show different trending than the majority of the transcripts, the trending of the transcript is the abundance throughout different stages of prostate cancer. We compare this model with standard hierarchical time-series clustering method based on Euclidean distance. Using time-series profile hierarchical clustering methods, we identified stage-specific mRNA species termed outlier transcripts that exhibit unique trending patterns as compared to most other transcripts during disease progression. This method is able to identify those outliers rather than finding patterns among the trending transcripts compared to the hierarchical clustering method based on Euclidean distance. A wet-lab experiment on a biomarker (CAM2G gene) confirmed the result of the computational model. Genes related to these outlier transcripts were found to be strongly associated with cancer, and in particular, prostate cancer. Further investigation of these outlier transcripts in prostate cancer may identify them as potential stage-specific biomarkers that can predict the progression of the disease. Breast cancer, on the other hand, is a widespread type of cancer in females and accounts for a lot of cancer cases and deaths in the world. Identifying the subtype of breast cancer plays a crucial role in selecting the best treatment. In the third contribution, we propose an optimized hierarchical classification model that is used to predict the breast cancer subtype. Suitable filter feature selection methods and new hybrid feature selection methods are utilized… Advisors/Committee Members: Luis Rueda.

Subjects/Keywords: Breast Cancer; Cancer Progression; Machine Learning; Prostate Cancer; RNA-Seq; Survivability; Computer Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Abedalrhman, A. (2018). Machine Learning Approaches for Cancer Analysis. (Doctoral Dissertation). University of Windsor. Retrieved from https://scholar.uwindsor.ca/etd/7597

Chicago Manual of Style (16^th Edition):

Abedalrhman, Alkhateeb. “Machine Learning Approaches for Cancer Analysis.” 2018. Doctoral Dissertation, University of Windsor. Accessed March 06, 2021. https://scholar.uwindsor.ca/etd/7597.

MLA Handbook (7^th Edition):

Abedalrhman, Alkhateeb. “Machine Learning Approaches for Cancer Analysis.” 2018. Web. 06 Mar 2021.

Vancouver:

Abedalrhman A. Machine Learning Approaches for Cancer Analysis. [Internet] [Doctoral dissertation]. University of Windsor; 2018. [cited 2021 Mar 06]. Available from: https://scholar.uwindsor.ca/etd/7597.

Council of Science Editors:

Abedalrhman A. Machine Learning Approaches for Cancer Analysis. [Doctoral Dissertation]. University of Windsor; 2018. Available from: https://scholar.uwindsor.ca/etd/7597

University of Michigan

15. Moore, Heather Marie. The Role of EZH2 in Breast Cancer Progression and Metastasis.

Degree: PhD, Cellular and Molecular Biology, 2013, University of Michigan

URL: http://hdl.handle.net/2027.42/100098

► Understanding how breast cancer cells disseminate and metastasize is essential to develop better treatments and to improve survival. Enhancer of Zeste Homolog 2 (EZH2) is… (more)

▼ Understanding how breast cancer cells disseminate and metastasize is essential to develop better treatments and to improve survival. Enhancer of Zeste Homolog 2 (EZH2) is a Polycomb group protein characterized as a transcriptional repressor through histone trimethylation. We previously found EZH2 overexpression in human invasive breast carcinomas to associate with worse survival. Here, we have focused on elucidating the mechanisms by which EZH2 promotes aggressive breast carcinomas with metastatic potential. We have found that EZH2 regulates two important processes for metastasis: the epithelial-to-mesenchymal transition and migration, and breast cancer stem cell numbers. We discovered that EZH2 downregulation in breast cancer cells promoted a mesenchymal-to-epithelial transition, reduced invasion and motility, and decreased spontaneous pulmonary metastasis. EZH2 was found to induce the p38 signaling pathway, an established regulator of breast cancer invasion and metastasis. EZH2 was demonstrated to bind phosphorylated-p38 (p-p38) in association with other members of the Polycomb Repressive Complex 2 (PRC2). The effect of p-p38 was confirmed in vivo and correlated with decreased spontaneous metastasis. Through analysis of invasive human breast cancers, EZH2 expression was upregulated in all metastatic cases, and EZH2 and p-p38 were co-expressed in 63% of cases, consistent with the functional results. In our studies on the role of EZH2 on breast cancer stem cells, we found that EZH2 expression levels regulate stem cell numbers in nontumorigenic and malignant breast cells. We revealed a role of EZH2 in activating Notch1 signaling by binding the Notch1 promoter independently of PRC2 and methyltransferase activity. Notch1 inhibition was sufficient in preventing the EZH2-induced expansion of stem cell numbers. In a transgenic model with targeted EZH2 overexpression, we found that EZH2 promoted earlier breast cancer initiation and correlated with Notch1 expression. Additionally, EZH2, Notch1 and stem cell markers were found to correlate in human breast cancer. Altogether, these findings reveal important and novel functional links between EZH2, stem cells and breast cancer migration and invasion, and the underlying mechanisms involving EZH2-mediated regulation of the p38 and Notch1 signaling pathways. This work establishes EZH2 as a regulator of breast cancer progression and metastasis, and identifies potential targets for treatment of this malignancy. Advisors/Committee Members: Kleer, Celina G. (committee member), Dlugosz, Andrzej A. (committee member), Dressler, Gregory R. (committee member), Varambally, Sooryanarayana (committee member), Merajver, Sofia D. (committee member).

Subjects/Keywords: Breast Cancer Progression and Metastasis; EZH2; Polycomb; Pathology; Health Sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Moore, H. M. (2013). The Role of EZH2 in Breast Cancer Progression and Metastasis. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/100098

Chicago Manual of Style (16^th Edition):

Moore, Heather Marie. “The Role of EZH2 in Breast Cancer Progression and Metastasis.” 2013. Doctoral Dissertation, University of Michigan. Accessed March 06, 2021. http://hdl.handle.net/2027.42/100098.

MLA Handbook (7^th Edition):

Moore, Heather Marie. “The Role of EZH2 in Breast Cancer Progression and Metastasis.” 2013. Web. 06 Mar 2021.

Vancouver:

Moore HM. The Role of EZH2 in Breast Cancer Progression and Metastasis. [Internet] [Doctoral dissertation]. University of Michigan; 2013. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/2027.42/100098.

