You searched for subject:(Hepatocellular Carcinoma).
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456 total matches.
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1.
Adebayo, Adeola O.
Unraveling the Transcriptomic and Proteomic Profile of
mTOR-Inhibited Progenitor-Derived Focal Lesions in a Rat Model of
Hepatocellular Carcinoma.
Degree: PhD, Pathobiology, 2016, Brown University
URL: https://repository.library.brown.edu/studio/item/bdr:674281/ 
► In 1977, Emmanuel Farber, Dennis Solt and Alan Medline reported carcinogen-induced hyperplastic lesions in a model of liver carcinogenesis. Lesions that grew following this protocol…
(more)
▼ In 1977, Emmanuel Farber, Dennis Solt and Alan Medline
reported carcinogen-induced hyperplastic lesions in a model of
liver carcinogenesis. Lesions that grew following this protocol
were seen as precursors to cancer, because they were resistant to
growth-inhibitory hepatotoxins. This model consists of a single
carcinogenic dose of diethylnitrosamine, which initiates rapid cell
proliferation, followed by 2-acetylaminofluorene, a liver toxicant
that subdues the growth of normal hepatocytes, and partial
hepatectomy, which serves as a growth stimulus. The cells that
proliferate after partial hepatectomy are observed to be a subset
of liver progenitor (oval) cells. Oval cell proliferation is not
suppressed by 2-AAF, and therefore proliferate to preneoplastic
lesions and adenomas, and evidence show them as the precursors of
some
hepatocellular carcinoma. Decades later, this protocol, now
termed the Solt-Farber or Resistance Hepatocyte Model, continues to
be utilized as the model to study hepatic carcinogenesis. Research
has turned to signaling mechanisms behind lesion proliferation, and
progression in this model, to characterize targeted therapies for
patients with
hepatocellular carcinoma. This dissertation is
focused on the role of mTOR-signaling pathway during development
and progression of focal lesions, with emphasis on global gene
profile and proteomic changes in lesions affected by mTOR
inhibition. The first aim characterized the gene expression
signature of rat liver exposed to rapamycin during early
development of preneoplastic lesions. Aim 2 extended to changes in
global gene expression as lesions progress and become persistent.
Aim 3 investigated the proteome of persistent focal lesions
affected by rapamycin. The overall results showed that there is
sustained effect of rapamycin long after exposure is stopped. In
addition, at the mRNA level, lesions affected by rapamycin
administration gained a gene profile that was similar to normal
liver. However, this phenomenon was not observed at the level of
the proteome. This dissertation concludes that complex
modifications of several proteins after translation may contribute
to the dissimilarities in mRNA and protein results. A study of
post-translational processes may provide information on the effect
of mTOR inhibition on focal lesions and lead to other studies on
chemopreventative strategies for
hepatocellular
carcinoma.
Advisors/Committee Members: Gruppuso, Philip (Director), Boekelheide, Kim (Reader), Wands, Jack (Reader), Sanders, Jennifer (Reader), Britt, Deborah (Reader).
Subjects/Keywords: Hepatocellular carcinoma
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APA (6th Edition):
Adebayo, A. O. (2016). Unraveling the Transcriptomic and Proteomic Profile of
mTOR-Inhibited Progenitor-Derived Focal Lesions in a Rat Model of
Hepatocellular Carcinoma. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:674281/
Chicago Manual of Style (16th Edition):
Adebayo, Adeola O. “Unraveling the Transcriptomic and Proteomic Profile of
mTOR-Inhibited Progenitor-Derived Focal Lesions in a Rat Model of
Hepatocellular Carcinoma.” 2016. Doctoral Dissertation, Brown University. Accessed January 15, 2021.
https://repository.library.brown.edu/studio/item/bdr:674281/.
MLA Handbook (7th Edition):
Adebayo, Adeola O. “Unraveling the Transcriptomic and Proteomic Profile of
mTOR-Inhibited Progenitor-Derived Focal Lesions in a Rat Model of
Hepatocellular Carcinoma.” 2016. Web. 15 Jan 2021.
Vancouver:
Adebayo AO. Unraveling the Transcriptomic and Proteomic Profile of
mTOR-Inhibited Progenitor-Derived Focal Lesions in a Rat Model of
Hepatocellular Carcinoma. [Internet] [Doctoral dissertation]. Brown University; 2016. [cited 2021 Jan 15].
Available from: https://repository.library.brown.edu/studio/item/bdr:674281/.
Council of Science Editors:
Adebayo AO. Unraveling the Transcriptomic and Proteomic Profile of
mTOR-Inhibited Progenitor-Derived Focal Lesions in a Rat Model of
Hepatocellular Carcinoma. [Doctoral Dissertation]. Brown University; 2016. Available from: https://repository.library.brown.edu/studio/item/bdr:674281/
2.
Lizarazo, Diana.
Aspartyl-Asparaginyl-β-Hydroxylase (AAH) Regulation and
Function in Liver Disease.
Degree: PhD, Molecular Pharmacology, Physiology, and
Biotechnology, 2014, Brown University
URL: https://repository.library.brown.edu/studio/item/bdr:386169/
► Aspartyl-asparaginyl-β-hydroxylase (AAH) is a ~86 kD protein abundantly expressed in hepatocellular carcinoma (HCC) and downregulated by chronic ethanol exposure, contributing to alcoholic liver disease (ALD).…
(more)
▼ Aspartyl-asparaginyl-β-hydroxylase (AAH) is a ~86 kD
protein abundantly expressed in
hepatocellular carcinoma (HCC) and
downregulated by chronic ethanol exposure, contributing to
alcoholic liver disease (ALD). AAH expression is stimulated by
insulin and insulin-like growth factor-1 (IGF-1) signaling
networks. Insulin/IGF-1 signaling is over-activated in HCCs, but
inhibited by ethanol exposure, partly due to aberrant ceramide
accumulation. AAH promotes cell adhesion, migration, and invasion
partly through the hydroxylation of Notch-1 and Jagged-1 and
attendant activation of Notch signaling. Insulin/IGF-1 signaling
networks regulate AAH at the transcriptional, as well as the
post-translational levels. More specifically, AAH may be
post-translationally regulated by phosphorylation since inhibition
of glycogen synthase kinase-3β (GSK-3β) increases AAH protein and
migration, while GSK-3β overexpression yields the opposite effects.
Correspondingly, sub-sequence analysis of AAH protein demonstrated
a number of potential phosphorylation sites corresponding to
GSK-3β, as well as protein kinase A (PKA), protein kinase C (PKC),
and casein kinase 2 (CK2). To investigate the regulation of AAH in
the liver, liver tissue or liver slice cultures from Long Evans
rats were exposed to ethanol and a ceramide inhibitor or insulin
sensitizing treatments to examine the effects on insulin/IGF-1,
AAH, and Notch signaling activation. Human hepatoma-derived Huh7
cells served to characterize the effects of IGF-1 stimulation on
AAH protein and the post-translational regulation of AAH by
phosphorylation, using chemical inhibitors of GSK-3β, PKA, PKC, or
CK2, or using AAH mutants lacking individual phosphorylation sites.
The findings demonstrated that inhibition of ceramide synthesis
restored ethanol-impaired insulin/IGF-1 signaling, expression of
AAH and Notch signaling proteins in the liver. Furthermore, IGF-1
signaling promoted AAH expression and subcellular trafficking with
consequences on the activation of Notch signaling. Lastly, the
findings suggest AAH protein is post-translationally regulated by
phosphorylation at multiple sites, possibly through priming
mechanisms of phosphorylation. The investigations shed light on the
regulation of AAH protein expression and function as it relates to
the activation of Notch signaling and its dysregulation in HCC and
ALD.
Advisors/Committee Members: de la Monte, Suzanne (Director), Wands, Jack (Reader), Salomon, Arthur (Reader), Harnett, Karen (Reader), Britt, Deborah (Reader).
Subjects/Keywords: hepatocellular carcinoma
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APA (6th Edition):
Lizarazo, D. (2014). Aspartyl-Asparaginyl-β-Hydroxylase (AAH) Regulation and
Function in Liver Disease. (Doctoral Dissertation). Brown University. Retrieved from https://repository.library.brown.edu/studio/item/bdr:386169/
Chicago Manual of Style (16th Edition):
Lizarazo, Diana. “Aspartyl-Asparaginyl-β-Hydroxylase (AAH) Regulation and
Function in Liver Disease.” 2014. Doctoral Dissertation, Brown University. Accessed January 15, 2021.
https://repository.library.brown.edu/studio/item/bdr:386169/.
MLA Handbook (7th Edition):
Lizarazo, Diana. “Aspartyl-Asparaginyl-β-Hydroxylase (AAH) Regulation and
Function in Liver Disease.” 2014. Web. 15 Jan 2021.
Vancouver:
Lizarazo D. Aspartyl-Asparaginyl-β-Hydroxylase (AAH) Regulation and
Function in Liver Disease. [Internet] [Doctoral dissertation]. Brown University; 2014. [cited 2021 Jan 15].
Available from: https://repository.library.brown.edu/studio/item/bdr:386169/.
Council of Science Editors:
Lizarazo D. Aspartyl-Asparaginyl-β-Hydroxylase (AAH) Regulation and
Function in Liver Disease. [Doctoral Dissertation]. Brown University; 2014. Available from: https://repository.library.brown.edu/studio/item/bdr:386169/
University of Alberta
3.
Abdualmjid,Reem J.
Mitochondrial Dysfunction and Induction of Apoptosis in
Hepatocellular Carcinoma and Cholangiocarcinoma Cell Lines by
Thymoquinone.
Degree: MS, Laboratory Medicine and Pathology, 2014, University of Alberta
URL: https://era.library.ualberta.ca/files/sj139469q
► Thymoquinone, the plant-based bioactive constituent derived from the volatile oil of Nigella sativa, has been shown to possess considerable anti-neoplastic activity. The present study aimed…
(more)
▼ Thymoquinone, the plant-based bioactive constituent
derived from the volatile oil of Nigella sativa, has been shown to
possess considerable anti-neoplastic activity. The present study
aimed to investigate the anti-tumour property of TQ against
hepatocellular carcinoma (HepG2) and cholangiocarcinoma (HuCCT1)
cells, the two most common primary hepatic tumours. All cell lines
were treated with increasing concentrations of TQ for varying
durations. The anti-proliferative effect of TQ was measured using
the MTS assay and resulted in dose- and time-dependent growth
inhibition in both cell lines. The analysis of cell cycle
distribution, determination of apoptosis, assessment of
morphological alterations and measurement of mitochondrial membrane
potential changes were also investigated. TQ caused cell cycle
arrest at different phases in the two cell types and induced
apoptosis in both cell lines through the mitochondrial pathway.
Overall, these findings suggest that TQ possesses promising
therapeutic potential as an anti-tumour agent for treating
hepatocellular carcinoma and cholangiocarcinoma.
Subjects/Keywords: Apoptosis; Hepatocellular carcinoma; Thymoquinone; Cholangiocarcinoma
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APA ·
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APA (6th Edition):
J, A. (2014). Mitochondrial Dysfunction and Induction of Apoptosis in
Hepatocellular Carcinoma and Cholangiocarcinoma Cell Lines by
Thymoquinone. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/sj139469q
Chicago Manual of Style (16th Edition):
J, Abdualmjid,Reem. “Mitochondrial Dysfunction and Induction of Apoptosis in
Hepatocellular Carcinoma and Cholangiocarcinoma Cell Lines by
Thymoquinone.” 2014. Masters Thesis, University of Alberta. Accessed January 15, 2021.
https://era.library.ualberta.ca/files/sj139469q.
MLA Handbook (7th Edition):
J, Abdualmjid,Reem. “Mitochondrial Dysfunction and Induction of Apoptosis in
Hepatocellular Carcinoma and Cholangiocarcinoma Cell Lines by
Thymoquinone.” 2014. Web. 15 Jan 2021.
Vancouver:
J A. Mitochondrial Dysfunction and Induction of Apoptosis in
Hepatocellular Carcinoma and Cholangiocarcinoma Cell Lines by
Thymoquinone. [Internet] [Masters thesis]. University of Alberta; 2014. [cited 2021 Jan 15].
Available from: https://era.library.ualberta.ca/files/sj139469q.
Council of Science Editors:
J A. Mitochondrial Dysfunction and Induction of Apoptosis in
Hepatocellular Carcinoma and Cholangiocarcinoma Cell Lines by
Thymoquinone. [Masters Thesis]. University of Alberta; 2014. Available from: https://era.library.ualberta.ca/files/sj139469q
Tulane University
4.
Harmon, Jonah.
Gas embolization as a minimally invasive therapy for the treatment of hepatocellular carcinoma.
Degree: 2020, Tulane University
URL: https://digitallibrary.tulane.edu/islandora/object/tulane:119707
► [email protected]
Hepatocellular carcinoma is an intractable cancer with a high mortality rate. Transarterial chemoembolization, a non-curative method, is the first line therapy for intermediate stage…
(more)
▼ [email protected]
Hepatocellular carcinoma is an intractable cancer with a high mortality rate. Transarterial chemoembolization, a non-curative method, is the first line therapy for intermediate stage patients. This effectively extends patient survival but requires a complicated intraarterial catheterization procedure and is poorly suited to repeated administration. Gas embolization has been proposed as a fast, easily administered, more spatially selective, and less invasive alternative. This process involves generating emboli in situ using acoustic droplet vaporization, the noninvasive focused ultrasound-mediated conversion of intravenously administered perfluorocarbon microdroplets into microbubbles. The work presented in this dissertation provides the first evidence of the feasibility and efficacy of gas embolization in vivo. Following confirmation of the cessation of tumor growth after treatment in a preliminary study, two additional preclinical studies were conducted. Varying treatment parameters and the use of systemic chemotherapy alongside gas embolization resulted in consistent, substantial tumor regression and a suppression of tumor recurrence following the cessation of treatment. Subsequent steps toward optimizing the treatment method, primarily intended to mitigate off-target tissue damage and to maximize the uniformity of treatment coverage across a lesion, involved the implementation of two specialized imaging modes for tumor detection and treatment planning and the development of an ultrasound-guided treatment method. Finally, retention of the lipid droplet shell upon vaporization was investigated in the context of selective targeting for localized drug delivery. The dissertation closes with a discussion of the implications of the presented work and proposed future studies.
1
Jonah Harmon
Advisors/Committee Members: Bull, Joseph (Thesis advisor), School of Science & Engineering Biomedical Engineering (Degree granting institution).
