subject:(liver cancer)

Penn State University

1. Balandaram, Gayathri. The role of peroxisome proliferator-activated receptor β/δ in viral protein-induced liver pathogenesis.

Degree: 2015, Penn State University

URL: https://submit-etda.libraries.psu.edu/catalog/27232

► PPARβ/δ has an established role in attenuating preneoplastic conditions in the liver such as inflammation, steatosis, proliferation and oxidative stress pointing to a chemopreventive role… (more)

▼ PPARβ/δ has an established role in attenuating preneoplastic conditions in the liver such as inflammation, steatosis, proliferation and oxidative stress pointing to a chemopreventive role for this nuclear receptor in the liver. However, not much is known about its part in orchestrating the progression of hepatocellular carcinoma. The present study examined the potential of this nuclear receptor in delaying the progression of chronic hepatocellular injury-induced liver cancer. In hepatitis B virus (HBV) transgenic mice, which develop progressive inflammation and cellular injury at the early stages (2-3 months of age), followed by hyperplasia, neoplasia and eventually hepatocellular carcinoma at later stages (12-18 months of age), long-term ligand activation (8 months) with PPARβ/δ ligand (GW0742), displayed a significant attenuation in tumor multiplicity and the average number of liver foci, which was not observed in HBV mice not treated with GW0742. Further, this attenuation in tumorigenesis was accompanied by a reduction in hepatic steatosis and markers of cellular proliferation CYCLIN D1 and c-MYC as well as an increase in a marker of apoptosis, cleaved PARP. Ligand activation of PPARβ/δ attenuated mRNA expression of hepatic inflammatory cytokine Tnfa and serum ALT at the early stages of disease pathogenesis in these mice. Ligand activation of PPARβ/δ attenuated LPS-induced mRNA expression of Tnfa in primary Kupffer cell cultures from wild-type but not in Kupffer cells from Pparβ/δ-null mice. LPS-induced mRNA expression of Tnfa was also found to be attenuated in Pparβ/δ-DBM (DNA binding mutant form of PPARβ/δ) Kupffer cells treated with GW0742, indicating that the anti-inflammatory effects of ligand activated PPARβ/δ occurs independent of the nuclear receptor binding to its PPREs. These effects were not observed in hepatocytes. Further, co-immunoprecipitation studies confirmed interaction of PPARβ/δ with p65 subunit of pro-inflammatory transcription factor NF-κB in LPS and GW0742 activated KC13-2 Kupffer cells. In the hepatitis C virus (HCV) transgenic mice expressing the core protein of the virus, preliminary histopathological analyses did not yield a conclusive role for PPARβ/δ in modulating hepatic inflammation and steatosis. However, PPARβ/δ was found to significantly increase the life span of HCV wild-type mice compared to that of HCV Pparβ/δ-null mice, independent of ligand activation of PPARβ/δ. Protein microarray displayed a consistent increase in Cofilin 1 and a decrease in SODD, SOCS2 and p27Kip1 expression levels, as well as a decrease in phosphorylation of PKCγ in livers of 18-month-old HCV Pparβ/δ-null mice compared to that of HCV wild-type mice. Combined, the present study confirms a hepatoprotective role for PPARβ/δ in mouse models of chronic hepatocellular injury-induced liver cancer and its potential as a possible therapeutic approach to treat hepatocarcinogenesis is promising and warrants further investigation. Advisors/Committee Members: Jeffrey Maurice Peters, Dissertation Advisor/Co-Advisor, Gary H Perdew, Committee Member, Andrew David Patterson, Committee Member, Connie Jo Rogers, Committee Member.

Subjects/Keywords: PPARβ/δ; liver; liver cancer

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

APA (6^th Edition):

Balandaram, G. (2015). The role of peroxisome proliferator-activated receptor β/δ in viral protein-induced liver pathogenesis. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/27232

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

Chicago Manual of Style (16^th Edition):

Balandaram, Gayathri. “The role of peroxisome proliferator-activated receptor β/δ in viral protein-induced liver pathogenesis.” 2015. Thesis, Penn State University. Accessed January 15, 2021. https://submit-etda.libraries.psu.edu/catalog/27232.

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

MLA Handbook (7^th Edition):

Balandaram, Gayathri. “The role of peroxisome proliferator-activated receptor β/δ in viral protein-induced liver pathogenesis.” 2015. Web. 15 Jan 2021.

Vancouver:

Balandaram G. The role of peroxisome proliferator-activated receptor β/δ in viral protein-induced liver pathogenesis. [Internet] [Thesis]. Penn State University; 2015. [cited 2021 Jan 15]. Available from: https://submit-etda.libraries.psu.edu/catalog/27232.

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

Council of Science Editors:

Balandaram G. The role of peroxisome proliferator-activated receptor β/δ in viral protein-induced liver pathogenesis. [Thesis]. Penn State University; 2015. Available from: https://submit-etda.libraries.psu.edu/catalog/27232

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

University of Adelaide

2. Tiong, Leong Ung. Improving the safety and efficacy of bimodal electric tissue ablation.

Degree: 2012, University of Adelaide

URL: http://hdl.handle.net/2440/74060

► Introduction: Bimodal electric tissue ablation (BETA) is a new method of ablation, which combines the process of electrolysis with radiofrequency ablation (RFA) to increase the… (more)

▼ Introduction: Bimodal electric tissue ablation (BETA) is a new method of ablation, which combines the process of electrolysis with radiofrequency ablation (RFA) to increase the size of tissue ablations. The cathode of the electrolytic circuit is connected to the radiofrequency (RF) electrode to increase the surrounding tissue hydration. This allows the RFA process to continue for a longer period of time and therefore produce larger ablations. Previous research has shown that BETA could produce larger ablations compared to standard RFA and that it did not produce any significant short or long-term complications. The studies described here aim to increase the knowledge on how BETA works to facilitate its translation into clinical practice to treat liver tumours. Materials & Methods The first study tested whether BETA really acts by increasing the hydration of tissues around the RF electrode. This was achieved by reversing the polarity of the electrolytic circuit, which theoretically would produce smaller ablations compared to standard RFA. The second study assessed where would be the best location (skin, parietal peritoneum or liver) for the anode of the electrolytic circuit during a BETA process. The third experiment determined whether the principle of BETA could be incorporated into the Cool-Tip RF system, which uses internally-cooled electrodes (ICEs). Results The duration of ablation when the polarity of the electrolytic circuit was reversed (called reversed polarity bimodal electric ablation, or RP-BEA) were significantly shorter compared to standard RFA and BETA (48s vs. 148s and 84s respectively, p=0.004). Consequently the size of ablations in RP-BEA was significantly smaller compared to RFA and BETA (9.1mm vs. 13.4mm and 11.6mm, p=0.001). The second experiment showed that the size of ablations were significantly larger when the anode of the electrolytic circuit was placed on the peritoneum or the liver, compared to when it was placed on the skin (19.7mm and 17.9mm vs. 12.4mm, p<0.001). Lastly, the third experiment showed that the principle of BETA could be incorporated into the Cool-Tip RF system to produce significantly larger ablations compared to standard RFA alone (23.1mm vs. 20.1mm, p<0.001). Discussion The results from this study confirmed the theory that BETA increases ablation size due to the effects of increased tissue hydration around the RF electrode. The increased hydration delays tissue desiccation during an ablation, thus allowing the process to continue for longer periods of time, therefore producing larger ablations. The efficacy of BETA depends on good electrical conductivity between the cathode and the anode of the DC circuit. Results from the second study showed that BETA works best when the anode of the electrolytic circuit was placed deep to the skin as the stratum corneum consisted of a layer of anucleated cells which have high electrical resistivity. Lastly, BETA could be incorporated into the Cool-Tip RF system (Covidien, ValleyLab), which is one of the popular RFA generators in… Advisors/Committee Members: Maddern, Guy John (advisor), Hewett, Peter J. (advisor), School of Medicine (school).

Subjects/Keywords: radio frequency ablation; liver cancer; liver metastases

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APA (6^th Edition):

Tiong, L. U. (2012). Improving the safety and efficacy of bimodal electric tissue ablation. (Thesis). University of Adelaide. Retrieved from http://hdl.handle.net/2440/74060

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

Chicago Manual of Style (16^th Edition):

Tiong, Leong Ung. “Improving the safety and efficacy of bimodal electric tissue ablation.” 2012. Thesis, University of Adelaide. Accessed January 15, 2021. http://hdl.handle.net/2440/74060.

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

MLA Handbook (7^th Edition):

Tiong, Leong Ung. “Improving the safety and efficacy of bimodal electric tissue ablation.” 2012. Web. 15 Jan 2021.

Vancouver:

Tiong LU. Improving the safety and efficacy of bimodal electric tissue ablation. [Internet] [Thesis]. University of Adelaide; 2012. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/2440/74060.

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

Council of Science Editors:

Tiong LU. Improving the safety and efficacy of bimodal electric tissue ablation. [Thesis]. University of Adelaide; 2012. Available from: http://hdl.handle.net/2440/74060

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

Michigan State University

3. Nath, Aritro. Investigating the role of elevated free fatty acids in epithelial-mesenchymal transition of hepatocellular carcinoma.