Council of Science Editors:

Moore HM. The Role of EZH2 in Breast Cancer Progression and Metastasis. [Doctoral Dissertation]. University of Michigan; 2013. Available from: http://hdl.handle.net/2027.42/100098

Cornell University

16. Mohanan Nair Padmini, Sunish. Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation.

Degree: PhD, Veterinary Medicine, 2014, Cornell University

URL: http://hdl.handle.net/1813/36176

► Numerous recent studies have shown that epigenetic modifications play a significant role in cancer pathogenesis. The PADs are a family of epigenetic enzymes that catalyze… (more)

▼ Numerous recent studies have shown that epigenetic modifications play a significant role in cancer pathogenesis. The PADs are a family of epigenetic enzymes that catalyze citrullination, a reaction by which PADs convert peptidyl-arginine to neutral citrulline, leading to the disruption of protein-protein interactions. Our lab has found that PAD2 has a critical role in breast cancer progression. The goal of this thesis research was to further elucidate the role of PAD2 in epithelial carcinogenesis using PAD2 overexpression tumor cell lines and a MMTV-FLAG-hPAD2 transgenic mouse model. We also aimed to evaluate how PAD2 may play a direct role in regulating chronic inflammation via macrophage extracellular chromatin trap release ("ETosis"). Interestingly, we found that 40% of the MMTV-FLAG-hPAD2 overexpressing transgenic mice developed proliferative skin lesions after five months of age. The tumors expressed the transgenic form of FLAG-hPAD2 and showed increased expression for inflammatory cytokines such as IL6 and IL8. As the next step we conducted a two-stage chemical carcinogenesis study to further evaluate the predilection of MMTV-FLAG-hPAD2 mice to develop more invasive skin tumors and compare the histopathology of these tumors with the WT tumors. We found that a higher percentage of MMTV-FLAG-hPAD2 mice developed skin papillomas and the transgenic tumors were more invasive. Furthermore, hPAD2 expression levels were highly positively correlated with chemokine levels and negatively correlated with the cell adhesion markers suggesting the role of PAD2 in assisting epithelial-mesenchymal transition. We had previously shown that PAD4 isozyme in neutrophils is involved in chromatin decondensation and extracellular chromatin trap release. In this thesis research we provide evidence on how PAD2 is involved in macrophage extracellular trap (MET) release. Using in vitro macrophage culture models, we found that PAD2 is critical in functional MET release and that METs contain high levels of histone H4 citrulline 3 (H4Cit3) modification. Using human tongue SCC tissue, we show that CD68+ macrophage associated ETs exist in tumor tissue and are highly positive for citrullinated histones. Additionally, we show that PAD2-rich macrophages associated with chronic subclinical inflammation in adipose tissue also release METs suggesting the significant role of PAD2 in chronic inflammation via MET release. Collectively, these studies provide strong experimental evidence establishing PAD2 as a potential oncogene, a therapeutic target for immunomodulation and a regulator of obesity and tumor associated inflammation. Advisors/Committee Members: Coonrod, Scott A. (chair), August, Avery (committee member), Fischbach, Claudia (committee member), Weiss, Robert S. (committee member).

Subjects/Keywords: Peptidylarginine deiminase 2 (PAD2); Cancer progression; Extracellular chromatin traps (ETosis)

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APA (6^th Edition):

Mohanan Nair Padmini, S. (2014). Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/36176

Chicago Manual of Style (16^th Edition):

Mohanan Nair Padmini, Sunish. “Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation.” 2014. Doctoral Dissertation, Cornell University. Accessed March 06, 2021. http://hdl.handle.net/1813/36176.

MLA Handbook (7^th Edition):

Mohanan Nair Padmini, Sunish. “Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation.” 2014. Web. 06 Mar 2021.

Vancouver:

Mohanan Nair Padmini S. Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation. [Internet] [Doctoral dissertation]. Cornell University; 2014. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/1813/36176.

Council of Science Editors:

Mohanan Nair Padmini S. Role Of Peptidylarginine Deiminase 2 (Pad2) In Epithelial Carcinogenesis And Tumor-Associated Inflammation. [Doctoral Dissertation]. Cornell University; 2014. Available from: http://hdl.handle.net/1813/36176

Harvard University

17. McFarland, Christopher Dennis. The role of deleterious passengers in cancer.

Degree: PhD, Biophysics, 2014, Harvard University

URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:13070047

► The development of cancer from a population of precancerous cells is a rapid evolutionary process. During progression, cells evolve several new traits for survive and… (more)

▼ The development of cancer from a population of precancerous cells is a rapid evolutionary process. During progression, cells evolve several new traits for survive and proliferation via a few key `driver' mutations. However, these few driver alterations reside in a cancer genome alongside tens of thousands of additional `passenger' mutations. Passengers are widely believed to have no role in cancer, yet many passengers fall within functional genomic elements that may have potentially deleterious effects on the cancer cells. Here we investigate the potential of moderately deleterious passengers to accumulate and alter neoplastic progression. Evolutionary simulations suggest that moderately-deleterious passengers accumulate during progression and largely evade natural selection. Accumulation is possible because of cancer's unique evolutionary constraints: an initially small population size, an elevated mutation rate, and a need to acquire several driver mutations within a short evolutionary timeframe. Cancer dynamics can be theoretically understood as a tug-of-war between rare, strongly-beneficial drives and frequent mildly-deleterious passengers. In this formalism, passengers present a barrier to cancer progression describable by a critical population size, below which most lesions fail to progress, and a critical mutation rate, above which cancers collapse. In essence, cancer progression can be subverted by its own unique evolutionary constraints. The collective burden of passengers explain several oncological phenomena that are difficult to explain otherwise. Genomics data confirms that many passengers are likely damaging and have largely evaded negative selection, while age-incidence curves and the distribution of mutation totals suggests that drivers and passengers exhibit competing effects. These data also provide estimates of the strength of drivers and passengers. Finally, we use our model to explore cancer treatments. We identify two broad regimes of adaptive evolutionary dynamics and use these regimes to understand outcomes from various treatment strategies. Our theory explains previously paradoxical treatment outcomes and suggest that passengers could serve as a biomarker of response to mutagenic therapies. Deleterious passengers are targetable by either (i) increasing the mutation rate or (ii) exacerbating their deleterious effects. Our results suggest a unique framework for understanding cancer progression as a balance between driver and passenger mutations. Advisors/Committee Members: Mirny, Leonid Alex (advisor), Desai, Michael (committee member), Getz, Gad (committee member), Van Allen, Eliezer (committee member).

Subjects/Keywords: Biophysics; Evolution & development; Genetics; Cancer Progression; Evolutionary Modeling; Genomics

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APA (6^th Edition):

McFarland, C. D. (2014). The role of deleterious passengers in cancer. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:13070047

Chicago Manual of Style (16^th Edition):

McFarland, Christopher Dennis. “The role of deleterious passengers in cancer.” 2014. Doctoral Dissertation, Harvard University. Accessed March 06, 2021. http://nrs.harvard.edu/urn-3:HUL.InstRepos:13070047.

MLA Handbook (7^th Edition):

McFarland, Christopher Dennis. “The role of deleterious passengers in cancer.” 2014. Web. 06 Mar 2021.

Vancouver:

McFarland CD. The role of deleterious passengers in cancer. [Internet] [Doctoral dissertation]. Harvard University; 2014. [cited 2021 Mar 06]. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:13070047.

Council of Science Editors:

McFarland CD. The role of deleterious passengers in cancer. [Doctoral Dissertation]. Harvard University; 2014. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:13070047

University of Toronto

18. Liu, Li Yang. Association of Tissue Promoter Methylation Levels of APC, RASSF1A, CYP26A1, and TBX15 with Prostate Cancer Progression.