Subjects/Keywords: Embolotherapy; Ultrasound; Hepatocellular Carcinoma
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APA (6th Edition):
Harmon, J. (2020). Gas embolization as a minimally invasive therapy for the treatment of hepatocellular carcinoma. (Thesis). Tulane University. Retrieved from https://digitallibrary.tulane.edu/islandora/object/tulane:119707
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Harmon, Jonah. “Gas embolization as a minimally invasive therapy for the treatment of hepatocellular carcinoma.” 2020. Thesis, Tulane University. Accessed January 15, 2021.
https://digitallibrary.tulane.edu/islandora/object/tulane:119707.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Harmon, Jonah. “Gas embolization as a minimally invasive therapy for the treatment of hepatocellular carcinoma.” 2020. Web. 15 Jan 2021.
Vancouver:
Harmon J. Gas embolization as a minimally invasive therapy for the treatment of hepatocellular carcinoma. [Internet] [Thesis]. Tulane University; 2020. [cited 2021 Jan 15].
Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:119707.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Harmon J. Gas embolization as a minimally invasive therapy for the treatment of hepatocellular carcinoma. [Thesis]. Tulane University; 2020. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:119707
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Harvard University
5.
Simon, Rachel.
Racial Disparities in In-Hospital Outcomes for Hepatocellular Carcinoma.
Degree: Doctor of Medicine, 2016, Harvard University
URL: http://nrs.harvard.edu/urn-3:HUL.InstRepos:40620217
► Background and Aims: Hepatocellular cancer (HCC) is increasing in incidence, contributing to morbidity and mortality. Racial disparities in therapeutic interventions and hospitalization outcomes have not…
(more)
▼ Background and Aims: Hepatocellular cancer (HCC) is increasing in incidence, contributing to morbidity and mortality. Racial disparities in therapeutic interventions and hospitalization outcomes have not been studied previously.
Methods: Using the 2011 Nationwide Inpatient Sample, the largest all-payer database of hospitalizations in the United States, we identified patients with HCC-related admissions using previously validated ICD-9-CM codes. Among these, we also identified those that were procedure-related (associated with liver transplantation, hepatic resection, radiofrequency ablation or transarterial chemoembolization (TACE). Multivariate regression was performed to identify the contribution of race to therapeutic interventions and outcomes.
Results: A total of 22,933 HCC-related hospitalizations were included of which 10,285 (45%) were procedure related. Blacks had a smaller proportion (35%) of procedure-related HCC hospitalizations compared to 46% for whites [Odds ratio (OR) 0.65, 95% confidence interval (CI) 0.49 – 0.86]. Specifically, blacks had lower odds of liver transplantation (OR 0.43, 95% CI 0.26-0.71), hepatic resection (OR 0.57, 95% CI 0.33-0.98) and ablation (0.46, 95% CI 0.29-0.74, p=0.002) when compared to whites. Overall, 10.9% of HCC-related admissions resulted in death among blacks compared to 6.4% among whites (OR 1.58, 95% CI 1.12 – 2.24).
Conclusion: Among HCC-related hospitalizations, blacks were less likely to receive liver transplantation, hepatic resection, and ablation when compared to whites and had higher in-patient mortality. Identifying racial disparities in health care is a necessary first step to appropriately address and eliminate them.
Scholarly Project
Subjects/Keywords: hepatocellular carcinoma; racial disparity
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APA (6th Edition):
Simon, R. (2016). Racial Disparities in In-Hospital Outcomes for Hepatocellular Carcinoma. (Doctoral Dissertation). Harvard University. Retrieved from http://nrs.harvard.edu/urn-3:HUL.InstRepos:40620217
Chicago Manual of Style (16th Edition):
Simon, Rachel. “Racial Disparities in In-Hospital Outcomes for Hepatocellular Carcinoma.” 2016. Doctoral Dissertation, Harvard University. Accessed January 15, 2021.
http://nrs.harvard.edu/urn-3:HUL.InstRepos:40620217.
MLA Handbook (7th Edition):
Simon, Rachel. “Racial Disparities in In-Hospital Outcomes for Hepatocellular Carcinoma.” 2016. Web. 15 Jan 2021.
Vancouver:
Simon R. Racial Disparities in In-Hospital Outcomes for Hepatocellular Carcinoma. [Internet] [Doctoral dissertation]. Harvard University; 2016. [cited 2021 Jan 15].
Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:40620217.
Council of Science Editors:
Simon R. Racial Disparities in In-Hospital Outcomes for Hepatocellular Carcinoma. [Doctoral Dissertation]. Harvard University; 2016. Available from: http://nrs.harvard.edu/urn-3:HUL.InstRepos:40620217
University of Toronto
6.
Bhat, Mamatha.
A Network-based Analysis of Hepatocellular Carcinoma.
Degree: PhD, 2019, University of Toronto
URL: http://hdl.handle.net/1807/94059
► Hepatocellular carcinoma (HCC) is a high-fatality cancer with complex pathogenesis, often arising in the setting of various chronic liver diseases when it is too late…
(more)
▼ Hepatocellular carcinoma (HCC) is a high-fatality cancer with complex pathogenesis, often arising in the setting of various chronic liver diseases when it is too late to offer any curative therapy. This PhD thesis is divided into two parts, the first of which was completed at McGill University under the supervision of Dr. Nahum Sonenberg, and evaluated inhibition of translation downstream of mTOR. This work was performed in the context of much interest in inhibiting the mTOR pathway in HCC, given its identification as a dominant pathway in this cancer. In the first part of this thesis, I evaluated how metformin inhibits HCC growth, by decreasing translation of anti-apoptotic proteins such as Mcl-1 downstream of mTOR. In the second part of this thesis, I sought to better understand the role of the mTOR pathway in relation to other commonly dysregulated pathways in HCC. All publicly available, high-throughput gene expression data in HCC was curated at http://ophid.utoronto.ca/CDIPLiver. Clinical variables such as etiology of liver disease and liver function parameters, important to understanding clinical relevance of gene expression data, were only available in around 50% of studies. Betweenness centrality calculation was performed on genes differentially expressed between HCC and corresponding background liver tissue, and revealed Estrogen Receptor 1 (ESR1) to be most central to the HCC Protein-Protein Interaction (PPI) network. HCC cells transfected with ESR1 and exposed to estradiol had significantly decreased proliferation and viability. Gene expression revealed that ESR1 upregulation significantly affected cellular processes such as histone methylation, transcription, and cell cycle. High expression of ESR1 in HCC tumors was found to be protective. Finally, we curated all publicly available whole exome sequencing, DNA methylation, microRNA, and proteomics data in HCC. Pathway analysis was performed on significantly dysregulated genes, and overlapping pathways identified. The following pathways overlapped among the 5 different datasets: Epidermal Growth Factor (EGFR), B1-integrin and axon guidance proteins, suggesting pathway dependencies in HCC. A systems biology approach to HCC allowed us to elucidate the role of sex-specific differences and importance of specific pathways in HCC biology, providing biological rationale for a more targeted therapeutic approach to HCC.
Advisors/Committee Members: Jurisica, Igor, Medical Biophysics.
Subjects/Keywords: Hepatocellular carcinoma; Network Analysis; 0307
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APA (6th Edition):
Bhat, M. (2019). A Network-based Analysis of Hepatocellular Carcinoma. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/94059
Chicago Manual of Style (16th Edition):
Bhat, Mamatha. “A Network-based Analysis of Hepatocellular Carcinoma.” 2019. Doctoral Dissertation, University of Toronto. Accessed January 15, 2021.
http://hdl.handle.net/1807/94059.
MLA Handbook (7th Edition):
Bhat, Mamatha. “A Network-based Analysis of Hepatocellular Carcinoma.” 2019. Web. 15 Jan 2021.
Vancouver:
Bhat M. A Network-based Analysis of Hepatocellular Carcinoma. [Internet] [Doctoral dissertation]. University of Toronto; 2019. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/1807/94059.
Council of Science Editors:
Bhat M. A Network-based Analysis of Hepatocellular Carcinoma. [Doctoral Dissertation]. University of Toronto; 2019. Available from: http://hdl.handle.net/1807/94059
University of Minnesota
7.
Sweet Kennedy, Kristin.
Hepatitis C: Hepatocellular carcinoma, mortality, and the impact of treatment.
Degree: PhD, Health Services Research, Policy and Administration, 2014, University of Minnesota
URL: http://hdl.handle.net/11299/174894
► Hepatitis C (HCV) infection is the most common bloodborne illness in the United States and the prevalence is highest in those born between 1945 and…
(more)
▼ Hepatitis C (HCV) infection is the most common bloodborne illness in the United States and the prevalence is highest in those born between 1945 and 1965. Most of those with HCV infection in this cohort have been infected for decades and some are now experiencing the long-term consequences of HCV infection, including cirrhosis and hepatocellular carcinoma. At the same time, this cohort is just reaching the age of eligibility for Medicare. The introduction of new treatment protocols including direct-acting antivirals for HCV infection has resulted in better outcomes for those undergoing treatment with many achieving a cure of their HCV infection. Despite an awareness of the potential burden of disease from HCV infection in this cohort, there is still a lack of information regarding hepatocellular carcinoma outcomes in persons with HCV and the impact of treatment for HCV outcomes and transmission. Using the Surveillance, Epidemiology, and End Results data linked to Medicare claims, this research describes (1) changes in risk factors for hepatocellular carcinoma, including HCV infection, over time and (2) differences in outcomes of persons with hepatocellular carcinoma by HCV infection status in the Medicare population. In addition, a state transition model with a transmission equation was used to compare the impact of treatment on mortality and HCV transmission using direct-acting antivirals to treat persons born between 1945 and 1965 in two risk populations, persons who inject drugs and persons who don't inject drugs. Overall, this research adds to our understanding of the consequences of HCV-infection-related hepatocellular carcinoma and the impact of treatment in the population with the highest prevalence of HCV infection.
Subjects/Keywords: Hepatitis C; Hepatocellular Carcinoma
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APA (6th Edition):
Sweet Kennedy, K. (2014). Hepatitis C: Hepatocellular carcinoma, mortality, and the impact of treatment. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/174894
Chicago Manual of Style (16th Edition):
Sweet Kennedy, Kristin. “Hepatitis C: Hepatocellular carcinoma, mortality, and the impact of treatment.” 2014. Doctoral Dissertation, University of Minnesota. Accessed January 15, 2021.
http://hdl.handle.net/11299/174894.
MLA Handbook (7th Edition):
Sweet Kennedy, Kristin. “Hepatitis C: Hepatocellular carcinoma, mortality, and the impact of treatment.” 2014. Web. 15 Jan 2021.
Vancouver:
Sweet Kennedy K. Hepatitis C: Hepatocellular carcinoma, mortality, and the impact of treatment. [Internet] [Doctoral dissertation]. University of Minnesota; 2014. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/11299/174894.
Council of Science Editors:
Sweet Kennedy K. Hepatitis C: Hepatocellular carcinoma, mortality, and the impact of treatment. [Doctoral Dissertation]. University of Minnesota; 2014. Available from: http://hdl.handle.net/11299/174894
University of Alberta
8.
Albahrani, Redha Mohammed.
Differential Expression of TWSG1, BMP4 and Shh Morphogens
Signaling Proteins in Hepatocellular Carcinoma and
Cholangiocellular Carcinoma.
Degree: MS, Medical Sciences- Laboratory Medicine and
Pathology, 2013, University of Alberta
URL: https://era.library.ualberta.ca/files/h415pb10b
► Hepatocellular carcinoma (HCC) and cholangiocellular carcinoma (CCA) constitute two of the most common liver malignancies in adults. The molecular mechanisms underlying their development remain poorly…
(more)
▼ Hepatocellular carcinoma (HCC) and cholangiocellular
carcinoma (CCA) constitute two of the most common liver
malignancies in adults. The molecular mechanisms underlying their
development remain poorly understood. Morphogen proteins, including
the hedgehog and the bone morphogenetic proteins pathway fulfill a
major role in embryonic development. Consequently, alterations in
these proteins may cause embryonic defects. Furthermore, abnormal
expression of morphogen proteins is found to correlate with cancer
development and progression. This thesis has demonstrated the
differential expression and co-localization of the morphogen
proteins, including sonic hedgehog (Shh), bone morphogenetic
protein (BMP)-4 and twisted gastrulation protein (TWSG)-1 in human
HCC and CCA tumors and cell lines. These proteins are strongly
expressed in CCA more than in HCC. Overall, these findings suggest
that morphogen proteins may play a crucial role during liver
carcinogenesis and progression, specifically in CCA. Moreover,
these proteins can serve as diagnostic biomarkers for HCC and
CCA.
Subjects/Keywords: Hepatocellular carcinoma; Tumor markers; Cholangiocellular carcinoma
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APA ·
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APA (6th Edition):
Albahrani, R. M. (2013). Differential Expression of TWSG1, BMP4 and Shh Morphogens
Signaling Proteins in Hepatocellular Carcinoma and
Cholangiocellular Carcinoma. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/h415pb10b
Chicago Manual of Style (16th Edition):
Albahrani, Redha Mohammed. “Differential Expression of TWSG1, BMP4 and Shh Morphogens
Signaling Proteins in Hepatocellular Carcinoma and
Cholangiocellular Carcinoma.” 2013. Masters Thesis, University of Alberta. Accessed January 15, 2021.
https://era.library.ualberta.ca/files/h415pb10b.
MLA Handbook (7th Edition):
Albahrani, Redha Mohammed. “Differential Expression of TWSG1, BMP4 and Shh Morphogens
Signaling Proteins in Hepatocellular Carcinoma and
Cholangiocellular Carcinoma.” 2013. Web. 15 Jan 2021.
Vancouver:
Albahrani RM. Differential Expression of TWSG1, BMP4 and Shh Morphogens
Signaling Proteins in Hepatocellular Carcinoma and
Cholangiocellular Carcinoma. [Internet] [Masters thesis]. University of Alberta; 2013. [cited 2021 Jan 15].
Available from: https://era.library.ualberta.ca/files/h415pb10b.
Council of Science Editors:
Albahrani RM. Differential Expression of TWSG1, BMP4 and Shh Morphogens
Signaling Proteins in Hepatocellular Carcinoma and
Cholangiocellular Carcinoma. [Masters Thesis]. University of Alberta; 2013. Available from: https://era.library.ualberta.ca/files/h415pb10b
NSYSU
9.
Chen, Ya-chun.
Studies on the relationship between autophagy and apoptosis in hepatocellular carcinoma-derived cells Huh7 by treatment with ABT-751.
Degree: Master, Institute of Biomedical Sciences, 2014, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0725114-131202
► The objective was to study the effects of ABT-751 on apoptosis and autophagy in hepatocellular carcinoma-derived cells. Hepatocellular carcinoma (HCC) is a common malignant tumor…
(more)
▼ The objective was to study the effects of ABT-751 on apoptosis and autophagy in
hepatocellular carcinoma-derived cells.