Degree: 2015, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:3740

►

Thesis Ph. D. Michigan State University. Genetics 2015

Hepatocellular carcinoma (HCC) is one of the deadliest forms of cancer world-wide with steadily increasing incidence and… (more)

▼

Thesis Ph. D. Michigan State University. Genetics 2015

Hepatocellular carcinoma (HCC) is one of the deadliest forms of cancer world-wide with steadily increasing incidence and mortality rates in the United States. Advanced HCC are characterized by increased prevalence of intrahepatic and extrahepatic metastases, and are associated with very poor survival rates. Epidemiological studies indicate elevated free fatty acid (FFA) levels, the physiological manifestation of obesity, may be associated with higher mortality rates in HCC patients. Here, we investigated the effects of elevated FFA uptake on the induction of epithelial to mesenchymal transition (EMT) program – a pathway involved in metastatic progression of human cancers. Our initial studies with saturated FFA palmitate (PA) revealed a significant loss of the obligate desmosomal protein desmoplakin (DSP) in HepG2 cells, indicating a loss of cell adhesion. We next observed enhanced migration and invasiveness in HepG2 and Hep3B cells in response to PA treatment and confirmed loss of cell adhesion in the two cell lines. PA treatment resulted in cytotoxicity and expression of EMT-markers in distinct populations within the treated cells. Additionally, we identified that the Wnt/β-catenin and TGF-β signaling pathways were activated, suggesting a possible mechanism of EMT induction by PA. We further assessed the association between CD36, a FFA uptake gene normally expressed at low levels in hepatocytes but found to be elevated in fatty liver, and the activation of EMT program in human HCC. Our analysis revealed a significant association between CD36 and expression of EMT markers in the cancer genome anatomy (TCGA) liver cancer mRNA expression dataset, which was confirmed with protein samples from human HCC tumor biopsies. Interestingly, both studies suggested that expression of EMT markers were not correlated with body mass index of the patients. Given the role of exogenous FFA uptake in promoting EMT and metastasis in HCC, we further analyzed somatic mutations, copy number variations, and gene expression profiles of fatty acid uptake and metabolism genes in context of metastatic progression in >8,000 samples from the TCGA database across 12-different cancer types. Our analysis revealed a significant and previously undocumented role of fatty acid uptake and fatty acid metabolism genes in the metastatic progression of multiple human cancers, and demonstrated the utility of genes involved in these pathways as strong prognostic biomarkers with significant influence on survival rates.

Description based on online resource;

Advisors/Committee Members: Chan, Christina, Yang, Chengfeng, Andrechek, Eran, Cui, Yuehua.

Subjects/Keywords: Fatty acids; Liver metastasis; Liver – Cancer; Genetics

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APA (6^th Edition):

Nath, A. (2015). Investigating the role of elevated free fatty acids in epithelial-mesenchymal transition of hepatocellular carcinoma. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:3740

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

Chicago Manual of Style (16^th Edition):

Nath, Aritro. “Investigating the role of elevated free fatty acids in epithelial-mesenchymal transition of hepatocellular carcinoma.” 2015. Thesis, Michigan State University. Accessed January 15, 2021. http://etd.lib.msu.edu/islandora/object/etd:3740.

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

MLA Handbook (7^th Edition):

Nath, Aritro. “Investigating the role of elevated free fatty acids in epithelial-mesenchymal transition of hepatocellular carcinoma.” 2015. Web. 15 Jan 2021.

Vancouver:

Nath A. Investigating the role of elevated free fatty acids in epithelial-mesenchymal transition of hepatocellular carcinoma. [Internet] [Thesis]. Michigan State University; 2015. [cited 2021 Jan 15]. Available from: http://etd.lib.msu.edu/islandora/object/etd:3740.

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

Council of Science Editors:

Nath A. Investigating the role of elevated free fatty acids in epithelial-mesenchymal transition of hepatocellular carcinoma. [Thesis]. Michigan State University; 2015. Available from: http://etd.lib.msu.edu/islandora/object/etd:3740

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

University of Hong Kong

4. Tzang, Fei-chuen. Radiofrequency ablation of hepatocellular carcinoma: identifying prognostic factors in long-term survivaloutcome.

Degree: 2008, University of Hong Kong

URL: http://hdl.handle.net/10722/51949

Subjects/Keywords: Liver - Cancer.

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

APA (6^th Edition):

Tzang, F. (2008). Radiofrequency ablation of hepatocellular carcinoma: identifying prognostic factors in long-term survivaloutcome. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/51949

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

Chicago Manual of Style (16^th Edition):

Tzang, Fei-chuen. “Radiofrequency ablation of hepatocellular carcinoma: identifying prognostic factors in long-term survivaloutcome.” 2008. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/51949.

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

MLA Handbook (7^th Edition):

Tzang, Fei-chuen. “Radiofrequency ablation of hepatocellular carcinoma: identifying prognostic factors in long-term survivaloutcome.” 2008. Web. 15 Jan 2021.

Vancouver:

Tzang F. Radiofrequency ablation of hepatocellular carcinoma: identifying prognostic factors in long-term survivaloutcome. [Internet] [Thesis]. University of Hong Kong; 2008. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/51949.

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

Council of Science Editors:

Tzang F. Radiofrequency ablation of hepatocellular carcinoma: identifying prognostic factors in long-term survivaloutcome. [Thesis]. University of Hong Kong; 2008. Available from: http://hdl.handle.net/10722/51949

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

University of Hong Kong

5. Kung, Hin-fung, Tony. The impact of heat on hepatocellular carcinoma (HCC).

Degree: 2008, University of Hong Kong

URL: http://hdl.handle.net/10722/52000

Subjects/Keywords: Liver - Cancer.

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

APA (6^th Edition):

Kung, Hin-fung, T. (2008). The impact of heat on hepatocellular carcinoma (HCC). (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/52000

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

Chicago Manual of Style (16^th Edition):

Kung, Hin-fung, Tony. “The impact of heat on hepatocellular carcinoma (HCC).” 2008. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/52000.

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

MLA Handbook (7^th Edition):

Kung, Hin-fung, Tony. “The impact of heat on hepatocellular carcinoma (HCC).” 2008. Web. 15 Jan 2021.

Vancouver:

Kung, Hin-fung T. The impact of heat on hepatocellular carcinoma (HCC). [Internet] [Thesis]. University of Hong Kong; 2008. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/52000.

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

Council of Science Editors:

Kung, Hin-fung T. The impact of heat on hepatocellular carcinoma (HCC). [Thesis]. University of Hong Kong; 2008. Available from: http://hdl.handle.net/10722/52000

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

University of Hong Kong

6. 馮偉業. The characterization of PAK 6 in liver cancer.

Degree: 2009, University of Hong Kong

URL: http://hdl.handle.net/10722/55680

Subjects/Keywords: Liver - Cancer.

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

APA (6^th Edition):

馮偉業. (2009). The characterization of PAK 6 in liver cancer. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/55680

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

Chicago Manual of Style (16^th Edition):

馮偉業. “The characterization of PAK 6 in liver cancer.” 2009. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/55680.

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

MLA Handbook (7^th Edition):

馮偉業. “The characterization of PAK 6 in liver cancer.” 2009. Web. 15 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

馮偉業. The characterization of PAK 6 in liver cancer. [Internet] [Thesis]. University of Hong Kong; 2009. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/55680.

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

Council of Science Editors:

馮偉業. The characterization of PAK 6 in liver cancer. [Thesis]. University of Hong Kong; 2009. Available from: http://hdl.handle.net/10722/55680

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

Hong Kong University of Science and Technology

7. Wang, Kwong Sang. Evaluation of causative relationship between candidate gene/gene cluster and hepatocellular carcinoma.

Degree: 2013, Hong Kong University of Science and Technology

URL: http://repository.ust.hk/ir/Record/1783.1-62355 ; https://doi.org/10.14711/thesis-b1250851 ; http://repository.ust.hk/ir/bitstream/1783.1-62355/1/th_redirect.html

► Cancer, which involves uncontrolled growth of cells, may occur almost anywhere in the body. There are risk factors correlating to carcinogenesis in different tissues. In… (more)

Subjects/Keywords: Liver ; Cancer ; Genetics ; Carcinogens

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APA (6^th Edition):

Wang, K. S. (2013). Evaluation of causative relationship between candidate gene/gene cluster and hepatocellular carcinoma. (Thesis). Hong Kong University of Science and Technology. Retrieved from http://repository.ust.hk/ir/Record/1783.1-62355 ; https://doi.org/10.14711/thesis-b1250851 ; http://repository.ust.hk/ir/bitstream/1783.1-62355/1/th_redirect.html

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

Chicago Manual of Style (16^th Edition):

Wang, Kwong Sang. “Evaluation of causative relationship between candidate gene/gene cluster and hepatocellular carcinoma.” 2013. Thesis, Hong Kong University of Science and Technology. Accessed January 15, 2021. http://repository.ust.hk/ir/Record/1783.1-62355 ; https://doi.org/10.14711/thesis-b1250851 ; http://repository.ust.hk/ir/bitstream/1783.1-62355/1/th_redirect.html.

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

MLA Handbook (7^th Edition):

Wang, Kwong Sang. “Evaluation of causative relationship between candidate gene/gene cluster and hepatocellular carcinoma.” 2013. Web. 15 Jan 2021.

Vancouver:

Wang KS. Evaluation of causative relationship between candidate gene/gene cluster and hepatocellular carcinoma. [Internet] [Thesis]. Hong Kong University of Science and Technology; 2013. [cited 2021 Jan 15]. Available from: http://repository.ust.hk/ir/Record/1783.1-62355 ; https://doi.org/10.14711/thesis-b1250851 ; http://repository.ust.hk/ir/bitstream/1783.1-62355/1/th_redirect.html.