Degree: 2012, University of Toronto

URL: http://hdl.handle.net/1807/33724

►

Aberrant promoter methylation is known to silence tumor-suppressor genes in prostate cancer. Using a quantitative real-time PCR assay(MethyLight), I determined promoter methylation levels of APC,… (more)

Subjects/Keywords: DNA Methylation; Prostate Cancer; Epigenetic Mechanism; Progression; Biochemical Recurrence; 0369; 0307

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APA (6^th Edition):

Liu, L. Y. (2012). Association of Tissue Promoter Methylation Levels of APC, RASSF1A, CYP26A1, and TBX15 with Prostate Cancer Progression. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/33724

Chicago Manual of Style (16^th Edition):

Liu, Li Yang. “Association of Tissue Promoter Methylation Levels of APC, RASSF1A, CYP26A1, and TBX15 with Prostate Cancer Progression.” 2012. Masters Thesis, University of Toronto. Accessed March 06, 2021. http://hdl.handle.net/1807/33724.

MLA Handbook (7^th Edition):

Liu, Li Yang. “Association of Tissue Promoter Methylation Levels of APC, RASSF1A, CYP26A1, and TBX15 with Prostate Cancer Progression.” 2012. Web. 06 Mar 2021.

Vancouver:

Liu LY. Association of Tissue Promoter Methylation Levels of APC, RASSF1A, CYP26A1, and TBX15 with Prostate Cancer Progression. [Internet] [Masters thesis]. University of Toronto; 2012. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/1807/33724.

Council of Science Editors:

Liu LY. Association of Tissue Promoter Methylation Levels of APC, RASSF1A, CYP26A1, and TBX15 with Prostate Cancer Progression. [Masters Thesis]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/33724

University of California – San Francisco

19. Brown, Christopher Michael. Technologies for Following Active Serine Proteases in Cancer Progression and Metastasis.

Degree: Biochemistry and Molecular Biology, 2010, University of California – San Francisco

URL: http://www.escholarship.org/uc/item/2sh048jb

► Serine proteases acting at the cell surface are a unique class of enzymes that carry out important cell signaling functions. By acting upstream of proteolytic… (more)

Subjects/Keywords: Biochemistry; activity-based probes; cancer progression; serine protease

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APA (6^th Edition):

Brown, C. M. (2010). Technologies for Following Active Serine Proteases in Cancer Progression and Metastasis. (Thesis). University of California – San Francisco. Retrieved from http://www.escholarship.org/uc/item/2sh048jb

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Brown, Christopher Michael. “Technologies for Following Active Serine Proteases in Cancer Progression and Metastasis.” 2010. Thesis, University of California – San Francisco. Accessed March 06, 2021. http://www.escholarship.org/uc/item/2sh048jb.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Brown, Christopher Michael. “Technologies for Following Active Serine Proteases in Cancer Progression and Metastasis.” 2010. Web. 06 Mar 2021.

Vancouver:

Brown CM. Technologies for Following Active Serine Proteases in Cancer Progression and Metastasis. [Internet] [Thesis]. University of California – San Francisco; 2010. [cited 2021 Mar 06]. Available from: http://www.escholarship.org/uc/item/2sh048jb.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Brown CM. Technologies for Following Active Serine Proteases in Cancer Progression and Metastasis. [Thesis]. University of California – San Francisco; 2010. Available from: http://www.escholarship.org/uc/item/2sh048jb

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queen Mary, University of London

20. Hervieu Vilches, Alexia. Understanding and targeting PI3K downstream of oncogenic Met mutant.

Degree: PhD, 2015, Queen Mary, University of London

URL: http://qmro.qmul.ac.uk/xmlui/handle/123456789/33935 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667429

► The Receptor Tyrosine Kinase (RTK) Met, overexpressed or mutated in cancer, plays a major role in cancer progression and represents an attractive target for cancer… (more)

Subjects/Keywords: 616.99; Tumour Biology; Receptor Tyrosine Kinase; cancer progression; Met oncogenicity

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APA (6^th Edition):

Hervieu Vilches, A. (2015). Understanding and targeting PI3K downstream of oncogenic Met mutant. (Doctoral Dissertation). Queen Mary, University of London. Retrieved from http://qmro.qmul.ac.uk/xmlui/handle/123456789/33935 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667429

Chicago Manual of Style (16^th Edition):

Hervieu Vilches, Alexia. “Understanding and targeting PI3K downstream of oncogenic Met mutant.” 2015. Doctoral Dissertation, Queen Mary, University of London. Accessed March 06, 2021. http://qmro.qmul.ac.uk/xmlui/handle/123456789/33935 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667429.

MLA Handbook (7^th Edition):

Hervieu Vilches, Alexia. “Understanding and targeting PI3K downstream of oncogenic Met mutant.” 2015. Web. 06 Mar 2021.

Vancouver:

Hervieu Vilches A. Understanding and targeting PI3K downstream of oncogenic Met mutant. [Internet] [Doctoral dissertation]. Queen Mary, University of London; 2015. [cited 2021 Mar 06]. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/33935 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667429.

Council of Science Editors:

Hervieu Vilches A. Understanding and targeting PI3K downstream of oncogenic Met mutant. [Doctoral Dissertation]. Queen Mary, University of London; 2015. Available from: http://qmro.qmul.ac.uk/xmlui/handle/123456789/33935 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.667429

University of Southern California

21. Tsen, Shao Hung Fred. The mechanism by which extracellular Hsp90α promotes cell migration: implications in wound healing and cancer.

Degree: PhD, Genetic, Molecular and Cellular Biology, 2013, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/236027/rec/6979

► Extracellular heat shock protein-90 (eHsp90) proteins, which include the membrane-bound, released and secreted forms were first cited in scientific literature late in the 70s. It… (more)

▼ Extracellular heat shock protein-90 (eHsp90) proteins, which include the membrane-bound, released and secreted forms were first cited in scientific literature late in the 70s. It was not until the recent decade that researchers began to understand the role of exported Hsp90 in normal and tumor cells. In normal cells, Hsp90 is secreted in response to tissue injury. Tumor cells, on the other hand, have managed to constitutively secrete Hsp90 for the purpose of tissue invasion. Cells abundantly store Hsp90 in their cytoplasm, insuring a sufficient supply of extracellular Hsp90 at a moment’s notice. A well-characterized function of secreted Hsp90α is to promote cell motility, a crucial event in both wound healing and cancer. One of the primary targets for extracellular Hsp90α is the cell surface LRP-1 receptor. The promotility activity of secreted Hsp90α resides within a fragment at the boundary between linker region and middle domain. Inhibiting Hsp90α secretion, neutralizing its extracellular function or blocking its signaling through the LRP-1 receptor prevent wound healing and tumor invasion both in vitro and in vivo. ❧ In regards to wound healing, topical application of F-5 promotes acute and diabetic wound healing far more effectively than US FDA-approved conventional growth factor therapy in mice. Moreover we demonstrated that, mechanistically, eHsp90α functions as signaling molecule to promote wound closure. eHsp90α binds to the subdomain II of the LRP-1 receptor and transmits the promotility signal through its NPVY motif located in its cytoplamic tail. The NPVY motif then relays the eHsp90α signal to the Akt1 and Akt2 kinases. We confirmed our findings using cross-rescuing experiments that suggest Akt1 and Akt2 work cooperatively to create a threshold of Akt kinase activity and promote cell migration. In vivo, eHsp90α accelerated wound closure in wild type mice, but not in its Akt1- and Akt2- knockout counterparts. ❧ In cancer, despite extensive efforts in the clinical and research fronts over the lasts two decades, it is still not clear why cancer cells are more susceptible to the toxicity of Hsp90 inhibitors compared to normal cells. We also do not understand why all cancer cell lines do not share this heightened sensitivity to Hsp90 inhibitors. Based on recent findings, we reason that the selected sensitivity of cancer cells to Hsp90 inhibitors, like17-AAG, is likely due to inhibition of the extracellular Hsp90 rather than intracellular Hsp90 action. Since not all tumor cells utilize eHsp90 for motility, invasion and metastasis, only eHsp90 dependent cancer cells display sensitivity to Hsp90 inhibitors. Based on this notion, pharmaceutical agents that specifically target eHsp90 function should be more effective on treating tumor cells and less toxic on normal cells than current inhibitors that do not discriminate between the extracellular Hsp90 promotility action from its intracellular ATPase dependent function. Advisors/Committee Members: Li, Wei (Committee Chair), Hong, Young-Kwon (Committee Member), Chuong, Cheng-Ming (Committee Member), Kobielak, Agnieszka (Committee Member).