Hepatocellular carcinoma (HCC) is a common malignant tumor in the world. In recent years, HCC was the second leading cause of cancer death in Taiwan. Recently, the effects of anti-cancer drugs usually are mediated by the inhibition of tumor angiogenesis and microtubule synthesis. ABT-751 arrest cells in the G2/M phase due to its inhibition of microtubule synthesis and induction of cell apoptosis. The objective of thesis is to study the relationship between autophagy and apoptosis in
hepatocellular carcinoma-derived cells Huh7 by treatment with ABT-751.
In this study, the cytotoxicity of ABT-751 to Huh7 cells was measured by MTT assay at 570 nm. The results indicated the IC50 of Huh7 treated with ABT-751 for 48 h was 1.5 µM. The assay of Cyto-ID, acridine orange staining and immunoblotting were used to determine the ABT-751-induced autophagy in Huh7 cells and the autophagy induced by ABT-751 has a role in cell survival. To investigate whether inhibition of autophagy could enhance apoptosis in Huh7 cells after the treatment of ABT-751. The results showed the inhibition of autophagy could enhance the effect of inducing Huh7 cells death due to the combinations of ABT-751 with the autophagy inhibitors 3-methylamphetamine (3-MA) or bafilomycin A1 (BafA1). Above results indicated that ABT-751 could inhibit microtubule polymerization and lead to autophagy, which promoted survival of cancer cells. Consequently, combinations of ABT-751 with the autophagy inhibitor, which will promote the effect of ABT-751 to induce cytotoxin.
Advisors/Committee Members: Yow-Ling Shiue (committee member), Hung-Wen Huamg (chair), Yao-tsung Yeh (chair).
Subjects/Keywords: Hepatocellular carcinoma; Autophagy; Apoptosis; Microtubule; ABT-751
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APA (6th Edition):
Chen, Y. (2014). Studies on the relationship between autophagy and apoptosis in hepatocellular carcinoma-derived cells Huh7 by treatment with ABT-751. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0725114-131202
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chen, Ya-chun. “Studies on the relationship between autophagy and apoptosis in hepatocellular carcinoma-derived cells Huh7 by treatment with ABT-751.” 2014. Thesis, NSYSU. Accessed January 15, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0725114-131202.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chen, Ya-chun. “Studies on the relationship between autophagy and apoptosis in hepatocellular carcinoma-derived cells Huh7 by treatment with ABT-751.” 2014. Web. 15 Jan 2021.
Vancouver:
Chen Y. Studies on the relationship between autophagy and apoptosis in hepatocellular carcinoma-derived cells Huh7 by treatment with ABT-751. [Internet] [Thesis]. NSYSU; 2014. [cited 2021 Jan 15].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0725114-131202.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chen Y. Studies on the relationship between autophagy and apoptosis in hepatocellular carcinoma-derived cells Huh7 by treatment with ABT-751. [Thesis]. NSYSU; 2014. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0725114-131202
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
10.
大野, 招伸.
Aberrant expression of monocarboxylate transpoter 4 (MCT4) in tumor cells predicts an unfavorable outcome in patients with hepatocellular carcinoma : 肝細胞癌におけるmonocarboxylate transpoter 4 (MCT4) の発現は、肝癌患者の予後推定因子である。.
Degree: 博士(医学), 2014, University of Miyazaki / 宮崎大学
URL: http://hdl.handle.net/10458/5035
以下に掲載:Liver International. 2014, 34, 6, p.942-952, doi:10.1111/liv.12466.
This is the accepted version of the following article: Liver International. 2014, 34, 6, p.942-952, which has been published in final form at http://dx.doi.org/10.1111/liv.12466.
Subjects/Keywords: hepatocellular carcinoma; MCT4; prognosis; tumour-associated macrophages
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APA (6th Edition):
大野, . (2014). Aberrant expression of monocarboxylate transpoter 4 (MCT4) in tumor cells predicts an unfavorable outcome in patients with hepatocellular carcinoma : 肝細胞癌におけるmonocarboxylate transpoter 4 (MCT4) の発現は、肝癌患者の予後推定因子である。. (Thesis). University of Miyazaki / 宮崎大学. Retrieved from http://hdl.handle.net/10458/5035
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
大野, 招伸. “Aberrant expression of monocarboxylate transpoter 4 (MCT4) in tumor cells predicts an unfavorable outcome in patients with hepatocellular carcinoma : 肝細胞癌におけるmonocarboxylate transpoter 4 (MCT4) の発現は、肝癌患者の予後推定因子である。.” 2014. Thesis, University of Miyazaki / 宮崎大学. Accessed January 15, 2021.
http://hdl.handle.net/10458/5035.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
大野, 招伸. “Aberrant expression of monocarboxylate transpoter 4 (MCT4) in tumor cells predicts an unfavorable outcome in patients with hepatocellular carcinoma : 肝細胞癌におけるmonocarboxylate transpoter 4 (MCT4) の発現は、肝癌患者の予後推定因子である。.” 2014. Web. 15 Jan 2021.
Vancouver:
大野 . Aberrant expression of monocarboxylate transpoter 4 (MCT4) in tumor cells predicts an unfavorable outcome in patients with hepatocellular carcinoma : 肝細胞癌におけるmonocarboxylate transpoter 4 (MCT4) の発現は、肝癌患者の予後推定因子である。. [Internet] [Thesis]. University of Miyazaki / 宮崎大学; 2014. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/10458/5035.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
大野 . Aberrant expression of monocarboxylate transpoter 4 (MCT4) in tumor cells predicts an unfavorable outcome in patients with hepatocellular carcinoma : 肝細胞癌におけるmonocarboxylate transpoter 4 (MCT4) の発現は、肝癌患者の予後推定因子である。. [Thesis]. University of Miyazaki / 宮崎大学; 2014. Available from: http://hdl.handle.net/10458/5035
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of California – San Diego
11.
Huo, Yuchen.
Towards improving Thermal Ablation and Embolization for Hepatocellular Carcinoma Through Cancer Stem Cell Inhibition.
Degree: Biology, 2018, University of California – San Diego
URL: http://www.escholarship.org/uc/item/7ms0h9bf
► Percutaneous thermal ablation (PTA) and transarterial embolization (TAE) represent vital alternatives for patients with early or intermediate stage hepatocellular carcinoma (HCC), for whom surgery is…
(more)
▼ Percutaneous thermal ablation (PTA) and transarterial embolization (TAE) represent vital alternatives for patients with early or intermediate stage hepatocellular carcinoma (HCC), for whom surgery is not an option. Nonetheless, incomplete ablation or embolization can lead to local recurrence or the development of new foci of disease. Studies suggest that the sublethal heat stress induced by incomplete PTA and hypoxia induced by TAE can enrich the proportion of the cancer stem cells (CSC), a rare subpopulation of self-renewing cells capable of recapitulating the entire HCC tumor. Their quiescence and self-protective mechanisms make CSC resistant to standard cancer therapies aimed at the rapidly-dividing cells that comprise the bulk of the tumor. If surviving HCC CSC give rise to disease recurrence after PTA or TAE, combining PTA or TAE with HCC CSC inhibitors could improve disease response and decrease recurrence. The current study tested this hypothesis in vitro by subjecting HCC cells to conditions simulating incomplete PTA with sublethal heat stress or TAE in a hypoxia chamber with serum starvation, without or with HCC CSC inhibitors. Surviving cells were analyzed by flow cytometry, cell culture assays, immunoblotting and immunofluorescence results. Our results demonstrated conditions simulating PTA and TAE resulted in an enrichment of cells bearing CSC markers and HCC CSC inhibitors decreased this enrichment. In conclusion, incomplete PTA and TAE activates the cancer stem cell populations in HCC and can generate more aggressive disease. The adjuvant treatments with CSC inhibitors can abolish the enrichment and improve the efficacy of treatments.
Subjects/Keywords: Biology; cancer stem cell; hepatocellular carcinoma
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APA ·
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APA (6th Edition):
Huo, Y. (2018). Towards improving Thermal Ablation and Embolization for Hepatocellular Carcinoma Through Cancer Stem Cell Inhibition. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/7ms0h9bf
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Huo, Yuchen. “Towards improving Thermal Ablation and Embolization for Hepatocellular Carcinoma Through Cancer Stem Cell Inhibition.” 2018. Thesis, University of California – San Diego. Accessed January 15, 2021.
http://www.escholarship.org/uc/item/7ms0h9bf.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Huo, Yuchen. “Towards improving Thermal Ablation and Embolization for Hepatocellular Carcinoma Through Cancer Stem Cell Inhibition.” 2018. Web. 15 Jan 2021.
Vancouver:
Huo Y. Towards improving Thermal Ablation and Embolization for Hepatocellular Carcinoma Through Cancer Stem Cell Inhibition. [Internet] [Thesis]. University of California – San Diego; 2018. [cited 2021 Jan 15].
Available from: http://www.escholarship.org/uc/item/7ms0h9bf.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Huo Y. Towards improving Thermal Ablation and Embolization for Hepatocellular Carcinoma Through Cancer Stem Cell Inhibition. [Thesis]. University of California – San Diego; 2018. Available from: http://www.escholarship.org/uc/item/7ms0h9bf
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
NSYSU
12.
Chou, Chien-Ting.
Study on ABT-751-suppressed growth on hepatocellular carcinoma-derived Hep-3B cells.
Degree: Master, Institute of Biomedical Sciences, 2017, NSYSU
URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0731117-120743
► One of the most prone to diagnosed cancer in the world, Hepatocellular carcinoma (HCC) is a common malignant tumor. Besides, the latest statistics show that…
(more)
▼ One of the most prone to diagnosed cancer in the world,
Hepatocellular carcinoma (HCC) is a common malignant tumor. Besides, the latest statistics show that HCC is the second most common cancer in men and forth in women in Taiwan. In this study, data show that in
hepatocellular carcinoma cell line, Hep-3B, ABT-751 can induce autophagy and apoptosis. This study is aim to investigate the mechanism of ABT-751-induced autophagy and apoptosis in Hep-3B.ABT-751 is a novel oral administration of anti-microtubule drugs. In previous studies, it has been demonstrated that ABT-751 can bond with β-tubulin to inhibit microtubules. In our research, we decided to use 2 μM as the application concentration by MTT test. ABT-751 is found to inhibit the splitting of Hep-3B cells by affecting microtubules. Besides, results of Cyto-ID, Acridine orange staining and western blotting show that ABT-751 induced autophagy at 24 and 48 hours. By using the autophagy inhibitors 3-Methyladenine (3-MA) and bafilomycin A1 (BafA1), we tend to investigate the role of autophagy during this study, results show that when autophagy is inhibited, the percentage of apoptotic cell would increase. In all, results indicated that ABT-751 inhibited splitting of Hep-3B by affecting microtubules, still, ABT-751 induced the occurrence of autophagy. Additionally, the proportion of apoptotic cells will increase, when the autophagy is inhibited.
Advisors/Committee Members: Chien-Feng Li (chair), Hung-Wen Huang (chair), Cheng-Tang Pan (chair), Yow-Ling Shiue (committee member).
Subjects/Keywords: Apoptosis; Autophagy; Microtubule; ABT-751; Hepatocellular carcinoma
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APA ·
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APA (6th Edition):
Chou, C. (2017). Study on ABT-751-suppressed growth on hepatocellular carcinoma-derived Hep-3B cells. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0731117-120743
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Chou, Chien-Ting. “Study on ABT-751-suppressed growth on hepatocellular carcinoma-derived Hep-3B cells.” 2017. Thesis, NSYSU. Accessed January 15, 2021.
http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0731117-120743.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Chou, Chien-Ting. “Study on ABT-751-suppressed growth on hepatocellular carcinoma-derived Hep-3B cells.” 2017. Web. 15 Jan 2021.
Vancouver:
Chou C. Study on ABT-751-suppressed growth on hepatocellular carcinoma-derived Hep-3B cells. [Internet] [Thesis]. NSYSU; 2017. [cited 2021 Jan 15].
Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0731117-120743.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Chou C. Study on ABT-751-suppressed growth on hepatocellular carcinoma-derived Hep-3B cells. [Thesis]. NSYSU; 2017. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0731117-120743
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Drexel University
13.
Kim, John.
Quantification of Hepatitis B Surface Antigen (HBsAg) in a Haimen City, China Cohort.
Degree: 2012, Drexel University
URL: http://hdl.handle.net/1860/3953
► Background: Liver cancer is the fifth most frequently diagnosed cancer, with hepatocellular carcinoma (HCC) constituting the majority of cases. Chronic hepatitis B (CHB) can incur…
(more)
▼ Background: Liver cancer is the fifth most frequently diagnosed cancer, with hepatocellular carcinoma (HCC) constituting the majority of cases. Chronic hepatitis B (CHB) can incur a 25 to 30% lifetime risk for HCC. Along with demographic factors, serum hepatitis B surface antigen (HBsAg) quantitation may aid in HCC risk prediction among those with CHB. Objectives: A method to classify quantitative levels of HBsAg was developed to evaluate the association of demographic factors and other baseline exposure variables with HBsAg levels. HBsAg levels and known HCC risk factors were assessed to predict the risk for HCC mortality. Methods: This prospective study included participants with initial serum HBsAg quantity (n = 3,917) who were followed for HCC mortality from 1992 to 2010. Tertile distributions of sAg quantity were created and ordinal logistic regression was performed to assess explanatory risk variables against polytomous sAg group outcomes. Known risk factors for HCC were assessed with sAg group to predict HCC mortality using Cox proportional hazards. Results: This study demonstrated that participants with higher sAg quantity had a decreased risk for HCC. Among males, hepatitis history, family HCC history, and HBV DNA positivity were important indicators for HCC. Among females, hepatitis history was an important indicator for HCC. Conclusions: The rising incidence of HCC indicates a need to identify risk factors for HCC mortality in clinical practice. Among those with CHB, known demographic and medical history factors are associated with an increased risk of HCC. In addition, HBsAg quantitation may help predict HCC mortality among those with established CHB.
M.P.H., Public Health – Drexel University, 2012
Advisors/Committee Members: Evans, Alison.
Subjects/Keywords: Public Health; Hepatitis B; China; Hepatocellular Carcinoma
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APA (6th Edition):
Kim, J. (2012). Quantification of Hepatitis B Surface Antigen (HBsAg) in a Haimen City, China Cohort. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/3953
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kim, John. “Quantification of Hepatitis B Surface Antigen (HBsAg) in a Haimen City, China Cohort.” 2012. Thesis, Drexel University. Accessed January 15, 2021.
http://hdl.handle.net/1860/3953.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kim, John. “Quantification of Hepatitis B Surface Antigen (HBsAg) in a Haimen City, China Cohort.” 2012. Web. 15 Jan 2021.