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

Council of Science Editors:

Wang KS. Evaluation of causative relationship between candidate gene/gene cluster and hepatocellular carcinoma. [Thesis]. Hong Kong University of Science and Technology; 2013. Available from: http://repository.ust.hk/ir/Record/1783.1-62355 ; https://doi.org/10.14711/thesis-b1250851 ; http://repository.ust.hk/ir/bitstream/1783.1-62355/1/th_redirect.html

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

University of Hong Kong

8. Zhu, Lixin. Mechanism of spontaneous rupture of hepatocellular carcinoma.

Degree: 1998, University of Hong Kong

URL: http://hdl.handle.net/10722/39574

Subjects/Keywords: Liver - Cancer.

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APA (6^th Edition):

Zhu, L. (1998). Mechanism of spontaneous rupture of hepatocellular carcinoma. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/39574

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

Chicago Manual of Style (16^th Edition):

Zhu, Lixin. “Mechanism of spontaneous rupture of hepatocellular carcinoma.” 1998. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/39574.

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

MLA Handbook (7^th Edition):

Zhu, Lixin. “Mechanism of spontaneous rupture of hepatocellular carcinoma.” 1998. Web. 15 Jan 2021.

Vancouver:

Zhu L. Mechanism of spontaneous rupture of hepatocellular carcinoma. [Internet] [Thesis]. University of Hong Kong; 1998. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/39574.

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

Council of Science Editors:

Zhu L. Mechanism of spontaneous rupture of hepatocellular carcinoma. [Thesis]. University of Hong Kong; 1998. Available from: http://hdl.handle.net/10722/39574

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

University of Arizona

9. Sweeney, Nathan. Investigating the Role of Obesity and Obstructive Sleep Apnea in Hepatocellular Carcinoma Progression .

Degree: 2018, University of Arizona

URL: http://hdl.handle.net/10150/628049

► Primary liver cancer is the seventh most common cancer worldwide and the second highest cause of cancer mortality. The incidence of hepatocellular carcinoma (HCC) has… (more)

▼ Primary liver cancer is the seventh most common cancer worldwide and the second highest cause of cancer mortality. The incidence of hepatocellular carcinoma (HCC) has increased 80% in the past two decades and now comprises 85% of all primary liver cancer. Obesity increases the risk of developing HCC two-fold in women and five-fold in men. Co-morbidities common to obesity including non-alcoholic steatohepatitis (NASH), hepatic inflammation, and lipid accumulation increase the risk of developing HCC. Obstructive sleep apnea (OSA), a state of chronic intermittent hypoxia which is common in obese individuals, also increases the incidence of NASH. With a U.S. population that is approximately 33% obese, having OSA at 30-50%, we estimate the co-incidence of obesity and OSA is 10-16.5% of the entire U.S. population. Diet-induced obesity or intermittent hypoxia induces hepatic lipid accumulation and diet-induced obesity was recently shown to promote HCC tumor development. Whether obesity, chronic intermittent hypoxia, and their combination hasten hepatic lipid accumulation and HCC tumor progression remains unclear. In our studies, we monitored tumor development utilizing micro-computed tomography imaging and discovered that tumors developed fastest in mice that consumed a high fat diet. Upon further investigation, these mice also tended to have higher serum levels of AST and ALT and gained more weight than their counterparts. However, the addition of hypoxia lead to a decrease in weight gained, as well as a reduction in hepatic lipid accumulation and tumor formation. Extraction of mRNA from mouse livers revealed an up-regulation HIF-1α in mice fed a high fat diet without treatment with hypoxia that correlated strongly with tumorigenesis. Remarkably, hypoxia was found in mice treated with hypoxia as well as the mice that were fed a high fat diet only. These findings suggest that hepatic lipid accumulation produces endogenous hepatic hypoxia which associates with increased hepatic HIF-1α expression that correlates with tumorigenesis. Collectively, these data reveal a mechanism that potentially explains progression from early liver disease to HCC. Advisors/Committee Members: Martinez, Jesse (advisor), Breihl, Margaret (committeemember), Cherrington, Nathan (committeemember), Doetschman, Tom (committeemember), Tax, Frans (committeemember).

Subjects/Keywords: Liver Cancer; Obesity; Sleep Apnea

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APA (6^th Edition):

Sweeney, N. (2018). Investigating the Role of Obesity and Obstructive Sleep Apnea in Hepatocellular Carcinoma Progression . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/628049

Chicago Manual of Style (16^th Edition):

Sweeney, Nathan. “Investigating the Role of Obesity and Obstructive Sleep Apnea in Hepatocellular Carcinoma Progression .” 2018. Doctoral Dissertation, University of Arizona. Accessed January 15, 2021. http://hdl.handle.net/10150/628049.

MLA Handbook (7^th Edition):

Sweeney, Nathan. “Investigating the Role of Obesity and Obstructive Sleep Apnea in Hepatocellular Carcinoma Progression .” 2018. Web. 15 Jan 2021.

Vancouver:

Sweeney N. Investigating the Role of Obesity and Obstructive Sleep Apnea in Hepatocellular Carcinoma Progression . [Internet] [Doctoral dissertation]. University of Arizona; 2018. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10150/628049.

Council of Science Editors:

Sweeney N. Investigating the Role of Obesity and Obstructive Sleep Apnea in Hepatocellular Carcinoma Progression . [Doctoral Dissertation]. University of Arizona; 2018. Available from: http://hdl.handle.net/10150/628049

University of Hong Kong

10. Ma, Tung, Lily. Studies of liver cancers in man and in rats, with special reference totheir fine structure as seen by electron microscopy.

Degree: 1977, University of Hong Kong

URL: http://hdl.handle.net/10722/34901

Subjects/Keywords: Liver - Cancer.

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

APA (6^th Edition):

Ma, Tung, L. (1977). Studies of liver cancers in man and in rats, with special reference totheir fine structure as seen by electron microscopy. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/34901

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

Chicago Manual of Style (16^th Edition):

Ma, Tung, Lily. “Studies of liver cancers in man and in rats, with special reference totheir fine structure as seen by electron microscopy.” 1977. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/34901.

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

MLA Handbook (7^th Edition):

Ma, Tung, Lily. “Studies of liver cancers in man and in rats, with special reference totheir fine structure as seen by electron microscopy.” 1977. Web. 15 Jan 2021.

Vancouver:

Ma, Tung L. Studies of liver cancers in man and in rats, with special reference totheir fine structure as seen by electron microscopy. [Internet] [Thesis]. University of Hong Kong; 1977. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/34901.

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

Council of Science Editors:

Ma, Tung L. Studies of liver cancers in man and in rats, with special reference totheir fine structure as seen by electron microscopy. [Thesis]. University of Hong Kong; 1977. Available from: http://hdl.handle.net/10722/34901

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

11. Drakaki, Alexandra. Η διερεύνηση νέων microRNA που παίζουν ρόλο στην δημιουργία καρκίνου ήπατος μέσα από υψηλής τεχνολογίας ανάλυση.

Degree: 2015, University of Crete (UOC); Πανεπιστήμιο Κρήτης

URL: http://hdl.handle.net/10442/hedi/36997

► Identification of Novel MicroRNAs Involved in Hepatocellular Carcinogenesis by High Throughput screening. Abstract-background: Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death in… (more)

▼ Identification of Novel MicroRNAs Involved in Hepatocellular Carcinogenesis by High Throughput screening. Abstract-background: Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death in men and the sixth in women. Those numbers reflect the aggressiveness of this disease while at the same time mirror the absence of effective therapeutic regimens. There have been conducted hundreds of clinical trials in which either combination chemotherapies or small molecule inhibitors and recently immune checkpoint inhibitors have been studied. However the only FDA approved drug for unresectable or metastatic HCC is sorafenib which is a tyrosine kinase inhibitor. Our interest was to identify genes that play a role in liver oncogenesis and so we directed our focus to study a novel class of small non coding RNAs, the microRNAs.MicroRNAs have been involved in the pathogenesis of different types of cancers, including liver cancer. Specific microRNA signatures have been identified to be deregulated in HCC patient tissues and also to correlate with different clinicopathological parameters including survival. Having all this in mind our mission was to identify microRNAs that have both functional and clinical relevance in HCC and examine their downstream signaling effectors. Methods: In this study, we have screened the human microRNAome, aiming to identify microRNAs that are potent regulators of HCC invasiveness. Initially we received 24 tissues from patients with liver cancer along with 14 from adjacent non tumor specimens. RNA extraction was performed and microRNA and gene expression levels were measured by quantitative real-time RT-PCR. We determined the expression levels of miR-9, miR-21 and miR-224 in those samples. Simultaneously a novel microRNA library screen was done after plating SNU-449 liver cancer cells in 96-well plates. Those were transfected with a microRNA library consisting of 316 microRNA mimics and 2 negative controls. 48hrs post transfection we evaluated the SNU-449 cell invasiveness. We also performed invasion assays in SNU-449 cells 24hrs after transfection specifically with miR-9 and anti-miR-9 and their respective controls. A TargetScan algorithm was used to identify miR-9 downstream direct targets based on bioinformatics. Those analyses were validated by performing 3’UTR luciferase assay. Precisely, we transfected SNU-449 cells with the reporter vectors carrying the 3’UTR of CDH1 or PPARA. The constructs harbored the seed sequence of miR-9 (wildtype) or had a deletion of this sequence (miR-9 mutant). At 24 hours, they were transfected with miR-9 or miR-control and at 48 hours luciferase activity was measured. We have also performed transfection with microRNA mimic for mir-9 overexpression as well as microRNA inihibitor to suppress the miR-9 activity and observed the expression levels of the downstream targets CDH1, PPARA, PDK4 and vimentin. Furthermore we performed cell proliferation as well as assessed sphere formation and colony assay in SNU-449 and HepG2 liver cancer cell lines, both…