Subjects/Keywords: wound healing; cell motility; cancer progression; secreted Hsp90; and LRP-1

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APA (6^th Edition):

Tsen, S. H. F. (2013). The mechanism by which extracellular Hsp90α promotes cell migration: implications in wound healing and cancer. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/236027/rec/6979

Chicago Manual of Style (16^th Edition):

Tsen, Shao Hung Fred. “The mechanism by which extracellular Hsp90α promotes cell migration: implications in wound healing and cancer.” 2013. Doctoral Dissertation, University of Southern California. Accessed March 06, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/236027/rec/6979.

MLA Handbook (7^th Edition):

Tsen, Shao Hung Fred. “The mechanism by which extracellular Hsp90α promotes cell migration: implications in wound healing and cancer.” 2013. Web. 06 Mar 2021.

Vancouver:

Tsen SHF. The mechanism by which extracellular Hsp90α promotes cell migration: implications in wound healing and cancer. [Internet] [Doctoral dissertation]. University of Southern California; 2013. [cited 2021 Mar 06]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/236027/rec/6979.

Council of Science Editors:

Tsen SHF. The mechanism by which extracellular Hsp90α promotes cell migration: implications in wound healing and cancer. [Doctoral Dissertation]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/236027/rec/6979

Queensland University of Technology

22. Shokoohmand, Ali. Identifying the molecular mediators of VN and the IGF:VN complex-stimulated breast cancer cell survival.

Degree: 2015, Queensland University of Technology

URL: https://eprints.qut.edu.au/85436/

► This project has identified a molecular signature involved in functions critical to breast cancer progression and metastasis mediated by vitronectin, an abundant protein in human… (more)

Subjects/Keywords: vitronectin; breast cancer; cancer progression; extracellular matrix; insulin-like growth factor; Attachment; vitronectin-binding integrins

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APA (6^th Edition):

Shokoohmand, A. (2015). Identifying the molecular mediators of VN and the IGF:VN complex-stimulated breast cancer cell survival. (Thesis). Queensland University of Technology. Retrieved from https://eprints.qut.edu.au/85436/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Shokoohmand, Ali. “Identifying the molecular mediators of VN and the IGF:VN complex-stimulated breast cancer cell survival.” 2015. Thesis, Queensland University of Technology. Accessed March 06, 2021. https://eprints.qut.edu.au/85436/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Shokoohmand, Ali. “Identifying the molecular mediators of VN and the IGF:VN complex-stimulated breast cancer cell survival.” 2015. Web. 06 Mar 2021.

Vancouver:

Shokoohmand A. Identifying the molecular mediators of VN and the IGF:VN complex-stimulated breast cancer cell survival. [Internet] [Thesis]. Queensland University of Technology; 2015. [cited 2021 Mar 06]. Available from: https://eprints.qut.edu.au/85436/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Shokoohmand A. Identifying the molecular mediators of VN and the IGF:VN complex-stimulated breast cancer cell survival. [Thesis]. Queensland University of Technology; 2015. Available from: https://eprints.qut.edu.au/85436/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

23. Dardenne, Étienne. Rôle des ARN hélicases Ddx5 et Ddx17 dans la progression tumorale : Role of RNA helicases DDX5 and DDX17 in tumor progression.

Degree: Docteur es, Biologie moléculaire, 2014, Université Claude Bernard – Lyon I

URL: http://www.theses.fr/2014LYO10048

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La progression tumorale, qui conduit à la formation de métastases, est le résultat de profondes modifications des différents niveaux de régulation de l'expression des gènes… (more)

▼

La progression tumorale, qui conduit à la formation de métastases, est le résultat de profondes modifications des différents niveaux de régulation de l'expression des gènes comme la transcription ou l'épissage alternatif. Au cours de ma thèse, j'ai étudié le rôle de DDX5 et DDX17, deux ARN hélicases qui, au cours de la progression tumorale, sont impliquées dans la régulation transcriptionnelle, l'épissage alternatif et la biogénèse des microARNs. Pour cela, j'ai utilisé deux modèles de progression tumorale : le modèle murin 4T1, composé de cellules cancéreuses qui présentent des propriétés métastatiques différentes, et les cellules humaines MCF10A qui, après traitement au TGF-beta, sont capables de réaliser la transition épithélio-mésenchymateuse, un processus de trans-différenciation qui contribue à la formation des métastases. Dans le modèle 4T1, j'ai montré que Ddx17 et Ddx5 contribuent à l'invasivité des cellules tumorales en contrôlant des programmes transcriptionnels et d'épissage alternatif. Plus précisément, j'ai démontré que Ddx5 et Ddx17 favorisent l'agressivité des cellules cancéreuses en régulant l'épissage des variants de l'histone macroH2A1 qui, à leur tour, contrôlent l'expression de gènes impliqués dans la progression tumorale. Dans le modèle MCF10A où la transition épithélio-mésenchymateuse peut être induite sous TGF-beta, j'ai montré que DDX5 et DDX17 orchestrent dynamiquement des programmes transcriptionnels et d'épissage. Le travail effectué pendant ma thèse met en évidence l'importance des ARN hélicases DDX5 et DDX17 comme régulateurs clés de la progression tumorale, et souligne le rôle de l'épissage alternatif lors de la progression tumorale. De plus, ce travail met l'accent sur l'importance d'intégrer les différents niveaux de régulation de l'expression des gènes (transcription, épissage, microARN) pour une compréhension globale de la progression tumorale

Tumor progression leading to the formation of metastases result from deep modifications of gene expression programs at several levels, including transcription and splicing. During my PhD, I investigated the role in tumor progression of DDX5 and DDX17, two highly related multifunctional DEAD box RNA helicases that are involved in transcription and splicing as well as in microRNA biogenesis. For this purpose, I used two breast cancer models of tumor progression : the 4T1 mouse model composed of cancer cells that exhibit different metastatic properties and MCF10a human cells that undergo epithelial-to-mesenchymal transition upon Tgf-beta treatment, a trans-differentiation process contributes to metastasis formation. In the 4T1 mouse model, I showed that Ddx17 and Ddx5 contribute to tumor-cell invasiveness by controlling both transcriptional and splicing programs. More specifically, I demonstrated that Ddx5 and Ddx17 promote cancer cells aggressiveness by regulating the splicing of the macroH2A1 histone which in turn impacts on the expression of genes implicated in tumor cell invasiveness. In the Tgf-beta induced epithelial-to-mesenchymal…

Advisors/Committee Members: Auboeuf, Didier (thesis director).