Vancouver:
Kim J. Quantification of Hepatitis B Surface Antigen (HBsAg) in a Haimen City, China Cohort. [Internet] [Thesis]. Drexel University; 2012. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/1860/3953.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kim J. Quantification of Hepatitis B Surface Antigen (HBsAg) in a Haimen City, China Cohort. [Thesis]. Drexel University; 2012. Available from: http://hdl.handle.net/1860/3953
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Boston University
14.
Pratt, Michelle Sherman.
Comparison of linear, bi-dimensional, and volumetric measurements in evaluating tumor response of hepatocellular carcinoma lesions in the arterial and portal venous phases on MRI.
Degree: MS, Clinical Investigation, 2015, Boston University
URL: http://hdl.handle.net/2144/15617
► There are unmet needs in evaluating treatment response of hepatocellular carcinoma in research protocols. Early predictors, such as imaging biomarkers, could allow for earlier judgment…
(more)
▼ There are unmet needs in evaluating treatment response of hepatocellular carcinoma in research protocols. Early predictors, such as imaging biomarkers, could allow for earlier judgment of treatment effect. Currently RECIST is the most widely accepted criterion in clinical trials. A modified RECIST (mRECIST) criterion was developed to take into account the unique imaging characteristics of HCC lesions. Much discussion has occurred regarding linear measurements and their appropriateness for evaluating change in tumor burden over time. The simplicity of currently accepted criteria differs with the increasing sophistication of imaging techniques. Tumor volume change on 3D imaging can provide insight into actual action of treatment rather than an estimate of action as shown by linear and bi-dimensional measurements. It was the aim of this study to determine whether linear, bi-dimensional, and volumetric percent changes of HCC lesions, in both the arterial and portal venous phases, are significantly comparable.
27 HCC lesions (identified on 25 subjects) were measured at two timepoints by each method on 3D GRE MRI scans in both phases. Percent change was calculated per lesion for each measurement type in both the arterial and portal venous phases. Signed rank tests, paired t tests, and comparison of change tests were run to evaluate the data.
Significant differences between the percent changes of linear measurements versus volumetric measurements were observed using a Wilcoxon signed-rank test which showed p = 0.0000. A simple correlation assessment showed positive correlations for all measurements, with the lowest being correlations 0.8679 for the arterial linear percent change versus the arterial volumetric percent change and 0.8434 for the portal venous linear percent change versus the portal venous volumetric percent change. Differences between percent changes of linear versus bi-dimensional measurements and bi-dimensional versus volumetric measurements were significant as well (Linear versus bi-dimensional p = 0.0001, bi-dimensional versus volumetric p = 0.0004).
To conclude, the differences in the percent changes when comparing the measurement types are statistically significant, particularly when comparing linear and volumetric measurements. Establishing a reproducible volumetric criterion could lead to improvements in the implementation of clinical trials.
Subjects/Keywords: Medical imaging; Arterial; Hepatocellular carcinoma; MRI; RECIST
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APA ·
Chicago ·
MLA ·
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CSE |
Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Pratt, M. S. (2015). Comparison of linear, bi-dimensional, and volumetric measurements in evaluating tumor response of hepatocellular carcinoma lesions in the arterial and portal venous phases on MRI. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/15617
Chicago Manual of Style (16th Edition):
Pratt, Michelle Sherman. “Comparison of linear, bi-dimensional, and volumetric measurements in evaluating tumor response of hepatocellular carcinoma lesions in the arterial and portal venous phases on MRI.” 2015. Masters Thesis, Boston University. Accessed January 15, 2021.
http://hdl.handle.net/2144/15617.
MLA Handbook (7th Edition):
Pratt, Michelle Sherman. “Comparison of linear, bi-dimensional, and volumetric measurements in evaluating tumor response of hepatocellular carcinoma lesions in the arterial and portal venous phases on MRI.” 2015. Web. 15 Jan 2021.
Vancouver:
Pratt MS. Comparison of linear, bi-dimensional, and volumetric measurements in evaluating tumor response of hepatocellular carcinoma lesions in the arterial and portal venous phases on MRI. [Internet] [Masters thesis]. Boston University; 2015. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/2144/15617.
Council of Science Editors:
Pratt MS. Comparison of linear, bi-dimensional, and volumetric measurements in evaluating tumor response of hepatocellular carcinoma lesions in the arterial and portal venous phases on MRI. [Masters Thesis]. Boston University; 2015. Available from: http://hdl.handle.net/2144/15617
Université Paris-Sud – Paris XI
15.
Degli Esposti, Davide.
Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis.
Degree: Docteur es, Physiopathologie moléculaire et cellulaire, 2011, Université Paris-Sud – Paris XI
URL: http://www.theses.fr/2011PA114809
► Le foie est un organe essentiel à la vie chez tous les mammifères. C’est un organe central du métabolisme énergétique et de la détoxification des…
(more)
▼ Le foie est un organe essentiel à la vie chez tous les mammifères. C’est un organe central du métabolisme énergétique et de la détoxification des substances xénobiotiques auxquelles l’individu est exposé. Le foie est la cible d’agressions diverses, telles que les virus, l’alcool, les substances chimiques présentes dans l’alimentation ou l’environnement. Il peut également subir destransformations pathologiques profondes, lors du diabète ou de l’obésité par exemple.La stéatose hépatique, caractérisée par une accumulation de triglycérides sous forme de vésiculesgénérant une réponse inflammatoire, est connue depuis de nombreuses années. Son étude a permisde définir un modèle en deux étapes (« two hits ») indispensables à la genèse d’une stéatohépatite ou NASH. La première est l’accumulation de lipides, la seconde consiste en la genèse d’un stress oxydant et la libération de cytokines. La NASH est une des conséquences pathologiques du syndrome métabolique au cours duquel une résistance des tissus à l’insuline se développe.Récemment, la composition des lipides accumulés dans la NASH a été décrite et montre la présence de cholestérol libre et de différents métabolites des acides gras dont la toxicité est grande mais variable. De façon surprenante, une nouvelle hypothèse tend à émerger quant aux rôles protecteurs de certaines catégories de lipides. En effet, le stockage des triglycérides sous forme de vésicules pourrait être un mécanisme de survie cellulaire (Neuschwander-Tetri, 2010). Il s’agirait principalement d’une tolérance à la mort cellulaire par nécrose ou apoptose. Dans ce contexte,l’activation de l’autophagie serait capitale et la nécrose ne serait plus un mécanisme non contrôlé,mais au contraire un système finement régulé.Des données expérimentales récentes suggèrent l’existence d’un réseau complexe d’interactions moléculaires qui lient, dans la NASH comme dans le cas de la cancérogenèse, le métabolisme énergétique, la réponse inflammatoire systémique et tissulaire et des altérations subcellulaires, telles que les lésions des mitochondries et du réticulum endoplasmique.Nous avons utilisé le cas particulier du préconditionnement ischémique, une technique chirurgicale qui consiste, grâce à de courtes périodes d’occlusion vasculaire avant l’ischémie, à conférer au tissu une protection contre les lésions d’ischémie/reperfusion (I/R), pour étudier les mécanismes de survie mis en place par les hépatocytes stéatosiques au cours d’un stress d’I/R. Dans deux contextes différents, celui d’une ischémie chaude au cours d’une hépatectomie partielle et celui d’une ischémie froide au cours de la transplantation hépatique, nous avons montré que l’autophagie peut jouer un rôle central dans la protection des hépatocytes stéatosiques. Cependant, il est envisageable qu’un dysfonctionnement de l’autophagie pourrait conduire à la genèse d’altérations cellulaires comme une instabilité génomique, caractéristique de la transformation cancéreuse. L’équilibre entre la survie et la mort cellulaire dépend donc de l’intégration de cette…
Advisors/Committee Members: Poüs, Christian (thesis director), Lemoine, Antoinette (thesis director).
Subjects/Keywords: Autophagie; Steatosis; Autophagy; Hepatocellular carcinoma; Cancer; Liver
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Manager
APA (6th Edition):
Degli Esposti, D. (2011). Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis. (Doctoral Dissertation). Université Paris-Sud – Paris XI. Retrieved from http://www.theses.fr/2011PA114809
Chicago Manual of Style (16th Edition):
Degli Esposti, Davide. “Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis.” 2011. Doctoral Dissertation, Université Paris-Sud – Paris XI. Accessed January 15, 2021.
http://www.theses.fr/2011PA114809.
MLA Handbook (7th Edition):
Degli Esposti, Davide. “Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis.” 2011. Web. 15 Jan 2021.
Vancouver:
Degli Esposti D. Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis. [Internet] [Doctoral dissertation]. Université Paris-Sud – Paris XI; 2011. [cited 2021 Jan 15].
Available from: http://www.theses.fr/2011PA114809.
Council of Science Editors:
Degli Esposti D. Les mécanismes de réponse à l'inflammation chronique dans le foie stéatosique et les conséquences sur l'homéostasie cellulaire et la cancérogénèse : Response mechanisms to chronic inflammation in steatotic liver and consequences on cellular homeostasy and carcinogenesis. [Doctoral Dissertation]. Université Paris-Sud – Paris XI; 2011. Available from: http://www.theses.fr/2011PA114809
Virginia Commonwealth University
16.
Lewis, Benjamin C.
Radiotherapy Response Using Intravoxel Incoherent Motion Magnetic Resonance Imaging in Liver Patients Treated with Stereotactic Body Radiotherapy.
Degree: PhD, Radiation Oncology, 2019, Virginia Commonwealth University
URL: https://doi.org/10.25772/DSD8-6593
;
https://scholarscompass.vcu.edu/etd/5821
► Magnetic resonance imaging is utilized as an important tool in radiation oncology for delineation of healthy and cancerous tissues, and evaluating the functionality of…
(more)
▼ Magnetic resonance imaging is utilized as an important tool in radiation oncology for delineation of healthy and cancerous tissues, and evaluating the functionality of those tissues, structures, and organs. Currently, the clinical imaging protocol at Virginia Commonwealth University includes anatomical imaging for tissue and structure delineation, and to observe treatment induced changes. Diffusion weighted imaging (DWI) is also acquired for calculation of apparent diffusion coefficient (ADC) values to provide quantitative information on tissue diffusivity and microstructure. However, anatomical images and ADC values may not display the true extent of changes in tissue. This work seeks to further utilize the capabilities of MRI and expand its role in treatment response monitoring for liver cancer patients treated with stereotactic body radiotherapy (SBRT). To do so, an imaging protocol and image analysis methodology to evaluate treatment changes on pre- and post-treatment image sets was developed. An extension of DWI, termed intravoxel incoherent motion (IVIM) imaging, was utilized to quantitatively assess levels of perfusion and diffusion within the liver and tumor. Acquisition of high-quality diffusion weighted images of the liver necessitated the development of an MR safe respiratory motion management device, which was designed, constructed and evaluated in this work. An imaging protocol was developed providing anatomical and functional images of the liver, acquired under breath hold, utilizing the respiratory motion management device. An IVIM parameter calculation and texture analysis workflow was developed using MATLAB, and applied to acquired data sets from multiple studies, including past clinical cases, investigator, healthy volunteer, and liver cancer patient . Differences in IVIM and texture analysis parameters were investigated for healthy and diseased tissue, and for select dose regions from pre- and post-treatment imaging sessions. Significant differences, at a voxel level, were found between healthy and diseased tissue, and pre- and post-treatment volumes, for multiple parameters, including apparent diffusion coefficient, pure diffusion, and perfusion, as well as for various texture features. Overall, this study showed the potential of IVIM and texture analysis to be used for discriminating between healthy and diseased tissues in the liver, and for indication of treatment response.
Advisors/Committee Members: Siyong Kim, Taeho Kim, William Song, Joel Steinberg.
Subjects/Keywords: IVIM; DWI; MRI; SBRT; Liver; Hepatocellular Carcinoma
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APA (6th Edition):
Lewis, B. C. (2019). Radiotherapy Response Using Intravoxel Incoherent Motion Magnetic Resonance Imaging in Liver Patients Treated with Stereotactic Body Radiotherapy. (Doctoral Dissertation). Virginia Commonwealth University. Retrieved from https://doi.org/10.25772/DSD8-6593 ; https://scholarscompass.vcu.edu/etd/5821
Chicago Manual of Style (16th Edition):
Lewis, Benjamin C. “Radiotherapy Response Using Intravoxel Incoherent Motion Magnetic Resonance Imaging in Liver Patients Treated with Stereotactic Body Radiotherapy.” 2019. Doctoral Dissertation, Virginia Commonwealth University. Accessed January 15, 2021.
https://doi.org/10.25772/DSD8-6593 ; https://scholarscompass.vcu.edu/etd/5821.
MLA Handbook (7th Edition):
Lewis, Benjamin C. “Radiotherapy Response Using Intravoxel Incoherent Motion Magnetic Resonance Imaging in Liver Patients Treated with Stereotactic Body Radiotherapy.” 2019. Web. 15 Jan 2021.
Vancouver:
Lewis BC. Radiotherapy Response Using Intravoxel Incoherent Motion Magnetic Resonance Imaging in Liver Patients Treated with Stereotactic Body Radiotherapy. [Internet] [Doctoral dissertation]. Virginia Commonwealth University; 2019. [cited 2021 Jan 15].
Available from: https://doi.org/10.25772/DSD8-6593 ; https://scholarscompass.vcu.edu/etd/5821.
Council of Science Editors:
Lewis BC. Radiotherapy Response Using Intravoxel Incoherent Motion Magnetic Resonance Imaging in Liver Patients Treated with Stereotactic Body Radiotherapy. [Doctoral Dissertation]. Virginia Commonwealth University; 2019. Available from: https://doi.org/10.25772/DSD8-6593 ; https://scholarscompass.vcu.edu/etd/5821
17.
Takano, Masato; Shimada, Keiji; Fujii, Tomomi; Morita, Kohei; Takeda, Maiko; Nakajima, Yoshiyuki; Nonomura, Akitaka; Konishi, Noboru.
Keratin 19 as a key molecule in progression of human hepatocellular carcinomas through invasion and angiogenesis. : 浸潤および血管新生を通しての人肝細胞癌の進行におけるケラチン19分子の役割.