Subjects/Keywords: Καρκίνος ήπατος; MicroRNAs; Liver cancer

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

APA (6^th Edition):

Drakaki, A. (2015). Η διερεύνηση νέων microRNA που παίζουν ρόλο στην δημιουργία καρκίνου ήπατος μέσα από υψηλής τεχνολογίας ανάλυση. (Thesis). University of Crete (UOC); Πανεπιστήμιο Κρήτης. Retrieved from http://hdl.handle.net/10442/hedi/36997

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

Chicago Manual of Style (16^th Edition):

Drakaki, Alexandra. “Η διερεύνηση νέων microRNA που παίζουν ρόλο στην δημιουργία καρκίνου ήπατος μέσα από υψηλής τεχνολογίας ανάλυση.” 2015. Thesis, University of Crete (UOC); Πανεπιστήμιο Κρήτης. Accessed January 15, 2021. http://hdl.handle.net/10442/hedi/36997.

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

MLA Handbook (7^th Edition):

Drakaki, Alexandra. “Η διερεύνηση νέων microRNA που παίζουν ρόλο στην δημιουργία καρκίνου ήπατος μέσα από υψηλής τεχνολογίας ανάλυση.” 2015. Web. 15 Jan 2021.

Vancouver:

Drakaki A. Η διερεύνηση νέων microRNA που παίζουν ρόλο στην δημιουργία καρκίνου ήπατος μέσα από υψηλής τεχνολογίας ανάλυση. [Internet] [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2015. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10442/hedi/36997.

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

Council of Science Editors:

Drakaki A. Η διερεύνηση νέων microRNA που παίζουν ρόλο στην δημιουργία καρκίνου ήπατος μέσα από υψηλής τεχνολογίας ανάλυση. [Thesis]. University of Crete (UOC); Πανεπιστήμιο Κρήτης; 2015. Available from: http://hdl.handle.net/10442/hedi/36997

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

University of Sydney

12. Lee, Aimei Yen-Jia. The glycoprotein Basigin in liver disease .

Degree: 2016, University of Sydney

URL: http://hdl.handle.net/2123/17163

► Basigin (Bsg) is a membrane glycoprotein expressed by many different cell types. Bsg is instrumental in tissue development, extracellular matrix (ECM) remodelling, and has been… (more)

Subjects/Keywords: liver; cancer; biomarker; glycosylation

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

APA (6^th Edition):

Lee, A. Y. (2016). The glycoprotein Basigin in liver disease . (Thesis). University of Sydney. Retrieved from http://hdl.handle.net/2123/17163

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

Chicago Manual of Style (16^th Edition):

Lee, Aimei Yen-Jia. “The glycoprotein Basigin in liver disease .” 2016. Thesis, University of Sydney. Accessed January 15, 2021. http://hdl.handle.net/2123/17163.

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

MLA Handbook (7^th Edition):

Lee, Aimei Yen-Jia. “The glycoprotein Basigin in liver disease .” 2016. Web. 15 Jan 2021.

Vancouver:

Lee AY. The glycoprotein Basigin in liver disease . [Internet] [Thesis]. University of Sydney; 2016. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/2123/17163.

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

Council of Science Editors:

Lee AY. The glycoprotein Basigin in liver disease . [Thesis]. University of Sydney; 2016. Available from: http://hdl.handle.net/2123/17163

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

13. Fekir, Karim. Biomarqueurs et nouvelles approches thérapeutiques ciblant les cellules souches cancéreuses dans le carcinome hépatocellulaire : Biomarkers and new therapeutic approches targeting cancer stem cells in hepatocellular carcinoma.

Degree: Docteur es, Biologie et sciences de la santé, 2015, Rennes 1

URL: http://www.theses.fr/2015REN1B007

►

Le cancer primitif du foie, ou carcinome hépatocellulaire (CHC), est l’un des premiers cancers dans le monde chez l’homme adulte. L'identité des cellules à l'origine… (more)

▼

Le cancer primitif du foie, ou carcinome hépatocellulaire (CHC), est l’un des premiers cancers dans le monde chez l’homme adulte. L'identité des cellules à l'origine des CHC est controversée, toutefois l'existence de cellules souches/progénitrices (CS/P) dans certaines tumeurs a été rapportée. Ces tumeurs ont un phénotype très agressif, sont associées à un mauvais pronostic et ont tendance à échapper aux thérapies conventionnelles. Ainsi, des traitements ciblant spécifiquement les cellules souches cancéreuses pourraient constituer des compléments thérapeutiques efficaces aux traitements actuels. Pour cela, il est nécessaire de disposer de biomarqueurs afin d’identifier les sous-types de CHC dérivant de CS/P mais également de modèles cellulaires permettant de tester des molécules thérapeutiques. Les CS/P pourraient provenir soit du compartiment de cellules souches hépatiques soit de la dédifférenciation d’hépatocytes à l'intérieur de la tumeur. Aussi dans le cadre de cette thèse nous nous sommes attachés à étudier les mécanismes cellulaires et moléculaires impliqués 1) dans la retrodifférenciation des hépatocytes en CS/P et 2) dans le maintien des propriétés souches. Pour cette étude nous avons utilisé la lignée HepaRG issue d’un CHC sur infection virale C qui présente des caractéristiques de progéniteurs hépatiques se différenciant en hépatocytes et cholangiocytes. Dans la première partie de ce travail nous avons montré qu’un environnement inflammatoire favorise la retrodifferenciation d’hépatocytes HepaRG en CS/P. Alors que les voies activées par le TNF et l’IL-6 sont impliquées dans la perte du phénotype hépatocytaire, la voie TGF induit une transition épithélio-mésenchymateuse. Dans ces CS/P, nous observons l’enrichissement de signatures moléculaires associées à des souches embryonnaires et à des CHC avec mauvais pronostic. De plus, nous avons identifié plusieurs molécules pouvant inhiber ce processus de rétrodifférenciation des hépatocytes-HepaRG comme la trichostatine A. Dans une seconde partie nous avons montré que l’acquisition et le maintien des caractéristiques souches des cellules HepaRG étaient associés à une production de cytokines, à l’expression de métalloprotéinases impliquées dans les processus de migration et d’invasion, de facteur pro-angiogenique et à un changement dans l’activité mitochondriale conduisant à une reprogrammation métabolique. Les voies de signalisation impliquant l’angiopoïétine-like 4, PI3K et ERK régulent ces changements. De façon intéressante, nous montrons que le rétablissement de l’activité mitochondriale réduit la résistance des CS/P aux anticancéreux. Notre étude nous a permis d’acquérir une meilleure compréhension des voies de signalisation activées dans les cellules souches/progénitrices hépatiques cancéreuses et des mécanismes impliqués dans la rétro-différenciation des cellules matures tumorales, deux phénomènes probablement impliqués dans la récidive tumorale et la chimiorésistance.

Biomarkers and new therapeutic approches targeting cancer stem cells in…

Advisors/Committee Members: Corlu, Anne (thesis director).

Subjects/Keywords: Foie; Cancer; Cellules souches; Liver cells; Cancer

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

APA (6^th Edition):

Fekir, K. (2015). Biomarqueurs et nouvelles approches thérapeutiques ciblant les cellules souches cancéreuses dans le carcinome hépatocellulaire : Biomarkers and new therapeutic approches targeting cancer stem cells in hepatocellular carcinoma. (Doctoral Dissertation). Rennes 1. Retrieved from http://www.theses.fr/2015REN1B007

Chicago Manual of Style (16^th Edition):

Fekir, Karim. “Biomarqueurs et nouvelles approches thérapeutiques ciblant les cellules souches cancéreuses dans le carcinome hépatocellulaire : Biomarkers and new therapeutic approches targeting cancer stem cells in hepatocellular carcinoma.” 2015. Doctoral Dissertation, Rennes 1. Accessed January 15, 2021. http://www.theses.fr/2015REN1B007.

MLA Handbook (7^th Edition):

Fekir, Karim. “Biomarqueurs et nouvelles approches thérapeutiques ciblant les cellules souches cancéreuses dans le carcinome hépatocellulaire : Biomarkers and new therapeutic approches targeting cancer stem cells in hepatocellular carcinoma.” 2015. Web. 15 Jan 2021.

Vancouver:

Fekir K. Biomarqueurs et nouvelles approches thérapeutiques ciblant les cellules souches cancéreuses dans le carcinome hépatocellulaire : Biomarkers and new therapeutic approches targeting cancer stem cells in hepatocellular carcinoma. [Internet] [Doctoral dissertation]. Rennes 1; 2015. [cited 2021 Jan 15]. Available from: http://www.theses.fr/2015REN1B007.