Subjects/Keywords: DDX5; DDX17; Épissage alternatif; Cancer du sein; Transition épithélio-mésenchymateuse; Progression tumorale; Transcription; MicroARN; DDX5; DDX17; Splicing; Breast cancer; Epithelial-to-mesenchymal transition; Tumor progression; Transcription; MicroRNA; 572.8

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dardenne, E. (2014). Rôle des ARN hélicases Ddx5 et Ddx17 dans la progression tumorale : Role of RNA helicases DDX5 and DDX17 in tumor progression. (Doctoral Dissertation). Université Claude Bernard – Lyon I. Retrieved from http://www.theses.fr/2014LYO10048

Chicago Manual of Style (16^th Edition):

Dardenne, Étienne. “Rôle des ARN hélicases Ddx5 et Ddx17 dans la progression tumorale : Role of RNA helicases DDX5 and DDX17 in tumor progression.” 2014. Doctoral Dissertation, Université Claude Bernard – Lyon I. Accessed March 06, 2021. http://www.theses.fr/2014LYO10048.

MLA Handbook (7^th Edition):

Dardenne, Étienne. “Rôle des ARN hélicases Ddx5 et Ddx17 dans la progression tumorale : Role of RNA helicases DDX5 and DDX17 in tumor progression.” 2014. Web. 06 Mar 2021.

Vancouver:

Dardenne E. Rôle des ARN hélicases Ddx5 et Ddx17 dans la progression tumorale : Role of RNA helicases DDX5 and DDX17 in tumor progression. [Internet] [Doctoral dissertation]. Université Claude Bernard – Lyon I; 2014. [cited 2021 Mar 06]. Available from: http://www.theses.fr/2014LYO10048.

Council of Science Editors:

Dardenne E. Rôle des ARN hélicases Ddx5 et Ddx17 dans la progression tumorale : Role of RNA helicases DDX5 and DDX17 in tumor progression. [Doctoral Dissertation]. Université Claude Bernard – Lyon I; 2014. Available from: http://www.theses.fr/2014LYO10048

24. Pez, Floriane. Implication de la lysyl oxydase dans la réponse hypoxique et dans la progression tumorale des cellules de carcinome colorectal humain : Role of lysyl oxidase in hypoxic response and tumor progression of Human colorectal carcinoma.

Degree: Docteur es, Biologie cellulaire, 2010, Université Claude Bernard – Lyon I

URL: http://www.theses.fr/2010LYO10141

►

Au sein d’une tumeur des régions hypoxiques se forment ce qui conduit à l’activation du facteur de transcription HIF1. HIF1, composé des deux protéines HIF1a… (more)

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Au sein d’une tumeur des régions hypoxiques se forment ce qui conduit à l’activation du facteur de transcription HIF1. HIF1, composé des deux protéines HIF1a et HIF1b, permet l’adaptation des cellules à des faibles concentrations d’oxygène en activant la transcription de gène cible. Un de ces gènes est celui codant pour la lysyl oxydase (LOX). Cette enzyme structure la matrice extracellulaire et est impliquée dans la tumorigénèse. Pour comprendre les liens entre LOX et HIF1a, nous avons modulé leurs expressions dans des lignées humaines de carcinome du côlon. En condition hypoxique, HIF1a contrôle l’expression de LOX et réciproquement, LOX régule la synthèse protéique d’HIF1a via l’activation de la voie de signalisation PI3K/AKT. Nous avons donc mis en évidence l’existence d’une boucle de régulation positive entre LOX et HIF1 en conditions hypoxique. Sachant que ces deux protéines sont des acteurs majeurs de la progression tumorale, nous avons cherché à comprendre le rôle de cette régulation mutuelle dans ce processus. Nos résultats démontrent que l’activité enzymatique de LOX promeut la croissance tumorale in vitro et in vivo et que son action est potentialisée par la présence de son partenaire HIF1a. De plus, LOX et HIF1a agissent en synergie afin d’augmenter la potentiel métastatiques des cellules tumorale de côlon in vitro. Ainsi, ce travail de thèse a permis de mettre en évidence l’existence d’une boucle de régulation entre HIF1a et LOX qui est critique dans la progression tumorale et semble également être impliquée dans le processus métastatiques

The microenvironment of solid tumors is exposed to hypoxic conditions which lead to the activation of Hypoxia‐Inducible Factor 1 (HIF1). HIF1, composed by a heterodimer of HIF1a and HIF1b protein, is a key transcription factor involved in cellular adaptation to changes in oxygen level, inducing the expression of several transcriptional targets such as Lysyl Oxidase (LOX). LOX is an amine oxidase that catalyzes crosslinking of fibrillar collagens and elastin in the extracellular matrix. Furthermore, LOX is implied in tumor progression. To clarify, the link between LOX and HIF1a, their expression were modulated in human colorectal carcinoma cell lines. We pointed out that besides HIF1‐dependant regulation of LOX, LOX can also act on the HIF1 pathway under hypoxic conditions. Indeed, LOX enzymatic activity upregulates HIF1a protein synthesis, and this action is mediated by the PI3K/AKT pathway. Thus, these results emphasize the existence of a regulation loop between HIF‐1a and LOX, which represent two main actors of tumoral progression. Thus, we wanted to determine the implication of this amplification loop in tumor progression. Our results show that LOX enzymatic activity increase tumor growth in vitro and in vivo, and this role is partially dependant of its partner HIF1a. Furthermore, we established that that LOX and HIF1a act in synergy to foster metastatic potential in colorectal carcinoma cell lines. Taken together, our results demonstrate a regulation loop…

Advisors/Committee Members: Sommer, Pascal (thesis director), Reynaud, Caroline (thesis director).

Subjects/Keywords: Lysyl oxydase; Hypoxie; Cancer; HIF1; PI3K/AKT; Progression tumorale; Métastases; Carcinome colorectal; Lysyl oxidase; Hypoxia; Cancer; HIF1; PI3K/AKT; Tumor progression; Metastasis; Colorectal carcinoma; 614.5999

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pez, F. (2010). Implication de la lysyl oxydase dans la réponse hypoxique et dans la progression tumorale des cellules de carcinome colorectal humain : Role of lysyl oxidase in hypoxic response and tumor progression of Human colorectal carcinoma. (Doctoral Dissertation). Université Claude Bernard – Lyon I. Retrieved from http://www.theses.fr/2010LYO10141

Chicago Manual of Style (16^th Edition):

Pez, Floriane. “Implication de la lysyl oxydase dans la réponse hypoxique et dans la progression tumorale des cellules de carcinome colorectal humain : Role of lysyl oxidase in hypoxic response and tumor progression of Human colorectal carcinoma.” 2010. Doctoral Dissertation, Université Claude Bernard – Lyon I. Accessed March 06, 2021. http://www.theses.fr/2010LYO10141.