Degree: 博士（医学）, 2017, Nara Medical University / 奈良県立医科大学
URL: http://hdl.handle.net/10564/3332
► BACKGROUND: Keratin (K) 19-positive hepatocellular carcinoma (HCC) is well known to have a higher malignant potential than K19-negative HCC: However, the molecular mechanisms involved in…
(more)
▼ BACKGROUND: Keratin (K) 19-positive hepatocellular carcinoma (HCC) is well known to have a higher malignant potential than K19-negative HCC: However, the molecular mechanisms involved in K19-mediated progression of HCC remain unclear. We attempted to clarify whether K19 directly affects cell survival and invasiveness in association with cellular senescence or epithelial-mesenchymal transition (EMT) in K19-positive HCC. METHODS: K19 expression was analysed in 136 HCC surgical specimens. The relationship of K19 with clinicopathological factors and survival was analysed. Further, the effect of K19 on cell proliferation, invasion, and angiogenesis was examined by silencing K19 in the human HCC cell lines, HepG2, HuH-7, and PLC/PRF/5. Finally, we investigated HCC invasion, proliferation, and angiogenesis using K19-positive HCC specimens. RESULTS: Analysis of HCC surgical specimens revealed that K19-positive HCC exhibited higher invasiveness, metastatic potential, and poorer prognosis. In vitro experiments using the human HCC cell lines revealed that K19 silencing suppressed cell growth by inducting apoptosis or upregulating p16 and p27, resulting in cellular senescence. In addition, transfection with K19 siRNA upregulated E-cadherin gene expression, significantly inhibited the invasive capacity of the cells, downregulated angiogenesis-related molecules such as vasohibin-1 (VASH1) and fibroblast growth factor 1 (FGFR1), and upregulated vasohibin-2 (VASH2). K19-positive HCC specimens exhibited a high MIB-1 labelling index, decreased E-cadherin expression, and high microvessel density around cancer foci. CONCLUSION: K19 directly promotes cancer cell survival, invasion, and angiogenesis, resulting in HCC progression and poor clinical outcome. K19 may therefore be a novel drug target for the treatment of K19-positive HCC.
博士（医学）・乙第1399号・平成29年3月15日
© The Author(s). 2016 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, andreproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link tothe Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
Subjects/Keywords: Keratin 19; Hepatocellular carcinoma; Senescence; Apoptosis; Angiogenesis
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APA (6th Edition):
Takano, Masato; Shimada, Keiji; Fujii, Tomomi; Morita, Kohei; Takeda, Maiko; Nakajima, Yoshiyuki; Nonomura, Akitaka; Konishi, N. (2017). Keratin 19 as a key molecule in progression of human hepatocellular carcinomas through invasion and angiogenesis. : 浸潤および血管新生を通しての人肝細胞癌の進行におけるケラチン19分子の役割. (Thesis). Nara Medical University / 奈良県立医科大学. Retrieved from http://hdl.handle.net/10564/3332
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Takano, Masato; Shimada, Keiji; Fujii, Tomomi; Morita, Kohei; Takeda, Maiko; Nakajima, Yoshiyuki; Nonomura, Akitaka; Konishi, Noboru. “Keratin 19 as a key molecule in progression of human hepatocellular carcinomas through invasion and angiogenesis. : 浸潤および血管新生を通しての人肝細胞癌の進行におけるケラチン19分子の役割.” 2017. Thesis, Nara Medical University / 奈良県立医科大学. Accessed January 15, 2021.
http://hdl.handle.net/10564/3332.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Takano, Masato; Shimada, Keiji; Fujii, Tomomi; Morita, Kohei; Takeda, Maiko; Nakajima, Yoshiyuki; Nonomura, Akitaka; Konishi, Noboru. “Keratin 19 as a key molecule in progression of human hepatocellular carcinomas through invasion and angiogenesis. : 浸潤および血管新生を通しての人肝細胞癌の進行におけるケラチン19分子の役割.” 2017. Web. 15 Jan 2021.
Vancouver:
Takano, Masato; Shimada, Keiji; Fujii, Tomomi; Morita, Kohei; Takeda, Maiko; Nakajima, Yoshiyuki; Nonomura, Akitaka; Konishi N. Keratin 19 as a key molecule in progression of human hepatocellular carcinomas through invasion and angiogenesis. : 浸潤および血管新生を通しての人肝細胞癌の進行におけるケラチン19分子の役割. [Internet] [Thesis]. Nara Medical University / 奈良県立医科大学; 2017. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/10564/3332.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Takano, Masato; Shimada, Keiji; Fujii, Tomomi; Morita, Kohei; Takeda, Maiko; Nakajima, Yoshiyuki; Nonomura, Akitaka; Konishi N. Keratin 19 as a key molecule in progression of human hepatocellular carcinomas through invasion and angiogenesis. : 浸潤および血管新生を通しての人肝細胞癌の進行におけるケラチン19分子の役割. [Thesis]. Nara Medical University / 奈良県立医科大学; 2017. Available from: http://hdl.handle.net/10564/3332
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
18.
호, 석광.
Blood Neutrophil-to-Lymphocyte Ratio predicts tumor recurrence in patients with hepatocellular carcinoma within Milan criteria after hepatectomy.
Degree: 2016, Ajou University
URL: http://repository.ajou.ac.kr/handle/201003/13046
;
http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000023056
► Purpose: The systemic inflammation biomarker, Neutrophil-to-Lymphocyte Ratio (NLR), has been reported as one of the adverse prognostic factors for HCC patient. The purpose of this…
(more)
▼ Purpose: The systemic inflammation biomarker, Neutrophil-to-Lymphocyte Ratio (NLR), has been reported as one of the adverse prognostic factors for HCC patient. The purpose of this study was to evaluate whether NLR could predict the risk of recurrence and death for the HCC patient confirming to Milan criteria after hepatectomy.
Methods: Retrospective analysis was performed on a database of HCC patients who underwent hepatectomy between March 2001 and December 2011. The cutoff value of NLR was decided by receiver operating characteristic (ROC) curve analysis. Univariate and multivariate regression analysis were performed to identify predictive factors of recurrence and death.
Results: A total of 213 patients were included in the present study. The median follow-up period was 48 months. One hundred and seven patients were experienced tumor recurrence; forty of them were recurred within 12 months (early recurrence). NLR≥1.505, albumin≤3.75g/dl, microvascular invasion and high grade of cirrhosis were found to be independent factors for adverse recurrence-free survival in multivariate regression analysis. And NLR≥1.945 was also found as a prognosis factor for early recurrence by univariate regression analysis.
Conclusions: Elevated preoperative NLR can be easily obtained and reliable biomarker for assessing the tumor recurrence and early recurrence of Milan criteria HCC after the initial hepatectomy.
Ⅰ. INTRODUCTION 1
Ⅱ. METHODS 3
A. Patients’ inclusion criterioa and characteristics 3
B. Follow-up strategy, recurrence and treatment pattern 4
C. To determined the optimal cutoff of continuous variavles 5
D. Statistical Analysis 10
Ⅲ. RESULTS 11
A. Survival outcomes 11
B. Prognositic facrors of tumor recurrence in HCC Patients within Milan criteria 14
C. Prognositic facrors of early recurrence in HCC patients within Milan criteria 17
Ⅳ. DISCUSSION 18
Ⅴ. CONCLUSION 23
REFERENCES 24
Doctor
Advisors/Committee Members: 대학원 의학과, 201325248, 호, 석광.
Subjects/Keywords: Neutrophils; lymphocytes; prognosis; hepatocellular carcinoma; hepatectomy
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APA (6th Edition):
호, . (2016). Blood Neutrophil-to-Lymphocyte Ratio predicts tumor recurrence in patients with hepatocellular carcinoma within Milan criteria after hepatectomy. (Thesis). Ajou University. Retrieved from http://repository.ajou.ac.kr/handle/201003/13046 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000023056
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
호, 석광. “Blood Neutrophil-to-Lymphocyte Ratio predicts tumor recurrence in patients with hepatocellular carcinoma within Milan criteria after hepatectomy.” 2016. Thesis, Ajou University. Accessed January 15, 2021.
http://repository.ajou.ac.kr/handle/201003/13046 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000023056.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
호, 석광. “Blood Neutrophil-to-Lymphocyte Ratio predicts tumor recurrence in patients with hepatocellular carcinoma within Milan criteria after hepatectomy.” 2016. Web. 15 Jan 2021.
Vancouver:
호 . Blood Neutrophil-to-Lymphocyte Ratio predicts tumor recurrence in patients with hepatocellular carcinoma within Milan criteria after hepatectomy. [Internet] [Thesis]. Ajou University; 2016. [cited 2021 Jan 15].
Available from: http://repository.ajou.ac.kr/handle/201003/13046 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000023056.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
호 . Blood Neutrophil-to-Lymphocyte Ratio predicts tumor recurrence in patients with hepatocellular carcinoma within Milan criteria after hepatectomy. [Thesis]. Ajou University; 2016. Available from: http://repository.ajou.ac.kr/handle/201003/13046 ; http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000023056
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
19.
Lopez Coral, Alfonso.
Functional and mutational analysis of the cytosolic N-terminal domains of MAL2 in hepatic cells.
Degree: 2019, The Catholic University of America
URL: http://hdl.handle.net/1961/cuislandora:213642
► A major focus of our lab is to study the role of MAL2 and its binding partners (STK16) in normal and malignant hepatic cells. Because…
(more)
▼ A major focus of our lab is to study the role of MAL2 and its binding partners (STK16) in normal and malignant hepatic cells. Because both MAL2 and STK16 have been shown to regulate exocytosis, we hypothesized that other constitutive phosphorylated substrates are required. Thus, one of the goals of this study was to identify STK16-mediated constitutively-phosphorylated substrates that regulate constitutive basolateral secretion in hepatic cells. To better assess the direct involvement for STK16-mediated secretion, we used a cell system that lacks MAL2. Using a proteomics approach, we overexpressed wild-type and kinase-dead versions of STK16 to screen for phosphorylated substrates. We identified WDR1 as one of many phosphorylated substrates containing consensus motifs for STK16 binding. We further determined that STK16-induced WDR1 phosphorylation is required for the actin-mediated basolateral secretion in hepatic cells.Since its discovery in breast carcinoma, the MAL2’s role in human cancers remains unknown. Previously, MAL2 overexpression in cancer patients has been proposed as a poor prognosis marker. However, MAL2 overexpression has been associated with benign and early stage cancers with more epithelial features. Also, its downregulation and/or silencing has been associated with more advanced and/or malignant forms of cancers. This confounding results create a paradox as to whether MAL2 has an oncogenic or tumor suppressive role in human carcinomas. Thus, another goal of this study was to unravel the MAL2 paradox in human carcinomas. Using polarized and nonpolarized hepatic-derived cancer cell lines, we determined that MAL2 functions as a tumor suppressor. We further characterized the mechanisms of how MAL2 exerts its tumor suppressor activity by a mutational analysis of the proline-rich regions of the MAL2’s cytosolic amino-terminal domains. Thus, we established that the MAL2 tumor suppressor activity is mediated via its FPAP motif. We propose that high MAL2 expression prevents key molecular markers from localizing at invadopodia sites. Rather, MAL2 promotes cell membrane actin-based protrusion formation associated with decreased cancer cell proliferation, migration and invasion. We further propose that in cancer cells, the chromosomal region 8q24 (a region that harbors the MAL2 gene) undergoes aberrant amplification leading to MAL2 overexpression. However, as cancer progresses MAL2 is downregulated and/or silenced. Therefore, the effect of MAL2 is beneficial but short-lived.
Cellular biology
Molecular biology
Hepatocellular carcinoma, Liver, MAL2, Mena, Polarity, TKs5
Biology
Degree Awarded: Ph.D. Biology. The Catholic University of America
Advisors/Committee Members: The Catholic University of America (Degree granting institution), Tuma, Pamela (Thesis advisor), Corsi, Ann (Committee member), Golin, John (Committee member), Knyazev, Vadim (Committee member), Clawson, Deborah (Committee member).
Subjects/Keywords: Hepatocellular carcinoma; Liver; MAL2; Mena; Polarity; TKs5
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APA (6th Edition):
Lopez Coral, A. (2019). Functional and mutational analysis of the cytosolic N-terminal domains of MAL2 in hepatic cells. (Thesis). The Catholic University of America. Retrieved from http://hdl.handle.net/1961/cuislandora:213642
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Lopez Coral, Alfonso. “Functional and mutational analysis of the cytosolic N-terminal domains of MAL2 in hepatic cells.” 2019. Thesis, The Catholic University of America. Accessed January 15, 2021.
http://hdl.handle.net/1961/cuislandora:213642.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Lopez Coral, Alfonso. “Functional and mutational analysis of the cytosolic N-terminal domains of MAL2 in hepatic cells.” 2019. Web. 15 Jan 2021.
Vancouver:
Lopez Coral A. Functional and mutational analysis of the cytosolic N-terminal domains of MAL2 in hepatic cells. [Internet] [Thesis]. The Catholic University of America; 2019. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/1961/cuislandora:213642.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Lopez Coral A. Functional and mutational analysis of the cytosolic N-terminal domains of MAL2 in hepatic cells. [Thesis]. The Catholic University of America; 2019. Available from: http://hdl.handle.net/1961/cuislandora:213642
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Boston University
20.
Clifford, Corinne.
A cross sectional analysis of the association between FGF19 tumor expression and serum AFP levels in advanced HCC patients.
Degree: MS, Clinical Investigation, 2017, Boston University
URL: http://hdl.handle.net/2144/23745
► PURPOSE: HCC is a complicated disease with high mortality rates and limited treatment options. No universal clinical or molecular classification established to inform better treatment…
(more)
▼ PURPOSE: HCC is a complicated disease with high mortality rates and limited treatment options. No universal clinical or molecular classification established to inform better treatment options. There has been very limited success in determining a molecular profile that represent valid drivers in HCC patients and thus no targeted agents have obtained marketing approval. However, emerging data suggest the FGF19-pathway as a HCC driver and a potential therapeutic target. This research study aims to investigate whether the HCC prognostic risk factor, serum AFP, is predictive of FGF19 protein expression as assessed by immunohistochemistry in advanced HCC patients.
METHODS: A cross-sectional analysis was performed from baseline data collected in a Phase 1 study conducted at various centers across the US, EU, and Asia. Only advanced HCC patients with adequate liver function were eligible for enrollment. Demographic data, detailed history of HCC, and any prior treatments or surgeries were recorded. Baseline laboratory values and prognostic factors including performance status (ECOG), lab values (i.e. bilirubin, albumin), and the number, size and biomarker status of the tumor(s) were collected. Differences between groups were assessed by t test, or Chi-square test, as appropriate. Multivariate logistic stepwise regression analyses were performed including all parameters with highly significant correlations in the multivariate analysis.
RESULTS: Only AFP, metastatic disease, and prior surgery met the criteria to be incorporated into the final model. Results indicated that high AFP had a statistically significant (p-value = .01) positive association (Wald chi-square statistic = 6.601) with positive FGF19 IHC status. The odds ratio for being FGF19 IHC+ was 12.216 among the high AFP subjects as compared to low AFP subjects, and also statistically significant but had a very wide 95% confidence interval (1.811, 82.79).