Council of Science Editors:

Fekir K. Biomarqueurs et nouvelles approches thérapeutiques ciblant les cellules souches cancéreuses dans le carcinome hépatocellulaire : Biomarkers and new therapeutic approches targeting cancer stem cells in hepatocellular carcinoma. [Doctoral Dissertation]. Rennes 1; 2015. Available from: http://www.theses.fr/2015REN1B007

14. Senni, Nadia. Reprogrammation métabolique des carcinomes hépatocellulaires présentant une activation aberrante de la beta-caténine : Consequences of beta-catenin pathway activation on hepatic metabolism.

Degree: Docteur es, Sciences de la vie et de la santé, 2017, Université Paris-Saclay (ComUE)

URL: http://www.theses.fr/2017SACLS075

►

Le carcinome hépatocellulaire constitue la 3ème cause de décès par cancer dans le monde. Il a été montré que des mutations activatrices du gène CTNNB1,… (more)

▼

Le carcinome hépatocellulaire constitue la 3ème cause de décès par cancer dans le monde. Il a été montré que des mutations activatrices du gène CTNNB1, codant la β-caténine, étaient à l’origine de 20 à 40% des CHC humains. Ces CHC sont peu prolifératifs et présentent un phénotype métabolique particulier associé notamment au développement d’une cholestase et à une absence de stéatose. De nombreuses tumeurs présentent un effet Warburg, c’est-à-dire une addiction au glucose et à la glutamine avec une hyperproduction de lactate, or il a été mis en évidence par l’équipe que les CHC activés pour la β-caténine étaient négatifs en PET-scan FDG et donc ne présentaient pas d’utilisation accrue du glucose.L’objectif de ce travail a été d’analyser la reprogrammation métabolique accompagnant la tumorigenèse β-caténine dans le foie. Nous disposons d’un modèle murin de tumorigenèse β-caténine, les souris TTR-Cre-Apclox/lox inductible au tamoxifène, dans lequel la perte d’Apc dans quelques hépatocytes conduit au développement de tumeurs β-caténine activée après quelques mois. Je dispose aussi d’un modèle dit « prénéoplasique » dans lequel la β-caténine est constitutivement active dans tout le lobule hépatique.Des analyses de flux métaboliques sur ces hépatocytes β-caténine activée a permis de mettre en évidence une absence d’effet Warburg : pas d’altération de la glycolyse ni de la production de lactate lors d’une activation anormale de la voie β-caténine. En revanche, le glucose est réorienté vers une hyperproduction de glutamine, qui n’est pas réutilisée par le cycle de Krebs. Ces hépatocytes présentent aussi une diminution de la lipogenèse avec une réorientation des acides gras produits dans la synthèse de phospholipides.D’autre part, nous avons pu mettre en évidence sur les hépatocytes et les tumeurs murines présentant une activation anormale de la β-caténine, une très forte augmentation de l’oxydation des acides gras et de la production de corps cétoniques. Cette augmentation de l’oxydation des acides gras est spécifique à la reprogrammation métabolique des CHC avec une activation anormale de la β-caténine, puisque nous ne l’avons pas retrouvée dans des CHC ne présentant pas d’hyperactivation de la β-caténine.De plus, l’invalidation d’Apc dans un modèle murin présentant un défaut d’oxydation des acides gras ne conduit pas au développement de tumeurs montrant ainsi que la -oxydation des acides gras serait primordiale pour la tumorigenèse associée à une suractivation de la -caténine. La β-caténine activerait donc un programme génique conduisant à une augmentation de l’oxydation des acides gras et cette reprogrammation métabolique est indispensable à la l’initiation tumorale.

Cancer cells are characterized by uncontrolled and rapid proliferation requiring metabolic adjustments to provide macromolecules and energy to fuel cell growth and division. Most tumors are characterized by a “Warburg effect” consisting in an addiction to glucose, at the basis for detecting them by fluorodeoxyglucose (FDG) positron emission tomography…

Advisors/Committee Members: Bossard, Pascale (thesis director).

Subjects/Keywords: Cancer; Métabolisme; Foie; Cancer; Metabolism; Liver

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

APA (6^th Edition):

Senni, N. (2017). Reprogrammation métabolique des carcinomes hépatocellulaires présentant une activation aberrante de la beta-caténine : Consequences of beta-catenin pathway activation on hepatic metabolism. (Doctoral Dissertation). Université Paris-Saclay (ComUE). Retrieved from http://www.theses.fr/2017SACLS075

Chicago Manual of Style (16^th Edition):

Senni, Nadia. “Reprogrammation métabolique des carcinomes hépatocellulaires présentant une activation aberrante de la beta-caténine : Consequences of beta-catenin pathway activation on hepatic metabolism.” 2017. Doctoral Dissertation, Université Paris-Saclay (ComUE). Accessed January 15, 2021. http://www.theses.fr/2017SACLS075.

MLA Handbook (7^th Edition):

Senni, Nadia. “Reprogrammation métabolique des carcinomes hépatocellulaires présentant une activation aberrante de la beta-caténine : Consequences of beta-catenin pathway activation on hepatic metabolism.” 2017. Web. 15 Jan 2021.

Vancouver:

Senni N. Reprogrammation métabolique des carcinomes hépatocellulaires présentant une activation aberrante de la beta-caténine : Consequences of beta-catenin pathway activation on hepatic metabolism. [Internet] [Doctoral dissertation]. Université Paris-Saclay (ComUE); 2017. [cited 2021 Jan 15]. Available from: http://www.theses.fr/2017SACLS075.

Council of Science Editors:

Senni N. Reprogrammation métabolique des carcinomes hépatocellulaires présentant une activation aberrante de la beta-caténine : Consequences of beta-catenin pathway activation on hepatic metabolism. [Doctoral Dissertation]. Université Paris-Saclay (ComUE); 2017. Available from: http://www.theses.fr/2017SACLS075

Deakin University

15. Ajji, Parminder Kaur. Functional characterization of a novel ribosome inactivating protein from Momordica balsamina.

Degree: School of Life and Environmental Sciences, 2016, Deakin University

URL: http://hdl.handle.net/10536/DRO/DU:30103049

► This study provides an insight into the cytotoxic potential of natural and recombinant ribosome-inactivating protein (Balsamin) from Momordica balsamina. It explores the molecular mechanism of… (more)

Subjects/Keywords: liver cancer therapy; breast cancer therapy; balsamin

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

APA (6^th Edition):

Ajji, P. K. (2016). Functional characterization of a novel ribosome inactivating protein from Momordica balsamina. (Thesis). Deakin University. Retrieved from http://hdl.handle.net/10536/DRO/DU:30103049

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

Chicago Manual of Style (16^th Edition):

Ajji, Parminder Kaur. “Functional characterization of a novel ribosome inactivating protein from Momordica balsamina.” 2016. Thesis, Deakin University. Accessed January 15, 2021. http://hdl.handle.net/10536/DRO/DU:30103049.

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

MLA Handbook (7^th Edition):

Ajji, Parminder Kaur. “Functional characterization of a novel ribosome inactivating protein from Momordica balsamina.” 2016. Web. 15 Jan 2021.

Vancouver:

Ajji PK. Functional characterization of a novel ribosome inactivating protein from Momordica balsamina. [Internet] [Thesis]. Deakin University; 2016. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10536/DRO/DU:30103049.

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

Council of Science Editors:

Ajji PK. Functional characterization of a novel ribosome inactivating protein from Momordica balsamina. [Thesis]. Deakin University; 2016. Available from: http://hdl.handle.net/10536/DRO/DU:30103049

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

University of Hong Kong

16. Lai, Cheuck-seen, Edward. Resection margin for hepatocellular carcinoma.

Degree: 1992, University of Hong Kong

URL: http://hdl.handle.net/10722/31251

Subjects/Keywords: Liver - Cancer - Surgery.; Liver - Cancer.

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

APA (6^th Edition):

Lai, Cheuck-seen, E. (1992). Resection margin for hepatocellular carcinoma. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/31251

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

Chicago Manual of Style (16^th Edition):

Lai, Cheuck-seen, Edward. “Resection margin for hepatocellular carcinoma.” 1992. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/31251.

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

MLA Handbook (7^th Edition):

Lai, Cheuck-seen, Edward. “Resection margin for hepatocellular carcinoma.” 1992. Web. 15 Jan 2021.

Vancouver:

Lai, Cheuck-seen E. Resection margin for hepatocellular carcinoma. [Internet] [Thesis]. University of Hong Kong; 1992. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/31251.

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

Council of Science Editors:

Lai, Cheuck-seen E. Resection margin for hepatocellular carcinoma. [Thesis]. University of Hong Kong; 1992. Available from: http://hdl.handle.net/10722/31251

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

University of Hong Kong

17. 呂愛蓮. Patho-biological prognostic factors in hepatocellular carcinoma.

Degree: 1994, University of Hong Kong

URL: http://hdl.handle.net/10722/26897

Subjects/Keywords: Liver - Cancer.; Liver - Cancer.; Cancer - Prognosis.

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

APA (6^th Edition):

呂愛蓮. (1994). Patho-biological prognostic factors in hepatocellular carcinoma. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/26897

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

Chicago Manual of Style (16^th Edition):

呂愛蓮. “Patho-biological prognostic factors in hepatocellular carcinoma.” 1994. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/26897.

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

MLA Handbook (7^th Edition):

呂愛蓮. “Patho-biological prognostic factors in hepatocellular carcinoma.” 1994. Web. 15 Jan 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

呂愛蓮. Patho-biological prognostic factors in hepatocellular carcinoma. [Internet] [Thesis]. University of Hong Kong; 1994. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/26897.