MLA Handbook (7^th Edition):

Pez, Floriane. “Implication de la lysyl oxydase dans la réponse hypoxique et dans la progression tumorale des cellules de carcinome colorectal humain : Role of lysyl oxidase in hypoxic response and tumor progression of Human colorectal carcinoma.” 2010. Web. 06 Mar 2021.

Vancouver:

Pez F. Implication de la lysyl oxydase dans la réponse hypoxique et dans la progression tumorale des cellules de carcinome colorectal humain : Role of lysyl oxidase in hypoxic response and tumor progression of Human colorectal carcinoma. [Internet] [Doctoral dissertation]. Université Claude Bernard – Lyon I; 2010. [cited 2021 Mar 06]. Available from: http://www.theses.fr/2010LYO10141.

Council of Science Editors:

Pez F. Implication de la lysyl oxydase dans la réponse hypoxique et dans la progression tumorale des cellules de carcinome colorectal humain : Role of lysyl oxidase in hypoxic response and tumor progression of Human colorectal carcinoma. [Doctoral Dissertation]. Université Claude Bernard – Lyon I; 2010. Available from: http://www.theses.fr/2010LYO10141

25. Da silva, Jordan. Relation entre HER2 et FHIT dans la progression tumorale des cancers broncho-pulmonaires : Relationship between HER2 and FHIT during lung tumor progression.

Degree: Docteur es, Aspects moléculaires et cellulaires de la biologie, 2020, Reims

URL: http://www.theses.fr/2020REIMS021

►

FHIT (fragile histidine triad) est un gène fréquemment inactivé dans le cancer du poumon. Nos travaux précédents ont montré que FHIT contrôle l’invasion des cellules… (more)

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FHIT (fragile histidine triad) est un gène fréquemment inactivé dans le cancer du poumon. Nos travaux précédents ont montré que FHIT contrôle l’invasion des cellules tumorales pulmonaires via la régulation de la transition épithélio-mésenchymateuse (TEM) et que son expression est liée à l’activation du récepteur HER2. Ici, nous avons recherché l’implication du lien FHIT/HER2 dans la progression tumorale broncho-pulmonaire et les potentielles retombées cliniques.Nous avons mis en évidence une corrélation inverse entre l'expression de FHIT et l’activation d’HER2 dans des cellules tumorales de patients atteints de CBNPC. De plus, la mise au point d’un modèle stable KO FHIT par CRISPR/Cas9 nous a permis de montrer que la perte de FHIT induit l’activation d’HER2 associée à une TEM via l’implication du récepteur LRP-1 et de la signalisation ERK. Nous avons également démontré que les drogues anti-HER2, irbinitinib et trastuzumab, restaurent un phénotype plus épithélial et contrecarrent l'invasivité et la croissance des cellules tumorales FHIT négatives in vitro et in vivo. Enfin, nous avons montré que le phénotype FHITfaible/pHER2élevé est associé à l’expression de vimentine et prédit la sensibilité à une thérapie anti-HER2 dans les cellules tumorales de patients atteints de CBNPC.Nos résultats montrent que FHIT régule l'activité d’HER2 et que des drogues anti-HER2 diminuent l'agressivité des cellules tumorales inactivées pour FHIT. Cette étude suggère que la plasticité phénotypique des cellules tumorales pourrait être un biomarqueur prédictif pour les thérapies ciblées et qu'une nouvelle sous-classe de patients atteints de CBNPC pourrait être éligible à une thérapie anti-HER2.

The lack or decrease of FHIT (fragile histidine triad) expression is a common event in lung cancer. We previously showed that FHIT controls the invasiveness of lung tumor cells by regulating the epithelial-mesenchymal transition (EMT) and that its expression is correlated with the activation of HER2 receptor. Here, we investigated the implication of the relationship between FHIT and HER2 during lung tumor progression and its potential clinical relevance.Firstly, we showed a negative correlation between FHIT expression and the activated form of HER2 in primary tumor cells from NSCLC patients. Moreover, a stable KO FHIT cell model, using CRISPR/cas9 technology, allowed to show that inhibition of FHIT expression induces HER2 activation associated with an EMT program through the involvement of LRP-1 receptor and ERK signaling. We also demonstrated that anti-HER2 drugs, irbinitinib and trastuzumab, restore a more epithelial phenotype and counteract invasiveness and growth of FHIT-silenced tumor cell lines. Finally, we showed that the FHITlow/pHER2high phenotype is associated with vimentin expression and predicts sensitivity to an anti-HER2 therapy in primary tumor cells from NSCLC patients.Our results showed that FHIT regulates the activity of HER2 receptor in lung tumor cells and that HER2 specific inhibitors decrease the aggressiveness of…

Advisors/Committee Members: Nawrocki-Raby, Béatrice (thesis director).

Subjects/Keywords: Cancer du poumon; Fhit; Her2; Progression tumorale; Transition épithélio-Mésenchymateuse; Thérapies ciblées; Lung cancer; Fhit; Her2; Tumor progression; Epithelial-Mesemchymal transition; Targeted therapies; 616

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Da silva, J. (2020). Relation entre HER2 et FHIT dans la progression tumorale des cancers broncho-pulmonaires : Relationship between HER2 and FHIT during lung tumor progression. (Doctoral Dissertation). Reims. Retrieved from http://www.theses.fr/2020REIMS021

Chicago Manual of Style (16^th Edition):

Da silva, Jordan. “Relation entre HER2 et FHIT dans la progression tumorale des cancers broncho-pulmonaires : Relationship between HER2 and FHIT during lung tumor progression.” 2020. Doctoral Dissertation, Reims. Accessed March 06, 2021. http://www.theses.fr/2020REIMS021.

MLA Handbook (7^th Edition):

Da silva, Jordan. “Relation entre HER2 et FHIT dans la progression tumorale des cancers broncho-pulmonaires : Relationship between HER2 and FHIT during lung tumor progression.” 2020. Web. 06 Mar 2021.

Vancouver:

Da silva J. Relation entre HER2 et FHIT dans la progression tumorale des cancers broncho-pulmonaires : Relationship between HER2 and FHIT during lung tumor progression. [Internet] [Doctoral dissertation]. Reims; 2020. [cited 2021 Mar 06]. Available from: http://www.theses.fr/2020REIMS021.

Council of Science Editors:

Da silva J. Relation entre HER2 et FHIT dans la progression tumorale des cancers broncho-pulmonaires : Relationship between HER2 and FHIT during lung tumor progression. [Doctoral Dissertation]. Reims; 2020. Available from: http://www.theses.fr/2020REIMS021

University of Illinois – Chicago

26. Pandey, Akshay. FoxM1 in Liver Cancer.

Degree: 2017, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/22070

► The work presented in this thesis elucidates the role of transcription factor FoxM1 in progression of hepatocellular carcinoma. In this work, I provide the genetic… (more)

Subjects/Keywords: Liver Cancer; Hepatocellular carcinoma; HCC; FoxM1; Ras; High grade progression; FoxA1; FoxA2

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pandey, A. (2017). FoxM1 in Liver Cancer. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/22070

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Pandey, Akshay. “FoxM1 in Liver Cancer.” 2017. Thesis, University of Illinois – Chicago. Accessed March 06, 2021. http://hdl.handle.net/10027/22070.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Pandey, Akshay. “FoxM1 in Liver Cancer.” 2017. Web. 06 Mar 2021.