CONCLUSIONS: The results indicated that HCC patients with high serum AFP levels have a twelve fold higher chance of having a positive FGF19 IHC status than those with low AFP levels. Further studies are warranted in order to replicate the data in a larger sample size to understand future clinical implications once treatment options become available for FGF19 IHC positive patients.
Subjects/Keywords: Oncology; AFP; FGF19; HCC; Hepatocellular carcinoma
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APA (6th Edition):
Clifford, C. (2017). A cross sectional analysis of the association between FGF19 tumor expression and serum AFP levels in advanced HCC patients. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/23745
Chicago Manual of Style (16th Edition):
Clifford, Corinne. “A cross sectional analysis of the association between FGF19 tumor expression and serum AFP levels in advanced HCC patients.” 2017. Masters Thesis, Boston University. Accessed January 15, 2021.
http://hdl.handle.net/2144/23745.
MLA Handbook (7th Edition):
Clifford, Corinne. “A cross sectional analysis of the association between FGF19 tumor expression and serum AFP levels in advanced HCC patients.” 2017. Web. 15 Jan 2021.
Vancouver:
Clifford C. A cross sectional analysis of the association between FGF19 tumor expression and serum AFP levels in advanced HCC patients. [Internet] [Masters thesis]. Boston University; 2017. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/2144/23745.
Council of Science Editors:
Clifford C. A cross sectional analysis of the association between FGF19 tumor expression and serum AFP levels in advanced HCC patients. [Masters Thesis]. Boston University; 2017. Available from: http://hdl.handle.net/2144/23745
University of Illinois – Chicago
21.
DeWaal, Dannielle C.
Hexokinase 2 in Liver Cancer.
Degree: 2016, University of Illinois – Chicago
URL: http://hdl.handle.net/10027/21322
► A major focus of cancer biologists is to identify novel therapeutic strategies to improve cancer-patient outcomes. One of the most prevalent cancer-specific phenotypes is glucose…
(more)
▼ A major focus of cancer biologists is to identify novel therapeutic strategies to improve cancer-patient outcomes. One of the most prevalent cancer-specific phenotypes is glucose addiction, manifest, by the specific upregulation of glycolysis in the presence of oxygen (aerobic glycolysis), and thus, cancer metabolism has been under investigation to learn how to best exploit this vulnerability to selectively eradicate cancer cells. Hexokinase (HK) enzymes catalyze the first, committed step of the glycolysis pathway, phosphorylating glucose to produce the product glucose-6-phosphate (G6P), that is used in a number of ways to support cell viability and proliferation. In liver cancer, an isoform switch is observed, whereby the normal, adult isoform, Glucokinase (GCK), is repressed and the embryonic form, Hexokinase 2 (HK2) is upregulated, and is the only isoform expressed. Therefore, liver cancer could be selectively targeted by HK2 ablation sparing the normal hepatocytes. We found that by targeting HK2 in two independent human HCC cell lines, HepG2 and Huh7, reduced hexokinase activity, proliferation, and tumorigenicity was observed in in-vitro and in-vivo assays. These phenotypes were rescued by exogenous expression of a rat, wt-HK2 orthologue that is resistant to silencing by shRNA used in the cells to target human HK2, but that both catalytic and mitochondrial-binding mutants could not, indicating that both of these functions are required for HK2 to exert tumorigenic potential. GCK could not phenocopy HK2 in rescue experiments either. Cells with HK2 knockdown that exhibited reductions in glycolysis also showed a compensatory upregulation in respiration. By targeting both glycolysis and OXPHOS, with HK2 shRNA and Metformin treatment, respectively, we were able to inhibit tumor growth in mouse tumorigenesis models. Treatment with Metformin in combination with HK2 loss also synergistically downregulates the mTORC1 signaling pathway through the REDD1 protein. Data suggests that targeting HK2 and Metformin co-treatment should be considered for HCC cancer therapy.
Advisors/Committee Members: Hay, Nissim (advisor), Tyner, Angela L. (committee member), Raychaudhuri, Pradip (committee member), Gapanko, Vadim (committee member), McLauchlan, Alan (committee member).
Subjects/Keywords: Hexokinase 2; cancer metabolism; Hepatocellular carcinoma
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Manager
APA (6th Edition):
DeWaal, D. C. (2016). Hexokinase 2 in Liver Cancer. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/21322
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
DeWaal, Dannielle C. “Hexokinase 2 in Liver Cancer.” 2016. Thesis, University of Illinois – Chicago. Accessed January 15, 2021.
http://hdl.handle.net/10027/21322.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
DeWaal, Dannielle C. “Hexokinase 2 in Liver Cancer.” 2016. Web. 15 Jan 2021.
Vancouver:
DeWaal DC. Hexokinase 2 in Liver Cancer. [Internet] [Thesis]. University of Illinois – Chicago; 2016. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/10027/21322.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
DeWaal DC. Hexokinase 2 in Liver Cancer. [Thesis]. University of Illinois – Chicago; 2016. Available from: http://hdl.handle.net/10027/21322
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Illinois – Chicago
22.
Liu, Jennifer Sue.
Engineering Culture Platforms to Study Human Liver Cancer and Fibrosis.
Degree: 2018, University of Illinois – Chicago
URL: http://hdl.handle.net/10027/22620
► The liver executes a plethora of functions such as drug metabolism, plasma protein secretion, and urea synthesis. Additionally, drug toxicity to the liver is a…
(more)
▼ The liver executes a plethora of functions such as drug metabolism, plasma protein secretion, and urea synthesis. Additionally, drug toxicity to the liver is a leading cause of drug attrition and liver cancer is the third leading cause of cancer-related deaths worldwide. Given differences between animals and humans in liver pathways, models of the human liver are essential for mechanistic studies and for drug screening. Unfortunately, human liver cells, both primary and cancer-derived, display low liver cell functions in conventional 2D monolayers. The micropatterned coculture (MPCC) platform, in which hepatocytes are organized onto collagen domains of empirically optimized dimensions and subsequently cocultured with fibroblasts, has been shown to induce high hepatocyte functions for several weeks. However, the current configuration of MPCCs lacks a key cell type of the liver, cholangiocytes (biliary epithelial cells), and it is not clear if MPCCs can be used for the development of a liver cancer screening system. This thesis aims to address these abovementioned limitations. Results obtained demonstrate that several liver cancer cell lines cultured in the MPCC platform maintain cell proliferation, higher liver cell functions, and can be effectively used to determine cytotoxicity of cancer drugs and detect cancer related gene expression. Furthermore, results show that while cholangiocytes cannot support primary human hepatocytes to the same extent as the fibroblasts, creation of a three-cell type model (hepatocytes, cholangiocytes, and fibroblasts) with higher ratio of fibroblasts and lower ratio of cholangiocytes allows high levels of functions in hepatocytes and retention of cholangiocyte morphology. Interestingly, three-cell type model also showed significantly inhibition of hepatic function and displayed increased microvascular steatosis which may suggest that the three-cell type model could be developed as a liver disease (e.g. fibrosis) model. In conclusion, the model systems developed are potentially useful for fundamental research in liver cancer and hepatocyte-cholangiocyte interactions, and for screening the cancer related pathways and efficacy and/or toxicity of drugs. In the future, the model systems can be integrated to study the effects of cholangiocytes in liver diseases or on liver cancer cells and to build models of both
hepatocellular carcinoma and cholangiocarcinoma (liver cancer subtypes).
Advisors/Committee Members: Khetani, Salman (advisor), Eddington, David (committee member), Lee, James (committee member), Khetani, Salman (chair).
Subjects/Keywords: Hepatocellular carcinoma; liver model; cholangiocyte; fibrosis
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APA (6th Edition):
Liu, J. S. (2018). Engineering Culture Platforms to Study Human Liver Cancer and Fibrosis. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/22620
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Liu, Jennifer Sue. “Engineering Culture Platforms to Study Human Liver Cancer and Fibrosis.” 2018. Thesis, University of Illinois – Chicago. Accessed January 15, 2021.
http://hdl.handle.net/10027/22620.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Liu, Jennifer Sue. “Engineering Culture Platforms to Study Human Liver Cancer and Fibrosis.” 2018. Web. 15 Jan 2021.
Vancouver:
Liu JS. Engineering Culture Platforms to Study Human Liver Cancer and Fibrosis. [Internet] [Thesis]. University of Illinois – Chicago; 2018. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/10027/22620.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Liu JS. Engineering Culture Platforms to Study Human Liver Cancer and Fibrosis. [Thesis]. University of Illinois – Chicago; 2018. Available from: http://hdl.handle.net/10027/22620
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Illinois – Chicago
23.
Yu, Wan-Ni.
The Effect of Akt Isoforms in Tumorigenesis and Glucose Homeostasis in Vivo.
Degree: 2014, University of Illinois – Chicago
URL: http://hdl.handle.net/10027/11305
► Germ line Akt1-deficient mice are resistant to cancer development which is driven by hyper-activation of PI3K-Akt signaling in mouse model. However, it is not clear…
(more)
▼ Germ line Akt1-deficient mice are resistant to cancer development which is driven by hyper-activation of PI3K-Akt signaling in mouse model. However, it is not clear whether Akt1 is required for tumor maintenance, and whether systemic Akt1 deficiency can block tumor progression in the mouse. It is also not known whether Akt1 deficiency could hinder tumorigenesis which is not driven by hyper-activation of PI3K-Akt signaling. Here, we use Akt1f/fRosa26CREERT2 mice, in which Akt1 could be systemically deleted after tamoxifen administration. These mice were crossed with p53-/-mice which are tumor prone. Systemic whole body Akt1-deficient mice substantially increased survival of these mice. Thymic lymphoma cell lines isolated from the mice undergone cell death and cell cycle arrest following by Akt1 deletion. Xenograft tumors of these mice are inhibited after Akt1 deletion.
PI3K-Akt signaling is frequently activated in human cancer. Therefore, Akt is a popular target for cancer therapy. However, the long-term effect is not well known since most of tests were done in the xenograft model. Here we used Akt1f/f; Akt2-/-; Rosa26CREERT2 mice and Akt1f/f; Akt2-/-; Albumin-Cre mice to generate combined Akt1 and Akt2 deleted adult mice and liver-specific deleted mice in order to mimic drug therapy condition. Akt1f/f; Akt2-/-; Rosa26CREERT2 adult mice could not survive after tam administration and Akt1hep-/-Akt2-/- mice developed severe diabetes and
hepatocellular carcinoma (HCC). Thus, using Akt inhibitors that target both Akt1 and Akt2 need to be aware of the side effects.
Advisors/Committee Members: Hay, Nissim (advisor), Raychaudhuri, Pradip (committee member), Lau, Lester F. (committee member), Merrill, Bradley (committee member), Schmidt, Jennifer (committee member).
Subjects/Keywords: Akt; p53; Lymphoma; Diabetes; Hepatocellular Carcinoma
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APA (6th Edition):
Yu, W. (2014). The Effect of Akt Isoforms in Tumorigenesis and Glucose Homeostasis in Vivo. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/11305
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Yu, Wan-Ni. “The Effect of Akt Isoforms in Tumorigenesis and Glucose Homeostasis in Vivo.” 2014. Thesis, University of Illinois – Chicago. Accessed January 15, 2021.
http://hdl.handle.net/10027/11305.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Yu, Wan-Ni. “The Effect of Akt Isoforms in Tumorigenesis and Glucose Homeostasis in Vivo.” 2014. Web. 15 Jan 2021.
Vancouver:
Yu W. The Effect of Akt Isoforms in Tumorigenesis and Glucose Homeostasis in Vivo. [Internet] [Thesis]. University of Illinois – Chicago; 2014. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/10027/11305.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Yu W. The Effect of Akt Isoforms in Tumorigenesis and Glucose Homeostasis in Vivo. [Thesis]. University of Illinois – Chicago; 2014. Available from: http://hdl.handle.net/10027/11305
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Cambridge
24.
Frake, Rebecca Astrid.
Vinexin regulates autophagy through YAP/TAZ: implications for health and disease.
Degree: PhD, 2018, University of Cambridge
URL: https://www.repository.cam.ac.uk/handle/1810/273360
► Macroautophagy (hereafter referred to as autophagy) is a highly conserved cellular process that promotes cytoplasmic homeostasis via lysosomal degradation of proteins and organelles. Dysfunctional autophagy…
(more)
▼ Macroautophagy (hereafter referred to as autophagy) is a highly conserved cellular process that promotes cytoplasmic homeostasis via lysosomal degradation of proteins and organelles. Dysfunctional autophagy occurs in numerous human pathologies, including neurodegeneration and cancer. Vinexin (encoded by SORBS3) is a physiologically important adaptor protein for two main reasons: 1. SORSB3 mRNA expression increases in normal human brain ageing, 2. SORBS3 is a candidate tumour suppressor in hepatocellular carcinoma (HCC).
This dissertation builds on published data from an siRNA screen for autophagy regulations under basal conditions, which indicates vinexin knockdown upregulates autophagy. I replicate this finding in multiple cell lines, before characterising the impact of siSORBS3 treatment on autophagy; autophagosome biogenesis is increased, while flux through the autophagy pathway remains intact. Having excluded several possible mechanisms suggested by the literature, I focus on the transcriptional coactivators YAP and TAZ. The rationale here is: 1. YAP/TAZ activity is implicated in autophagy, 2. YAP/TAZ and vinexin are both linked to HCC.
My data show that YAP/TAZ transcriptional activity is upregulated upon vinexin depletion. Moreover, increased autophagy following siSORBS3 treatment requires YAP and TAZ. A key focus of this dissertation is the mechanism by which vinexin knockdown upregulates YAP/TAZ and hence, autophagy. This centres on altered actin cytoskeleton dynamics; an increase in F-actin structures appears to compete with YAP/TAZ for binding to angiomotins, established sequesterers of YAP/TAZ in the cytosol. In this way, siSORBS3 treatment facilitates YAP/TAZ nuclear localisation and consequent transcriptional activity. Angiomotin overexpression therefore ameliorates the increase in autophagy caused by vinexin depletion.
Published RNA sequencing data is used to confirm that SORBS3 mRNA expression increases in normal brain ageing, not only in the frontal cortex (as previously published), but also in the hippocampus. This sits alongside decreased expression of core autophagy genes in both tissues. Accordingly, vinexin could contribute to the decline in autophagic potential thought to occur in normal brain ageing.
With regards to SORBS3 as a candidate tumour suppressor in HCC, I show that stably re-expressing vinexin in a HCC cell line downregulates YAP/TAZ and hence, autophagy. These cells also show reduced clonogenicity. My data therefore support the hypothesis that SORBS3 is a tumour suppressor in HCC; YAP and TAZ are well-known to increase proliferation and resistance to apoptosis, while autophagy can enable tumour cells to survive stressors such as nutrient starvation.