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

Council of Science Editors:

呂愛蓮. Patho-biological prognostic factors in hepatocellular carcinoma. [Thesis]. University of Hong Kong; 1994. Available from: http://hdl.handle.net/10722/26897

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

University of Illinois – Chicago

18. Kataria, Yachana. Integrating Biomarkers into Translational Research on Diet and Cancer.

Degree: 2015, University of Illinois – Chicago

URL: http://hdl.handle.net/10027/19769

► Here, we elucidate dietary factors that contribute to or protect against liver and prostate cancer, and their relationship with underlying pathophysiologic mechanisms. Alpha-methylacyl-CoA racemase (AMACR)… (more)

▼ Here, we elucidate dietary factors that contribute to or protect against liver and prostate cancer, and their relationship with underlying pathophysiologic mechanisms. Alpha-methylacyl-CoA racemase (AMACR) is an enzyme involved in fatty acid metabolism that is markedly over-expressed in virtually all prostate cancers (PCa), relative to benign tissue. Phytanic acid, one of AMACR’s primary substrates, is derived predominately from red meat and dairy product consumption. Epidemiological evidence suggests links between dairy/red meat intake, as well as phytanic acid levels, and elevated PCa risk. The first study investigates the relationships among dietary intake, serum and tissue concentrations of phytanic acid, and AMACR expression (mRNA and protein) in the histologically benign human prostate. Our data could not unify the hypothesis that excess levels of dietary phytanic acid are responsible for both the overexpression of AMACR in prostate cancer and the potential association between PCa risk and intake of dairy foods and red meat. The focus of the second part is vitamin A, iron, and the joint relationship of vitamin A and iron in patients at high risk for liver cancer. HCV patients with cirrhosis form the largest group of persons at high risk for hepatocellular carcinoma (HCC). Increased oxidative stress is regarded as a major mechanism of HCV-related liver disease progression. Deficiencies in retinoid and carotenoid antioxidants and increased iron may represent a major modifiable risk factor for HCC progression. We observed that a decrease in serum retinol, β-carotene, and RBP4 is associated with early stage HCV infection. Retinoid and carotenoid levels decline as disease progresses, and our data suggest that this decline occurs early in the disease process, even before fibrosis is apparent. Measures of oxidative stress are associated with fibrosis stage and concurrent antioxidant depletion. Vitamin A loss is accompanied by stellate cell activation in hepatic tissue. We observed an increase in serum iron biomarkers in CLD patients compared to controls. Serum retinoids were inversely associated with serum iron biomarkers. However, there was little evidence of a joint effect between iron and retinoids in early CLD. Advisors/Committee Members: Bosland, Maarten C. (advisor), Gann, Peter H. (committee member), Kajdacsy-Balla, Andre (committee member), Walden, William (committee member), Fantuzzi, Giamila (committee member).

Subjects/Keywords: Biomarkers; Prostate Cancer; Liver Cancer; Diet; Cancer; Epidemiology; Chemoprevention

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

APA (6^th Edition):

Kataria, Y. (2015). Integrating Biomarkers into Translational Research on Diet and Cancer. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/19769

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

Chicago Manual of Style (16^th Edition):

Kataria, Yachana. “Integrating Biomarkers into Translational Research on Diet and Cancer.” 2015. Thesis, University of Illinois – Chicago. Accessed January 15, 2021. http://hdl.handle.net/10027/19769.

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

MLA Handbook (7^th Edition):

Kataria, Yachana. “Integrating Biomarkers into Translational Research on Diet and Cancer.” 2015. Web. 15 Jan 2021.

Vancouver:

Kataria Y. Integrating Biomarkers into Translational Research on Diet and Cancer. [Internet] [Thesis]. University of Illinois – Chicago; 2015. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10027/19769.

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

Council of Science Editors:

Kataria Y. Integrating Biomarkers into Translational Research on Diet and Cancer. [Thesis]. University of Illinois – Chicago; 2015. Available from: http://hdl.handle.net/10027/19769

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

Univerzitet u Beogradu

19. Galun, Danijel A., 1974-. Izvodljivost velikih resekcija jetre kod bolesnika sa hepatocelularnim karcinomom i cirozom jetre primenom radiofrekventne energije.

Degree: Medicinski fakultet, 2018, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:19074/bdef:Content/get

►

Medicina - Hirurgija / Medicine - Surgery

kurativno lečenje primeni na što je moguće većem broju bolesnika. Budući da je transplantacija jetre ograničena definisanim kriterijumima… (more)

▼

Medicina - Hirurgija / Medicine - Surgery

kurativno lečenje primeni na što je moguće većem broju bolesnika. Budući da je transplantacija jetre ograničena definisanim kriterijumima i brojem donora, resekcija jetre predstavlja glavnu terapijsku opciju potencijalno kurativnog lečenja ali je ograničena funkcionalnim kapacitetom preostalog parenhima jetre. Radiofrekventna resekcija jetre uvažava sve principa savremene hirurgije jetre. Kako je hepatična cirkulacija kod ove tehnike prezervirana tokom transekcije parenhima, funkcija preostalog često cirotičnog parenhima jetre nije narušena ishemijsko-reperfuzionom lezijom. Time se resekcija jetre kao potencijalno kurativni modalitet lečenja može primeniti i kod bolesnika koji imaju ograničenu funkciju jetre. Cilj rada: Utvrditi izvodljivost velikih resekcija jetre kod bolesnika sa hepatocelularnim karcinomom na terenu cirotično imenjene jetre određivanjem postoperativnog morbiditeta i mortaliteta; odrediti preoperativne, intraoperativne i patohistološke prognostičke parametre povezane sa najvećim preživljavanjem i ispitati postoperativni oporavak funkcije cirotične jetre primenom statičkih i dinamičkih testova i merenjem nivoa TNFά i IL6 u prvih 48h posle resekcije jetre Metod: Kohortna studija delom retrospektivna delom prospektivna realizovana na Klinici za digestivnu hirurgiju Kliničkog centra Srbije u periodu od novembra 2001. godine do novembra 2012. godine. U navedenom periodu kod 41 bolesnika (20 sa cirozom, 21 bez ciroze jetre) sa histološki potvrđenim hepatocelularnim karcinomom urađena je radiofrekventna resekcije jetre i to velika resekcija (resekcija 3 i više segmenata). Isključeni su bolesnici sa mešovitim hepatocelularnim/holangiocelularnim karcinomom, bolesnici kod kojih je infiltrisana donja šuplja vena, glavno stablo portne vene i bolesnici sa ekstrahepatičnim širenjem bolesti. U studiji su korišćeni demografski podaci, anamnestički podaci, perioperativni parametri, patohistološke karakteristike tumora, laboratorijske analize, vrednosti lidokainskog testa, vrednosti nivoa TNFά i IL6 u serumu i tkivu jetre, praćen je postoperativni morbiditet i mortalitet. Za statističku obradu korišćen je statistički programski paket SPSS for Windows (18.0). Izbor testova za analizu numeričkih obeležja posmatranja vršen je zavisno od prirode njihove raspodele koja je ispitivana korišćenjem Koglomorov–Smirnov-og testa.U slučaju normalne raspodele podataka za testiranje razlike između dve grupe ispitanika korišćen je t-test dok je kod neparametarskih podataka korišćen Mann Whitney U test. Kaplan Majer-ovim krivama preživljavanja praćen je ishod kod ispitanika sa HCCom. Cox-ovom regresionom analizom ispitivani su prediktori preživljavanja. Granična vrednost za prihvatanje radne hipoteze postavljena je na p < 0.05 ...

Advisors/Committee Members: Milićević, Miroslav, 1949-.

Subjects/Keywords: Liver resection; cirrhosis; radiofrequent energy; hepatocellular cancer; primary liver tumor

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❌

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

APA (6^th Edition):

Galun, Danijel A., 1. (2018). Izvodljivost velikih resekcija jetre kod bolesnika sa hepatocelularnim karcinomom i cirozom jetre primenom radiofrekventne energije. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:19074/bdef:Content/get

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

Chicago Manual of Style (16^th Edition):

Galun, Danijel A., 1974-. “Izvodljivost velikih resekcija jetre kod bolesnika sa hepatocelularnim karcinomom i cirozom jetre primenom radiofrekventne energije.” 2018. Thesis, Univerzitet u Beogradu. Accessed January 15, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:19074/bdef:Content/get.

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

MLA Handbook (7^th Edition):

Galun, Danijel A., 1974-. “Izvodljivost velikih resekcija jetre kod bolesnika sa hepatocelularnim karcinomom i cirozom jetre primenom radiofrekventne energije.” 2018. Web. 15 Jan 2021.

Vancouver:

Galun, Danijel A. 1. Izvodljivost velikih resekcija jetre kod bolesnika sa hepatocelularnim karcinomom i cirozom jetre primenom radiofrekventne energije. [Internet] [Thesis]. Univerzitet u Beogradu; 2018. [cited 2021 Jan 15]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:19074/bdef:Content/get.