Vancouver:

Pandey A. FoxM1 in Liver Cancer. [Internet] [Thesis]. University of Illinois – Chicago; 2017. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/10027/22070.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pandey A. FoxM1 in Liver Cancer. [Thesis]. University of Illinois – Chicago; 2017. Available from: http://hdl.handle.net/10027/22070

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Western Ontario

27. Souter, Lesley H. A Model System for Rapid Identification and Functional Testing of Genes Involved in Early Breast Cancer Progression.

Degree: 2011, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/122

► Early breast cancer progression involves advancement through specific morphologic stages including atypical ductal hyperplasia (ADH), ductal carcinoma in situ (DCIS) and invasive mammary carcinoma (IMC),… (more)

▼ Early breast cancer progression involves advancement through specific morphologic stages including atypical ductal hyperplasia (ADH), ductal carcinoma in situ (DCIS) and invasive mammary carcinoma (IMC), although not always in a linear fashion. Histological studies have examined differences in breast tissues representing these stages of progression, but model systems which allow for experimental testing of factors influencing transition through these stages are scarce. The purpose of these studies was to develop a 3D in vitro model of early breast cancer progression that reflected the in vivo sequence of events, and to use this system to identify and functionally test genes important in controlling the processes. The 21T series cell lines, originally derived from the same patient with metastatic breast cancer, were shown to mimic specific stages of human breast cancer progression (21PT, ADH; 21NT, DCIS; 21MT-1, IMC) when grown in the mammary fat pad of nude mice. When grown in 3D Matrigel, the cell lines showed characteristic morphologies in which aspects of the stage-specific in vivo behaviours were recapitulated. Gene expression profiling of the 21T cells revealed characteristic patterns for each, with differential expression of certain key genes in common with clinical specimens. Subsequent studies focused on functionally characterizing the roles of VANGL1, S100A2 and TBX3 in breast cancer progression. Genes were up- or down-regulated to determine if alterations could affect transitioning between stages of progression. VANGL1 was differentially expressed in the ADH (21PT) to DCIS (21NT) transition (higher in DCIS) and was found functionally to promote the transition from ADH to a malignant phenotype (DCIS and even IMC). S100A2 and TBX3 were both differentially expressed in the DCIS to IMC (21MT-1) transition (S100A2 lower in IMC, TBX3 higher in IMC). S100A2 was found to functionally inhibit the transition from DCIS to IMC, while TBX3 promoted progression to invasion. These studies demonstrate that the 21T series cell lines provide a model of early breast cancer progression when grown in 3D. In addition, the model provides a means of testing the functional effects of genes on transitions between stages of pre-malignant to malignant growth, which may elucidate potential therapeutic targets.

Subjects/Keywords: breast cancer progression; atypical ductal hperplasia; ductal carcinoma in situ; invasive mammary carcinoma; Matrigel; Neoplasms

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Souter, L. H. (2011). A Model System for Rapid Identification and Functional Testing of Genes Involved in Early Breast Cancer Progression. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/122

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Souter, Lesley H. “A Model System for Rapid Identification and Functional Testing of Genes Involved in Early Breast Cancer Progression.” 2011. Thesis, University of Western Ontario. Accessed March 06, 2021. https://ir.lib.uwo.ca/etd/122.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Souter, Lesley H. “A Model System for Rapid Identification and Functional Testing of Genes Involved in Early Breast Cancer Progression.” 2011. Web. 06 Mar 2021.

Vancouver:

Souter LH. A Model System for Rapid Identification and Functional Testing of Genes Involved in Early Breast Cancer Progression. [Internet] [Thesis]. University of Western Ontario; 2011. [cited 2021 Mar 06]. Available from: https://ir.lib.uwo.ca/etd/122.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Souter LH. A Model System for Rapid Identification and Functional Testing of Genes Involved in Early Breast Cancer Progression. [Thesis]. University of Western Ontario; 2011. Available from: https://ir.lib.uwo.ca/etd/122

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Toronto

28. Kazazian, Karineh. Polo-Like Kinase 4 (PLK4) Function in Cancer Progression.

Degree: PhD, 2017, University of Toronto

URL: http://hdl.handle.net/1807/77481

► Invasion and metastasis are responsible for the majority of deaths from cancer, but the molecular mechanisms that facilitate execution of the metastatic cascade remain incompletely… (more)

▼ Invasion and metastasis are responsible for the majority of deaths from cancer, but the molecular mechanisms that facilitate execution of the metastatic cascade remain incompletely understood. One strategy is to identify genes that drive the metastatic process, and then target these drivers with biologic therapies in either the adjuvant or the metastatic setting. The polo family member polo-like kinase 4 (Plk4), is a serine-threonine kinase that is most highly expressed at the centrosome, where it is a master regulator of centriole duplication. Emerging evidence suggests that increased Plk4 levels in established malignancy may promote tumour progression; high levels of Plk4 expression have been reported in many tumour types, including breast, colorectal and pancreas, and its overexpression has been linked with resistance to therapy and death from cancer. While the critical role played by Plk4 in centriolar biogenesis is well-acknowledged, we recently discovered a novel and unexpected localization of Plk4 to the edges of lamellipodia and filopodia of motile cells, and identified a gene expression pattern predictive of reduced motility in Plk4+/- murine embryonic fibroblasts. I functionally validated this prediction in cancer cells, showing enhancement by Plk4 of cancer cell migration and invasion in vitro, and of MDA-MB-231 human breast cancer xenograft progression. Furthermore, this Plk4-driven invasive phenotype correlates with acquisition of an epithelial-to-mesenchymal transition (EMT) profile, cell polarity, spreading and enhanced directional protrusion formation. Investigation of pathways upstream of actin polymerization revealed that Plk4 regulates activation of the motility-related RhoGTPase Cdc42, and others have demonstrated that Plk4 promotes Rac1 activation, however this was insufficient for Plk4-induced motility in our system. In a BioID screen for Plk4 interactors, members of the Arp2/3 complex were identified, and I confirmed a novel physical and functional interaction between Plk4 and Arp2 in mediating Plk4-driven cancer cell movement. The interaction is mediated through the Plk4 PB1-PB2 domain, and results in phosphorylation of Arp2 at the T237/T238 activation site. These results provide a further rationale for application of targeted anti-Plk4 therapy in the clinical treatment of cancer patients, and reveal a new role for Plk4 in regulating Arp2/3-mediated actin cytoskeletal rearrangement. Advisors/Committee Members: Swallow, Carol J., Medical Science.

Subjects/Keywords: Arp2/3; BioID; Cancer Progression; Invasion and Metastasis; Plk4; Plk4 inhibitor; 0307

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kazazian, K. (2017). Polo-Like Kinase 4 (PLK4) Function in Cancer Progression. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/77481

Chicago Manual of Style (16^th Edition):

Kazazian, Karineh. “Polo-Like Kinase 4 (PLK4) Function in Cancer Progression.” 2017. Doctoral Dissertation, University of Toronto. Accessed March 06, 2021. http://hdl.handle.net/1807/77481.