The conclusions of this dissertation are that vinexin depletion upregulates autophagy in a YAP/TAZ-dependent manner and that this has physiologically important implications, especially with regards to HCC.
Subjects/Keywords: Autophagy; YAP/TAZ; Brain ageing; Hepatocellular carcinoma
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Chicago ·
MLA ·
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CSE |
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APA (6th Edition):
Frake, R. A. (2018). Vinexin regulates autophagy through YAP/TAZ: implications for health and disease. (Doctoral Dissertation). University of Cambridge. Retrieved from https://www.repository.cam.ac.uk/handle/1810/273360
Chicago Manual of Style (16th Edition):
Frake, Rebecca Astrid. “Vinexin regulates autophagy through YAP/TAZ: implications for health and disease.” 2018. Doctoral Dissertation, University of Cambridge. Accessed January 15, 2021.
https://www.repository.cam.ac.uk/handle/1810/273360.
MLA Handbook (7th Edition):
Frake, Rebecca Astrid. “Vinexin regulates autophagy through YAP/TAZ: implications for health and disease.” 2018. Web. 15 Jan 2021.
Vancouver:
Frake RA. Vinexin regulates autophagy through YAP/TAZ: implications for health and disease. [Internet] [Doctoral dissertation]. University of Cambridge; 2018. [cited 2021 Jan 15].
Available from: https://www.repository.cam.ac.uk/handle/1810/273360.
Council of Science Editors:
Frake RA. Vinexin regulates autophagy through YAP/TAZ: implications for health and disease. [Doctoral Dissertation]. University of Cambridge; 2018. Available from: https://www.repository.cam.ac.uk/handle/1810/273360
University of Sydney
25.
Henderson, James Matthew.
Dipeptidyl peptidases in experimental hepatocellular carcinoma
.
Degree: 2018, University of Sydney
URL: http://hdl.handle.net/2123/20017
► The urgent unmet need to develop hepatocellular carcinoma (HCC) therapies is addressed here by characterising a novel mouse model of HCC in the context of…
(more)
▼ The urgent unmet need to develop hepatocellular carcinoma (HCC) therapies is addressed here by characterising a novel mouse model of HCC in the context of ongoing liver damage and overnutrition. Male C57Bl/6J mice were treated with Diethylnitrosamine (DEN) and thioacetamide (TAA), and some were provided with an atherogenic high fat diet (HFD). Inflammation, steatosis, fibrosis, 87 genes, liver lesions and intratumoural leukocyte subsets were quantified up to 24 weeks of age. Mice treated on the DEN/TAA/HFD regime for 24-36 weeks were then treated with one of several compounds, ARI-4175, ARI-3996, ARI-6000 or vehicle controls. These compounds target the DPP4 enzyme family. The DPP4 enzyme family includes four atypical serine proteases: DPP4, Fibroblast activation protein (FAP), DPP8, and DPP9. These proteins mediate a diverse range of biological processes by releasing the N-terminal dipeptide of substrates that have a proline or alanine at the penultimate position. Livers were assessed for tumour and histopathological burdens. The expression and activity of DPP4, FAP, DPP8 and DPP9 were investigated to assess their biomarker utility and roles in liver carcinogenesis. Adding HFD to DEN/TAA increased fibrosis, steatosis and inflammation, and the incidence of both HCC and non-HCC dysplastic lesions. All lesions contained α-SMA positive fibroblasts. Macrophage marker F4/80 was not significantly different between treatment groups, but the macrophage-associated genes Arg-1 and Cd47 were differentially expressed. Fibrosis, cancer and cell death associated genes were upregulated in DEN/TAA/HFD livers. Fewer Kupffer cells and plasmacytoid dendritic cells were in tumours compared to control liver. FAP+ fibroblastic populations can be identified with a novel reagent 4613b FAP+ fibroblastic populations were acutely depleted from livers with FAP specific pro-drug ARI-3996. Depletion of FAP+ fibroblast populations with FAP-specific prodrugs ARI-3996 and ARI-6000 as a result of long term administration did not decrease liver fibrosis. ARI-6000 treatment showed a nonsignificant trend towards less inflammation and fibrosis. ARI-4175 administration increased liver fibrosis and decreased tumour burden in the liver. Liver DPP4, DPP8, and DPP9 enzymatic activity expression decreased with DEN/TAA/HFD treatment and DPP9 was enriched in tumours and dysplastic lesions. In conclusion, combining hepatotoxins with an atherogenic diet produced more intrahepatic tumours, dysplastic lesions and fibrosis compared to hepatotoxins alone. This new HCC model provides a relatively rapid means of examining primary HCC and potential therapies in the Preface xii context of multiple hepatotoxins including those derived from overnutrition. The DPP-family have shown potential as both HCC markers and potential therapeutic targets due to their tissue specific expression in the case of FAP and roles in liver carcinogenesis in the case of DPP4 and DPP9.
Subjects/Keywords: hepatocellular carcinoma;
dipeptidyl peptidase;
fibrosis;
liver disease
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APA ·
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Manager
APA (6th Edition):
Henderson, J. M. (2018). Dipeptidyl peptidases in experimental hepatocellular carcinoma
. (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/20017
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Henderson, James Matthew. “Dipeptidyl peptidases in experimental hepatocellular carcinoma
.” 2018. Thesis, University of Sydney. Accessed January 15, 2021.
http://hdl.handle.net/2123/20017.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Henderson, James Matthew. “Dipeptidyl peptidases in experimental hepatocellular carcinoma
.” 2018. Web. 15 Jan 2021.
Vancouver:
Henderson JM. Dipeptidyl peptidases in experimental hepatocellular carcinoma
. [Internet] [Thesis]. University of Sydney; 2018. [cited 2021 Jan 15].
Available from: http://hdl.handle.net/2123/20017.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Henderson JM. Dipeptidyl peptidases in experimental hepatocellular carcinoma
. [Thesis]. University of Sydney; 2018. Available from: http://hdl.handle.net/2123/20017
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Texas State University – San Marcos
26.
Kendrick, Katie.
Specificity of TLS11a Aptamer Towards Hepatocellular Carcinoma as a Means of Detection and Targeted Drug Delivery.
Degree: MS, Biology, 2017, Texas State University – San Marcos
URL: https://digital.library.txstate.edu/handle/10877/8503
► Liver cancer is the sixth most commonly occurring cancer and second leading cause of cancer-related deaths worldwide with an estimated 75% of all liver malignancy…
(more)
▼ Liver cancer is the sixth most commonly occurring cancer and second leading cause of cancer-related deaths worldwide with an estimated 75% of all liver malignancy cases being
hepatocellular carcinoma (HCC), the most common and most lethal form of liver cancer [1]. While the incidence rates for many cancers have slowly declined over the years, HCC incidence and death rates have been continuously rising due to late stage diagnoses and poor prognoses. This suggests that there is a lack of existing biomarkers and diagnostic equipment sensitive enough to identify this disease in early stages [2]. More sophisticated methods are needed to detect HCC in early stages and specifically target this disease. Recently, an HCC-specific aptamer was created and shown to effectively discriminate mouse HCC from normal liver in vitro [3]. In this thesis, the specificity of TLS11a towards HCC is addressed regarding human tissue. Specifically, immunohistochemical (IHC) staining of human tissue microarrays (TMA) was utilized to address what tissue types TLS11a can bind, if it can differentiate between normal liver and HCC tissue and if binding is correlated with tumor stage. Formalin fixed paraffin embedded (FFPE) TMAs were stained with fluorophore labeled TLS11a and imaged using epifluorescence microscopy. However, negative controls demonstrated high levels of autofluorescence (AF) which made aptamer-based fluorescence indistinguishable from background. Attempts to induce aptamer refolding, antigen retrieval and using alternate fluorophores were unsuccessful at increasing the signal to noise ratio. Colorimetric FFPE staining was also pursued; unfortunately, there was no indication of aptamer binding above background using these conditions either. Ultimately, this lack of specific binding between TLS11a and HCC tissue was attributed to disruption or loss of cell surface binding sites and epitopes during the formalin fixation and paraffin embedding process. Using immunofluorescence staining of fresh frozen (FF) TMAs, TLS11a was found to effectively distinguish between normal liver and HCC tissue (p<0.001) in human tissue with the mean integrated intensity increasing more than 10-fold on average in HCC tissues. TLS11a was also found to bind to other malignant tissue types including breast, lung, kidney and colon, among others, with little to no binding to normal tissues (p<0.0001). These results signify that TLS11a has the potential to be used for targeting multiple malignancies. Additional studies are needed to confirm these findings; however, these studies suggest TLS11a has the potential to be a tumor-specific marker, particularly with respect to HCC, and would be an excellent candidate for use in human studies for new HCC-targeted diagnostic and therapeutic applications.
Advisors/Committee Members: Weigum, Shannon (advisor), Koke, Joe (committee member), Garcia, Dana (committee member).
Subjects/Keywords: TLS11a; Hepatocellular carcinoma; Liver cancer; Aptamer; HCC
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APA (6th Edition):
Kendrick, K. (2017). Specificity of TLS11a Aptamer Towards Hepatocellular Carcinoma as a Means of Detection and Targeted Drug Delivery. (Masters Thesis). Texas State University – San Marcos. Retrieved from https://digital.library.txstate.edu/handle/10877/8503
Chicago Manual of Style (16th Edition):
Kendrick, Katie. “Specificity of TLS11a Aptamer Towards Hepatocellular Carcinoma as a Means of Detection and Targeted Drug Delivery.” 2017. Masters Thesis, Texas State University – San Marcos. Accessed January 15, 2021.
https://digital.library.txstate.edu/handle/10877/8503.
MLA Handbook (7th Edition):
Kendrick, Katie. “Specificity of TLS11a Aptamer Towards Hepatocellular Carcinoma as a Means of Detection and Targeted Drug Delivery.” 2017. Web. 15 Jan 2021.
Vancouver:
Kendrick K. Specificity of TLS11a Aptamer Towards Hepatocellular Carcinoma as a Means of Detection and Targeted Drug Delivery. [Internet] [Masters thesis]. Texas State University – San Marcos; 2017. [cited 2021 Jan 15].
Available from: https://digital.library.txstate.edu/handle/10877/8503.
Council of Science Editors:
Kendrick K. Specificity of TLS11a Aptamer Towards Hepatocellular Carcinoma as a Means of Detection and Targeted Drug Delivery. [Masters Thesis]. Texas State University – San Marcos; 2017. Available from: https://digital.library.txstate.edu/handle/10877/8503
27.
Banova-Chakarova, Sonya / Банова-Чакърова, Соня.
Risk Factors and Precanceroses for Hepatocellular Carcinoma /// Рискови фактори и преканцерози за хепатоцелуларен карцином.
Degree: 2018, Medical University of Varna
URL: http://repository.mu-varna.bg/handle/nls/409
► [EN] This dissertation aims to identify and analyse the risk factors and precancerous status of hepatocellular carcinoma (HCC) and its early detection by monitoring the…
(more)
▼ [EN] This dissertation aims to identify and analyse the risk factors and precancerous status of hepatocellular carcinoma (HCC) and its early detection by monitoring the predisposed groups of patients. Hepatocellular carcinoma develops most often in men with chronic viral infection (mainly HBV infection), in stage of liver cirrhosis. In HBV-HDV and HBV-HCV co-infected patient, malignant disease occurs at an earlier age, has faster progression and worse survival. The role of nutrition, harmful habits (alcohol and smoking) and lifestyle in the development of HCC are being studied. Factors rated as risky for HCC development include alcohol consumption, smoking, frequent intake of fruit and red meat, lack of regular coffee intake and overweight. For protective factor we accept the frequent consumption of vegetables. Antiviral therapy has a protective effect on disease progression in patients with chronic viral infection. These patients live longer. The study of serum glycopican-3 level and its tissue expression in biopsy showed it to be a reliable histological marker for HCC. The APRI index can be used as a non-invasive diagnostic and prognostic marker as well as a predictor of HCC related mortality. Established and applied in clinical practice algorithm of behavior in liver lesions in patients with elevated risk for HCC. /////////// /////////// [BG] Дисертацията има за цел да се определят и анализират рисковите фактори и преканцерозните състояние за развитие на хепатоцелуларния карцином (ХЦК) и възможностите за ранното му установяване чрез проследяване на предразположените групи пациенти. Хепатоцелуларният карцином се развива най-често при мъже с вирусна инфекция (основно HBV инфекция), в стадий на чернодробна цироза. При пациентите с HBV-HDV и HBV-HCV ко-инфекции малигненото заболяване възниква в по-ранна възраст, има по-бърза прогресия и по-лоша преживяемост. Изследва се ролята на храненето, вредните навици (прием на алкохол и тютюнопушене) и начина на живот в развитието на ХЦК. Факторите, оценени като рискови за развитието на му са: консумация на алкохол, тютюнопушенето, честата употреба на плодове и червено месо, липсата на редовен прием на кафе и наднорменото тегло. За протективни си приемат честата консумация на зеленчуци. Антивирусната терапия има протективен ефект върху развитието на заболяването при пациентите с хронична вирусна инфекция. Тези пациентите живеят по-дълго. Изследването на серумното равнище на глипикан-3 и тъканната му експресия в биопсичен материал показа, че той е надежден хистологичен маркер за ХЦК. APRI индексът може да се използва като неинвазивен диагностичен и прогностичен маркер, както и за предиктор за смъртност от ХЦК. Създаден и приложен в клиничната практика алгоритъм на поведение при чернодробни огнищни лезии при пациенти с повишен риск за ХЦК.
Subjects/Keywords: hepatocellular carcinoma (HCC); hepatic carcinoma; mixed hepatocellular and cholangiocellular carcinoma; nutrition; lifestyle hepatic carcinoma; Гастроентерология / Gastroenterology
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APA ·
Chicago ·
MLA ·
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Export
to Zotero / EndNote / Reference
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APA (6th Edition):
Banova-Chakarova, Sonya / Банова-Чакърова, . (2018). Risk Factors and Precanceroses for Hepatocellular Carcinoma /// Рискови фактори и преканцерози за хепатоцелуларен карцином. (Thesis). Medical University of Varna. Retrieved from http://repository.mu-varna.bg/handle/nls/409
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Banova-Chakarova, Sonya / Банова-Чакърова, Соня. “Risk Factors and Precanceroses for Hepatocellular Carcinoma /// Рискови фактори и преканцерози за хепатоцелуларен карцином.” 2018. Thesis, Medical University of Varna. Accessed January 15, 2021.
http://repository.mu-varna.bg/handle/nls/409.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Banova-Chakarova, Sonya / Банова-Чакърова, Соня. “Risk Factors and Precanceroses for Hepatocellular Carcinoma /// Рискови фактори и преканцерози за хепатоцелуларен карцином.” 2018. Web. 15 Jan 2021.