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

Council of Science Editors:

Galun, Danijel A. 1. Izvodljivost velikih resekcija jetre kod bolesnika sa hepatocelularnim karcinomom i cirozom jetre primenom radiofrekventne energije. [Thesis]. Univerzitet u Beogradu; 2018. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:19074/bdef:Content/get

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

University of Manitoba

20. Labine, Meaghan. Cyanobacterial toxins and liver cancer.

Degree: Pharmacology and Therapeutics, 2014, University of Manitoba

URL: http://hdl.handle.net/1993/23952

► Hepatocellular carcinoma (HCC) is the fifth most common cancer in the world today. Over the past decade, the incidence of HCC in Canada has been… (more)

▼ Hepatocellular carcinoma (HCC) is the fifth most common cancer in the world today. Over the past decade, the incidence of HCC in Canada has been increasing despite efforts to mitigate disease causing factors such as viral hepatitis B and C infection. Fresh water cyanobacteria are known to release potent hepatotoxins, such as microcystin-LR (MCLR), into drinking and recreational water sources, which have been associated with liver toxicity and HCC. Despite government efforts to limit MCRL contamination, chronic low-dose exposure continues to occur. The purpose of this thesis was to gain an understanding of the potential relationship between chronic low-dose MCLR exposure and HCC. The research contains five areas of investigation; 1) In vitro effects of low-dose MCLR exposure on various hepatocellular cell types, 2) in vitro effects of low-dose MCLR exposure on hepatic stellate cells and fibrosis, 3) in vivo effects of chronic low-dose MCLR exposure on HCC initiation and promotion, 4) in vivo effects of chronic low-dose MCLR exposure on hepatic fibrosis and 5) national and provincial epidemiological analysis investigating the potential association between cyanobacterial hepatotoxins and liver cancer. Our methodology involved; 1) exposing WB-F344, PLC and CFSC-2G hepatic cell lines to varying concentrations of MCLR and observing changes in cell proliferation, protein expression, wound healing and malignant transformation, 2) continuously exposing adult male mice to 1 µg/L of MCLR in their drinking water for seven months, and observing changes in body weight, liver histology, liver enzymes, hepatic fibrosis and HCC development, 3) conducting a national HCC epidemiological study, and determining the relative risk of developing HCC from up-stream factors contributing to cyanobacterial contamination of drinking water sources and 4) conducting a provincial epidemiological study that involved collecting liver cancer incidence data from the Manitoba cancer registry from 1985 to 2007, and temporally and spatially analyzing the association between cancer incidence and MCLR measured in Manitoba lakes. The in vitro results indicate that chronic low-dose exposure to MCLR does not significantly induce cellular characteristics associated with a malignant and/or pro-fibrotic phenotype. In vivo, there were no significant changes in liver pathology, plasma chemistry, histology or tumor development compared to negative controls. Epidemiological analyses conducted at the national and provincial levels revealed similar trends. HCC incidence in Canada was associated with urban residence, immigration and hepatitis B. However, HCC incidence was not found to be influenced by the up-stream cyanobacterial predictive factors; agriculture, cattle and swine density. In Manitoba, the increasing incidence of liver cancer did not temporally or spatially associate with MCLR contamination sites within the province. In conclusion, these results are reassuring in that they suggest that chronic low-dose exposure to MCLR does not… Advisors/Committee Members: Minuk, Gerald (Pharmacology and Therapeutics) (supervisor), Leygue, Etienne (Biochemistry and Medical Genetics) Hatch, Grant (Pharmacology and Therapeutics) Holmes, Charles (University of Alberta) (examiningcommittee).

Subjects/Keywords: Cyanobacteria; Liver cancer; microcystin; Liver disease; water; cyanotoxin; drinking water; Manitoba

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

APA (6^th Edition):

Labine, M. (2014). Cyanobacterial toxins and liver cancer. (Thesis). University of Manitoba. Retrieved from http://hdl.handle.net/1993/23952

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

Chicago Manual of Style (16^th Edition):

Labine, Meaghan. “Cyanobacterial toxins and liver cancer.” 2014. Thesis, University of Manitoba. Accessed January 15, 2021. http://hdl.handle.net/1993/23952.

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

MLA Handbook (7^th Edition):

Labine, Meaghan. “Cyanobacterial toxins and liver cancer.” 2014. Web. 15 Jan 2021.

Vancouver:

Labine M. Cyanobacterial toxins and liver cancer. [Internet] [Thesis]. University of Manitoba; 2014. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1993/23952.

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

Council of Science Editors:

Labine M. Cyanobacterial toxins and liver cancer. [Thesis]. University of Manitoba; 2014. Available from: http://hdl.handle.net/1993/23952

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

University of Illinois – Urbana-Champaign

21. Chen, Yung-Ju. Dietary broccoli impedes Western diet-enhanced fatty liver and hepatocellular carcinoma development.

Degree: PhD, Food Science & Human Nutrition, 2015, University of Illinois – Urbana-Champaign

URL: http://hdl.handle.net/2142/89169

► Liver is the metabolic center for energy homeostasis in our body, maintaining a balance between carbohydrate and fat metabolism. The “Westernized” dietary pattern, which is… (more)

▼ Liver is the metabolic center for energy homeostasis in our body, maintaining a balance between carbohydrate and fat metabolism. The “Westernized” dietary pattern, which is known for high saturated fat and refined sugar and rooted in the lifestyle of a large proportion of the world’s population, may greatly disrupt energy balance, resulting in obesity and obesity-related diseases. Non-alcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma, which is also a possible endpoint of NAFLD, are both enhanced by adiposity and inflammation, and almost symptomless until serious damage is caused in liver. However, these diseases can be preventable, by changing lifestyle and diet. Broccoli, a well-accepted brassica vegetable in the United States, has the potential to reduce cancer risk and ameliorate inflammation. Therefore, in this study, we aimed to understand the impact of dietary broccoli on the development of NAFLD and liver cancer in mice fed a Western diet. Accordingly, we proposed a whole dietary broccoli intervention. A combined Western diet-fed and diethylnitrosamine (DEN)-treated mouse liver cancer models was used in order to evaluate the changes in hepatic lipidosis, macrophage activation, and tumorigenesis after long-term consumption of broccoli. Our results show that dietary broccoli decreased hepatic lipidosis as early as 3 months after initiation, and effectively down-regulated liver damage. The enlarged hepatic triglyceride pool due to the Western diet was narrowed by dietary broccoli, lowering the influx of non-esterified fatty acids but increasing the excretion of very-low-density lipoprotein. Activation of hepatic macrophages, was lowered by continues consumption of broccoli. Furthermore, DEN-induced liver tumor size and hepatic neoplasm-related lesion formation were both decreased by dietary broccoli. In addition, as an incidental finding, intraperitoneal DEN-induced nasal epithelial neoplasm-related lesions in B6C3F1 mice are first reported in this study. Overall, whole broccoli dietary intervention has the potential to impede the progression of NAFLD, from hepatic steatosis, through steatohepatitis, to hepatocellular carcinoma. This study fills gaps of knowledge about the impact of broccoli on hepatic lipid metabolism, supports the cancer preventive effect of brassicas revealed by epidemiologic studies, and further encourages the whole food dietary intervention. Translation to clinical studies is needed. Advisors/Committee Members: Jeffery, Elizabeth H. (advisor), Erdman, John W. (Committee Chair), Pan, Yuan-Xiang (committee member), Wallig, Matthew A. (committee member).

Subjects/Keywords: Broccoli; Western diet; Non-Alcoholic Fatty Liver Disease (NAFLD); Liver cancer

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

APA (6^th Edition):

Chen, Y. (2015). Dietary broccoli impedes Western diet-enhanced fatty liver and hepatocellular carcinoma development. (Doctoral Dissertation). University of Illinois – Urbana-Champaign. Retrieved from http://hdl.handle.net/2142/89169

Chicago Manual of Style (16^th Edition):

Chen, Yung-Ju. “Dietary broccoli impedes Western diet-enhanced fatty liver and hepatocellular carcinoma development.” 2015. Doctoral Dissertation, University of Illinois – Urbana-Champaign. Accessed January 15, 2021. http://hdl.handle.net/2142/89169.

MLA Handbook (7^th Edition):

Chen, Yung-Ju. “Dietary broccoli impedes Western diet-enhanced fatty liver and hepatocellular carcinoma development.” 2015. Web. 15 Jan 2021.

Vancouver:

Chen Y. Dietary broccoli impedes Western diet-enhanced fatty liver and hepatocellular carcinoma development. [Internet] [Doctoral dissertation]. University of Illinois – Urbana-Champaign; 2015. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/2142/89169.

Council of Science Editors:

Chen Y. Dietary broccoli impedes Western diet-enhanced fatty liver and hepatocellular carcinoma development. [Doctoral Dissertation]. University of Illinois – Urbana-Champaign; 2015. Available from: http://hdl.handle.net/2142/89169

University of Melbourne

22. KOH, SHIR LIN. The role of the renin-angiotensin system in liver regeneration and colorectal cancer liver metastases.