MLA Handbook (7^th Edition):

Kazazian, Karineh. “Polo-Like Kinase 4 (PLK4) Function in Cancer Progression.” 2017. Web. 06 Mar 2021.

Vancouver:

Kazazian K. Polo-Like Kinase 4 (PLK4) Function in Cancer Progression. [Internet] [Doctoral dissertation]. University of Toronto; 2017. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/1807/77481.

Council of Science Editors:

Kazazian K. Polo-Like Kinase 4 (PLK4) Function in Cancer Progression. [Doctoral Dissertation]. University of Toronto; 2017. Available from: http://hdl.handle.net/1807/77481

University of Windsor

29. Singi Reddy, Siva Charan Reddy. USING MACHINE LEARNING TECHNIQUES FOR FINDING MEANINGFUL TRANSCRIPTS IN PROSTATE CANCER PROGRESSION.

Degree: MS, Computer Science, 2015, University of Windsor

URL: https://scholar.uwindsor.ca/etd/5433

► Prostate Cancer is one of the most common types of cancer among Canadian men. Next generation sequencing that uses RNA-Seq can be valuable in… (more)

Subjects/Keywords: Alternative Splicing; Classification; Feature Selection; Machine Learning; Next Generation Sequencing; Prostate Cancer Progression

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Singi Reddy, S. C. R. (2015). USING MACHINE LEARNING TECHNIQUES FOR FINDING MEANINGFUL TRANSCRIPTS IN PROSTATE CANCER PROGRESSION. (Masters Thesis). University of Windsor. Retrieved from https://scholar.uwindsor.ca/etd/5433

Chicago Manual of Style (16^th Edition):

Singi Reddy, Siva Charan Reddy. “USING MACHINE LEARNING TECHNIQUES FOR FINDING MEANINGFUL TRANSCRIPTS IN PROSTATE CANCER PROGRESSION.” 2015. Masters Thesis, University of Windsor. Accessed March 06, 2021. https://scholar.uwindsor.ca/etd/5433.

MLA Handbook (7^th Edition):

Singi Reddy, Siva Charan Reddy. “USING MACHINE LEARNING TECHNIQUES FOR FINDING MEANINGFUL TRANSCRIPTS IN PROSTATE CANCER PROGRESSION.” 2015. Web. 06 Mar 2021.

Vancouver:

Singi Reddy SCR. USING MACHINE LEARNING TECHNIQUES FOR FINDING MEANINGFUL TRANSCRIPTS IN PROSTATE CANCER PROGRESSION. [Internet] [Masters thesis]. University of Windsor; 2015. [cited 2021 Mar 06]. Available from: https://scholar.uwindsor.ca/etd/5433.

Council of Science Editors:

Singi Reddy SCR. USING MACHINE LEARNING TECHNIQUES FOR FINDING MEANINGFUL TRANSCRIPTS IN PROSTATE CANCER PROGRESSION. [Masters Thesis]. University of Windsor; 2015. Available from: https://scholar.uwindsor.ca/etd/5433

30. Kaparelou, Maria. Μελέτη της απουσίας της ισομορφής Ec του IGF-1 (MGF).

Degree: 2015, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)

URL: http://hdl.handle.net/10442/hedi/39741

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IGF-1 is one of the key molecules in cancer biology; however, little is known about the role of the preferential expression of the premature IGF-1… (more)

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IGF-1 is one of the key molecules in cancer biology; however, little is known about the role of the preferential expression of the premature IGF-1 isoforms in prostate cancer. We have examined the role of the cleaved COO- terminal peptide (PEc) of the third IGF-1 isoform, IGF-1Ec, in prostate cancer. Our evidence suggests that endogenously produced PEc induces cellular proliferation in the human prostate cancer cells (PC-3) in-vitro and in-vivo, by activating the ERK 1/2 pathway in an autocrine/paracrine manner. PEc overexpressing cells and tumors presented evidence of epithelial to mesenchymal transition, whereas the orthotopic injection of PEc overexpressing, normal prostate epithelium cells (HPrEC) in SCID mice was associated with increased metastatic rate. Our data underlies the action of PEc in prostate cancer biology and defines its potential role in tumor growth, progression and metastasis.

Ο IGF-1 αποτελεί ένα από τα μόρια κλειδιά στην βιολογία του καρκίνου, παρόλαυτα λίγα είναι αυτά που γνωρίζουμε για την εκλεκτική έκφραση των ισομορφών του στον καρκίνο του προστάτη. Σε αυτή την μελέτη εξετάσαμε τον ρόλο του COO- άκρου του πεπτιδίου (PEc) της τρίτης ισομορφής του IGF-1 στον καρκίνο του προστάτη. Τα αποτελέσματα μας προτείνουν ότι η παραγωγή πεπτιδίου Ec ενδογενώς επάγει τον κυτταρικό πολλαπλασιασμό σε προστατικά καρκινικά κύτταρα (PC3) τόσο in vitro όσο και in vivo, μέσω ενεργοποίησης του ERK μονοπατιού με έναν αυτοκρινή/παρακρινή τρόπο. Η υπερέκφραση του PEc σε κύτταρα και όγκους αποτελεί ένδειξη του φαινομένου EMT (epithelial-mesenchymal transition) και η ορθοτοπική έγχυση των προστατικών επιθηλιακών κυττάρων που υπερεκφράζουν PEc σε SCID ποντίκια φαίνεται να συνδέεται με αυξημένο ποσοστό για μετάσταση. Τα στοιχεία σε αυτή την μελέτη αποτελούν την βάση για την κατανόηση της δράσης του PEc στον καρκίνο του προστατη και καθορίζει τον πιθανό του ρόλο στην δημιουργία όγκου, στην εξέλιξή του και στην ικανότητά του να δίνει μεταστάσεις.

Subjects/Keywords: Πεπτίδιο Ec; Καρκίνος προστάτη; Εξέληξη όγκου; Igf1ec; Ec peptide; Prostate cancer; Tumor progression

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APA (6^th Edition):

Kaparelou, M. (2015). Μελέτη της απουσίας της ισομορφής Ec του IGF-1 (MGF). (Thesis). National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Retrieved from http://hdl.handle.net/10442/hedi/39741

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Kaparelou, Maria. “Μελέτη της απουσίας της ισομορφής Ec του IGF-1 (MGF).” 2015. Thesis, National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ). Accessed March 06, 2021. http://hdl.handle.net/10442/hedi/39741.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Kaparelou, Maria. “Μελέτη της απουσίας της ισομορφής Ec του IGF-1 (MGF).” 2015. Web. 06 Mar 2021.

Vancouver:

Kaparelou M. Μελέτη της απουσίας της ισομορφής Ec του IGF-1 (MGF). [Internet] [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2015. [cited 2021 Mar 06]. Available from: http://hdl.handle.net/10442/hedi/39741.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Kaparelou M. Μελέτη της απουσίας της ισομορφής Ec του IGF-1 (MGF). [Thesis]. National and Kapodistrian University of Athens; Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ); 2015. Available from: http://hdl.handle.net/10442/hedi/39741

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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