Vancouver:
Banova-Chakarova, Sonya / Банова-Чакърова . Risk Factors and Precanceroses for Hepatocellular Carcinoma /// Рискови фактори и преканцерози за хепатоцелуларен карцином. [Internet] [Thesis]. Medical University of Varna; 2018. [cited 2021 Jan 15].
Available from: http://repository.mu-varna.bg/handle/nls/409.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Banova-Chakarova, Sonya / Банова-Чакърова . Risk Factors and Precanceroses for Hepatocellular Carcinoma /// Рискови фактори и преканцерози за хепатоцелуларен карцином. [Thesis]. Medical University of Varna; 2018. Available from: http://repository.mu-varna.bg/handle/nls/409
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
28.
Kikuchi, Luciana Oba Onishi.
Análise da sobrevida de pacientes com carcinoma hepatocelular pequeno.
Degree: Mestrado, Gastroenterologia Clínica, 2007, University of São Paulo
URL: http://www.teses.usp.br/teses/disponiveis/5/5147/tde-13022008-095440/
;
► Introdução: O carcinoma hepatocelular (CHC) é o câncer primário de fígado mais comum. A cirrose hepática é o principal fator de risco para esse tumor.…
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▼ Introdução: O carcinoma hepatocelular (CHC) é o câncer primário de fígado mais comum. A cirrose hepática é o principal fator de risco para esse tumor. O rastreamento para o CHC em pacientes com cirrose tem sido recomendado há anos. Acredita-se que a detecção e o tratamento precoce do CHC melhorem a sobrevida dos pacientes. O objetivo deste estudo foi analisar a sobrevida dos pacientes cirróticos com CHC pequeno e identificar fatores preditivos de sobrevida no Brasil. Casuística e Métodos: Entre janeiro de 1998 e dezembro de 2003, 74 pacientes cirróticos com CHC foram avaliados. Eles preenchiam os seguintes critérios: CHC com até três nódulos e no máximo 30 mm de diâmetro cada. Os fatores preditores de sobrevida foram identificados através do método de Kaplan-Meier e o modelo de Cox. Resultados: A média de idade foi de 58 anos (32-77); 71% dos pacientes eram do sexo masculino; 64% tinham hepatite C; 60% eram Child-Pugh A, o valor mediano da pontuação de MELD foi de 11; 79% tinham hipertensão portal. No momento do diagnóstico, 71% tinham uma única lesão; o tamanho do principal tumor era menor que 20 mm em 47%; o valor médio de AFP foi de 131 ng/ml. Três pacientes tinham trombose de veia porta, sugestiva de invasão vascular. Cinqüenta pacientes (67,5%) foram incluídos na lista de transplante hepático, que foi realizado só em quatro pacientes. A ressecção cirúrgica do tumor foi possível em quatro pacientes. Quarenta e oito (64,8%) pacientes receberam tratamento ablativo percutâneo (ablação por radiofreqüência ou injeção percutânea de etanol). Nove pacientes não receberam nenhum tratamento específico para o tumor. A taxa de sobrevida geral foi de 80%; 62%; 41% e 17% em 12, 24, 36 e sessenta meses, respectivamente. O tempo médio de seguimento após o diagnóstico do CHC foi de 23 meses (mediana de 22 meses, variando de um a 86 meses) para todo o grupo. Durante o seguimento, ocorreram 39 óbitos ocorreram relacionados com insuficiência hepática ou progressão do CHC. A análise univariada dos 74 pacientes mostrou que escore MELD maior que 11 (p = 0,016), classificação de Child-Pugh B e C (p = 0,007), AFP > 100 ng/ml (p = 0,006), mais de uma lesão (p = 0,041), diâmetro do tumor > 20 mm (p = 0,009) e presença de invasão vascular (p < 0,0001) foram preditores independentes de sobrevida. A análise de regressão de Cox identificou invasão vascular (RR = 14,60 - IC 95% = 3,3 - 64,56 - p < 0,001) e tamanho do tumor > 20mm (RR = 2,14 - IC 95% = 1,07 - 4,2 - p = 0,030) como preditores independentes de pior sobrevida. O tratamento do CHC esteve relacionado com melhor sobrevida. Conclusão: A identificação de CHC pequeno com até 20 mm de diâmetro está relacionada com melhores taxas de sobrevida. Por outro lado, a presença de invasão vascular, apesar do tamanho pequeno das lesões, é um fator associado a péssimo prognóstico.
Introduction: Hepatocellular carcinoma (HCC) is the most common primary liver cancer. Liver cirrhosis is the major risk factor for this tumor. Screening for HCC in patients with cirrhosis has been recommended, in the…
Advisors/Committee Members: Carrilho, Flair José.
Subjects/Keywords: Carcinoma hepatocellular; Carcinoma hepatocelular; Diagnóstico precoce; Early diagnosis; Sobrevida; Survivorship
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APA (6th Edition):
Kikuchi, L. O. O. (2007). Análise da sobrevida de pacientes com carcinoma hepatocelular pequeno. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5147/tde-13022008-095440/ ;
Chicago Manual of Style (16th Edition):
Kikuchi, Luciana Oba Onishi. “Análise da sobrevida de pacientes com carcinoma hepatocelular pequeno.” 2007. Masters Thesis, University of São Paulo. Accessed January 15, 2021.
http://www.teses.usp.br/teses/disponiveis/5/5147/tde-13022008-095440/ ;.
MLA Handbook (7th Edition):
Kikuchi, Luciana Oba Onishi. “Análise da sobrevida de pacientes com carcinoma hepatocelular pequeno.” 2007. Web. 15 Jan 2021.
Vancouver:
Kikuchi LOO. Análise da sobrevida de pacientes com carcinoma hepatocelular pequeno. [Internet] [Masters thesis]. University of São Paulo; 2007. [cited 2021 Jan 15].
Available from: http://www.teses.usp.br/teses/disponiveis/5/5147/tde-13022008-095440/ ;.
Council of Science Editors:
Kikuchi LOO. Análise da sobrevida de pacientes com carcinoma hepatocelular pequeno. [Masters Thesis]. University of São Paulo; 2007. Available from: http://www.teses.usp.br/teses/disponiveis/5/5147/tde-13022008-095440/ ;
Universidade Estadual de Campinas
29.
Segatelli, Vanderlei, 1971-.
Avaliação da expressão de biomarcadores relacionados à hepatocarcinogênese em fígados cirróticos e não cirróticos, com estudo imuno-histoquímico: Evaluation of the expression of biomarkers related to hepatocarcinogenesis in cirrhotic and non-cirrhotis livers, with immunohistochemical study.
Degree: 2017, Universidade Estadual de Campinas
URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/330530
► Abstract: Introduction: Hepatocellular carcinoma (HCC) is a complex and heterogenous malignany, commonly associated with chronic liver disease and the development of cirrhosis. Hepatocarcinogenesis is multifactorial…
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▼ Abstract: Introduction:
Hepatocellular carcinoma (HCC) is a complex and heterogenous malignany, commonly associated with chronic liver disease and the development of cirrhosis. Hepatocarcinogenesis is multifactorial and occurs in multiple stages, involving genetic, epigenetic and environmental factors. Research into the differences in patterns of biomarker immunoexpression associated with hepatocarcinogenesis among
hepatocellular carcinomas that originated in cirrhotic livers and non-cirrhotic livers is still scarce in the world literature. Aims: Evaluation of biological markers related to hepatocarcinogenesis in
hepatocellular carcinomas originated in cirrhotic and non-cirrhotic livers using immunohistochemical study. Materials and methods: Paraffin blocks containing samples of 25 patients with HCC in cirrhotic livers from liver transplantations (group A) and 25 patients with
hepatocellular carcinoma in noncirrhotic livers were selected. Patient diagnosis was made on products (resection specimens) of partial hepatectomy or nodulectomy (group B), irrespective of etiologic factor, gender, color, age or ethnic group. The relationship between clinical variables and immunohistochemical markers (CK7, CK19, p53, p16, C-MET, beta-catenin, HSP-70, glutamine synthetase, glypican-3 and C-MYC) was evaluated by the chi-square, Fisher¿s or Mann-Whitney tests, considering p<0.05 statistically significant. Results: Group B showed greater variation in neoplastic size, greater association with metabolic syndrome factors and greater glutamine-synthetase immunoexpression in relation to group A. Conclusion: The increased immunoexpression of glutamine synthetase in group B may be associated with changes vascular and / or metabolic. Glutamine synthetase may be a useful biomarker in CHC in the background of metabolic syndrome
Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS (CRUESP), Escanhoela, Cecília Amélia Fazzio, 1958- (advisor), Universidade Estadual de Campinas. Faculdade de Ciências Médicas (institution), Programa de Pós-Graduação em Ciências Médicas (nameofprogram), Stucchi, Raquel Silveira Bello (committee member), Passador-Santos, Fabricio (committee member), Silva, Rita de Cassia Martins Alves da (committee member), Andrade, Liliana Aparecida Lucci de Angelo (committee member).
Subjects/Keywords: Carcinoma hepatocelular; Imuno-histoquímica; Cirrose hepática; Hepatocellular carcinoma; Immunohistochemistry; Liver cirrhosis
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APA ·
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APA (6th Edition):
Segatelli, Vanderlei, 1. (2017). Avaliação da expressão de biomarcadores relacionados à hepatocarcinogênese em fígados cirróticos e não cirróticos, com estudo imuno-histoquímico: Evaluation of the expression of biomarkers related to hepatocarcinogenesis in cirrhotic and non-cirrhotis livers, with immunohistochemical study. (Thesis). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/330530
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Segatelli, Vanderlei, 1971-. “Avaliação da expressão de biomarcadores relacionados à hepatocarcinogênese em fígados cirróticos e não cirróticos, com estudo imuno-histoquímico: Evaluation of the expression of biomarkers related to hepatocarcinogenesis in cirrhotic and non-cirrhotis livers, with immunohistochemical study.” 2017. Thesis, Universidade Estadual de Campinas. Accessed January 15, 2021.
http://repositorio.unicamp.br/jspui/handle/REPOSIP/330530.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Segatelli, Vanderlei, 1971-. “Avaliação da expressão de biomarcadores relacionados à hepatocarcinogênese em fígados cirróticos e não cirróticos, com estudo imuno-histoquímico: Evaluation of the expression of biomarkers related to hepatocarcinogenesis in cirrhotic and non-cirrhotis livers, with immunohistochemical study.” 2017. Web. 15 Jan 2021.
Vancouver:
Segatelli, Vanderlei 1. Avaliação da expressão de biomarcadores relacionados à hepatocarcinogênese em fígados cirróticos e não cirróticos, com estudo imuno-histoquímico: Evaluation of the expression of biomarkers related to hepatocarcinogenesis in cirrhotic and non-cirrhotis livers, with immunohistochemical study. [Internet] [Thesis]. Universidade Estadual de Campinas; 2017. [cited 2021 Jan 15].
Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/330530.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Segatelli, Vanderlei 1. Avaliação da expressão de biomarcadores relacionados à hepatocarcinogênese em fígados cirróticos e não cirróticos, com estudo imuno-histoquímico: Evaluation of the expression of biomarkers related to hepatocarcinogenesis in cirrhotic and non-cirrhotis livers, with immunohistochemical study. [Thesis]. Universidade Estadual de Campinas; 2017. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/330530
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
University of Florida
30.
Fitian, Asem I.
Non-Targeted Metabolomics and Targeted Proteomics toward the Discovery of Novel Hepatocellular Carcinoma Biomarkers.
Degree: MS, Medical Sciences - Medicine, 2013, University of Florida
URL: https://ufdc.ufl.edu/UFE0045980
► Hepatocellular carcinoma (HCC) is the world’s third most lethal cancer and has a five-year survival rate of 10%. Early detection of HCC improves patient outcome…
(more)
▼ Hepatocellular carcinoma (HCC) is the world’s third most lethal cancer and has a five-year survival rate of 10%. Early detection of HCC improves patient outcome but is exacerbated by the poor diagnostic accuracy of the principal HCC biomarker alpha-fetoprotein (AFP). Resource-poor areas of sub-Saharan Africa and East Asia suffer the brunt of HCC’s mortality rate, and coupled with HCC’s emergence as the fastest rising cause of cancer-related death in the United States, there has arisen an urgent and global need for an inexpensive, reproducible, and accurate HCC rapid diagnostic test that streamlines early detection and improves the curative outlook for HCC patients. Using liver cancer and cirrhosis patient serum, non-targeted liquid chromatography/mass spectrometry metabolomics was employed toward the discovery of HCC diagnostic biomarkers. Serendipitously during the metabolomics endeavor, potential biomarkers of cirrhosis were also identified. In a targeted proteomics investigation, ELISA and multivariate statistics were used to characterize the utility of immune factor soluble CD25 in diagnosing the presence and early stages of HCC. ( en )
Advisors/Committee Members: Cabrera, Roniel (committee chair), Cook, Robert L (committee member), Nelson, David R (committee member), Kraft, John (committee member).
Subjects/Keywords: Amino acids; Bile; Bile acids; Biological markers; Cirrhosis; Fatty acids; Hepatocellular carcinoma; Metabolism; Metabolites; Metabolomics; biomarker – biomarkers – carcinoma – hcc – hepatocellular – metabolomics
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APA ·
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APA (6th Edition):
Fitian, A. I. (2013). Non-Targeted Metabolomics and Targeted Proteomics toward the Discovery of Novel Hepatocellular Carcinoma Biomarkers. (Masters Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0045980
Chicago Manual of Style (16th Edition):
Fitian, Asem I. “Non-Targeted Metabolomics and Targeted Proteomics toward the Discovery of Novel Hepatocellular Carcinoma Biomarkers.” 2013. Masters Thesis, University of Florida. Accessed January 15, 2021.
https://ufdc.ufl.edu/UFE0045980.
MLA Handbook (7th Edition):
Fitian, Asem I. “Non-Targeted Metabolomics and Targeted Proteomics toward the Discovery of Novel Hepatocellular Carcinoma Biomarkers.” 2013. Web. 15 Jan 2021.
Vancouver:
Fitian AI. Non-Targeted Metabolomics and Targeted Proteomics toward the Discovery of Novel Hepatocellular Carcinoma Biomarkers. [Internet] [Masters thesis]. University of Florida; 2013. [cited 2021 Jan 15].
Available from: https://ufdc.ufl.edu/UFE0045980.
Council of Science Editors:
Fitian AI. Non-Targeted Metabolomics and Targeted Proteomics toward the Discovery of Novel Hepatocellular Carcinoma Biomarkers. [Masters Thesis]. University of Florida; 2013. Available from: https://ufdc.ufl.edu/UFE0045980
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Open Access Theses and Dissertations