Degree: 2012, University of Melbourne

URL: http://hdl.handle.net/11343/37714

► Background: Colorectal cancer (CRC) is the second most common cause of cancer related death in Australia with over 4700 deaths reported annually. CRC liver metastasis… (more)

▼ Background: Colorectal cancer (CRC) is the second most common cause of cancer related death in Australia with over 4700 deaths reported annually. CRC liver metastasis (CRCLM) contributes to over 70% of the disease mortality. While unresected patients rarely survive beyond 2 years, partial hepatectomy (PH) improves their survival to 25%-60% at 5 years. Blockade of the renin-angiotensin system(RAS) has been shown to enhance liver regeneration and, separately, to inhibit CRCLM. Targeting the RAS may offer a unique synergistic anti-cancer therapy by inhibiting CRCLM tumour growth while simultaneously enhancing liver regeneration following PH. Aim: This study investigated the expression of the RAS during liver regeneration and in CRCLM. The effects of RAS blockade on liver regeneration and CRCLM in the regenerating liver were determined to investigate its potential benefits as a therapeutic avenue for CRCLM patients. Methods: Male CBA mice (10-12 weeks) were used in this study. After 70% partial hepatectomy (PH) alone, captopril (750mg/kg) or saline (control), were administered intraperitoneally on a daily basis until the endpoints (days 1, 2, 4, 6 and 8 post-surgery). A mouse model of CRCLM in the regenerating liver was developed. Mice induced with CRCLM and subjected to 70% PH were treated with captopril (250mg/kg) daily until the endpoints (days 2, 6, 16 and 21). At study endpoints, liver regeneration was assessed by measuring the liver-to-body weight ratio. CRCLM tumour burden (percentage of liver metastases) was calculated using total liver and tumour volumes using quantitative stereology. Liver function tests were performed on mouse serum collected from days 2 and 6. The expression of the RAS components, cell proliferation, apoptosis, hepatic stellate cells (HSC) and liver endothelial cell densities, matrix metalloproteinase (MMP)-9, transforming growth factor (TGF)-β were quantified. Statistical analyses were performed using 2-sample independent T-test, one-way ANOVA with post-hoc analysis, or Kruskal Wallis followed by Mann-Whitney U tests as appropriate (SPSS v.18). P-value of <0.05 was considered statistically significant. Results: Captopril significantly inhibited CRCLM tumour growth and increased tumour cell apoptosis in the regenerating liver at day 21. Captopril also enhanced early liver regeneration and this was associated with an increase in hepatocyte proliferation at 6 hours after PH as well as an increase in HSC density and MMP-9 levels 2 days after PH. The decrease in hepatocyte proliferation at day 2 was transient. By day 4 onwards there was no significant difference between control and treated livers. Captopril also decreased the hepatocyte injury marker, alanine transaminase. The ability of captopril to increase human hepatocyte proliferation was confirmed in vitro. The RAS was expressed in the liver and tumours during liver regeneration and tumour growth phases.…

Subjects/Keywords: renin-angiotensin system; liver regeneration; colorectal cancer liver metastases

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

APA (6^th Edition):

KOH, S. L. (2012). The role of the renin-angiotensin system in liver regeneration and colorectal cancer liver metastases. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/37714

Chicago Manual of Style (16^th Edition):

KOH, SHIR LIN. “The role of the renin-angiotensin system in liver regeneration and colorectal cancer liver metastases.” 2012. Doctoral Dissertation, University of Melbourne. Accessed January 15, 2021. http://hdl.handle.net/11343/37714.

MLA Handbook (7^th Edition):

KOH, SHIR LIN. “The role of the renin-angiotensin system in liver regeneration and colorectal cancer liver metastases.” 2012. Web. 15 Jan 2021.

Vancouver:

KOH SL. The role of the renin-angiotensin system in liver regeneration and colorectal cancer liver metastases. [Internet] [Doctoral dissertation]. University of Melbourne; 2012. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/11343/37714.

Council of Science Editors:

KOH SL. The role of the renin-angiotensin system in liver regeneration and colorectal cancer liver metastases. [Doctoral Dissertation]. University of Melbourne; 2012. Available from: http://hdl.handle.net/11343/37714

University of Southern California

23. Chen, Wan-Ting. The roles of endoplasmic reticulum chaperones in regulating liver homeostasis and tumorigenesis.

Degree: PhD, Genetic, Molecular and Cellular Biology, 2014, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/459118/rec/7284

► Cancer progression is characterized by the overriding of growth arrest and rapid cell proliferation, which require increased protein synthesis. Additionally, the poor vascularization of cancer… (more)

▼ Cancer progression is characterized by the overriding of growth arrest and rapid cell proliferation, which require increased protein synthesis. Additionally, the poor vascularization of cancer tissues leads to glucose deprivation and hypoxia. Therefore, the tumor microenvironment represents physiological endoplasmic reticulum (ER) stress and activates the unfolded protein response (UPR) for survival. ER stress has been linked to a variety of human diseases, including liver steatosis and different cancers, and the conventional function of ER chaperones in protein quality control is updated to promote tumor progression, metastasis, and drug resistance. ❧ Liver cancer is one of the most common solid tumors with poor prognosis and high mortality. 40-50% of liver cancer patients have the tumor suppressor PTEN mutations or deletion, whereas the two major ER chaperones, glucose‐regulated protein 94 (GRP94) and glucose‐regulated protein 78 (GRP78), have been shown to be overexpressed in liver cancer. Thus, in this dissertation we established multiple mouse models with liver‐specific deletion of Grp94 (cGrp94ᶠ/ᶠ) or Grp78 alone (cGrp78ᶠ/ᶠ) or in combination with Pten (cPᶠ/ᶠ94ᶠ/ᶠ or cPᶠ/ᶠ78ᶠ/ᶠ) to investigate the roles of GRP94 and GRP78 in liver cancer development. First, we demonstrated that while deletion of GRP94 in the liver led to hyperproliferation of liver progenitor cells (LPCs), deletion of both GRP94 and PTEN accelerated development of liver tumors, including both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC), suggestive of progenitor cell origin. Moreover, at the premalignant stage, disturbance of cell adhesion proteins and minor liver injury were observed. When GRP94 was deleted in Pten‐null livers, ERK was selectively activated. ❧ Next, we further explored the long‐term effect of GRP94 deletion on liver tumorigenesis. cGrp94ᶠ/ᶠ livers showed small nodules at 15 months and spontaneously developed HCC and ductular reactions (DRs) by 21 months, associating with increased liver injury and fibrosis. Interestingly, GRP94‐positive hepatocytes progressively repopulated cGrp94ᶠ/ᶠ livers. At 15 months, we observed expansion of LPCs and mild DRs, as well as increase in cell proliferation. Analysis of signaling pathways revealed TGF‐β1 upregulaion, SMAD2/3, ERK, and JNK activation, and cyclin D1 upregulation in cGrp94ᶠ/ᶠ livers. The HCC was found to be GRP94‐positive, whereas the expanded LPCs and DRs remained GRP94‐negative. ❧ Interestingly, hepatic deletion of Grp78 led to a different story. Ablation of GRP78 was progressive but incomplete. At 3 months, cPᶠ/ᶠ78ᶠ/ᶠ livers showed lipogenic gene activation, exacerbated steatosis, and liver injury. In response to liver injury, increased proliferation of bile duct cells and LPCs was observed in cPᶠ/ᶠ78ᶠ/ᶠ livers, and GRP78 expression was intact in bile ducts and some LPCs. At 6 months, cPᶠ/ᶠ78ᶠ/ᶠ livers exhibited JNK activation, β‐catenin downregulation, along with PDGFRα upregulation. HCC and CC development was accelerated and evident in cPᶠ/ᶠ78ᶠ/ᶠ livers at 8-9… Advisors/Committee Members: Lee, Amy S. (Committee Chair), Stiles, Bangyan L. (Committee Member), Machida, Keigo (Committee Member).

Subjects/Keywords: ER chaperones; GRP94; GRP78; liver cancer; liver progenitor cells

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

APA (6^th Edition):

Chen, W. (2014). The roles of endoplasmic reticulum chaperones in regulating liver homeostasis and tumorigenesis. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/459118/rec/7284

Chicago Manual of Style (16^th Edition):

Chen, Wan-Ting. “The roles of endoplasmic reticulum chaperones in regulating liver homeostasis and tumorigenesis.” 2014. Doctoral Dissertation, University of Southern California. Accessed January 15, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/459118/rec/7284.

MLA Handbook (7^th Edition):

Chen, Wan-Ting. “The roles of endoplasmic reticulum chaperones in regulating liver homeostasis and tumorigenesis.” 2014. Web. 15 Jan 2021.

Vancouver:

Chen W. The roles of endoplasmic reticulum chaperones in regulating liver homeostasis and tumorigenesis. [Internet] [Doctoral dissertation]. University of Southern California; 2014. [cited 2021 Jan 15]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/459118/rec/7284.

Council of Science Editors:

Chen W. The roles of endoplasmic reticulum chaperones in regulating liver homeostasis and tumorigenesis. [Doctoral Dissertation]. University of Southern California; 2014. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/459118/rec/7284

University of Cambridge

24. Mastrogiovanni, Gianmarco. Establishment of new human and mouse liver cancer models and their use to uncover the role of RNF43 and ZNRF3 in liver homeostasis and repair.

Degree: PhD, 2018, University of Cambridge

URL: https://doi.org/10.17863/CAM.20368 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.745022

► Primary liver cancer (PLC) is the second most common cause of cancer death worldwide, preceded only by lung cancer. Current models for PLC either fail… (more)

▼ Primary liver cancer (PLC) is the second most common cause of cancer death worldwide, preceded only by lung cancer. Current models for PLC either fail to fully recapitulate tumour histology and architecture or are expensive, time consuming and do not allow for personalised drug testing. During the first part of my PhD, I have collaborated with Dr. Laura Broutier in order to established a new 3D in vitro model system for liver cancer. Based on the current knowledge on organoid cultures, we have managed to establish a system to grow primary human liver cancer cells long-term (Broutier et al., in press). Interestingly, the tumour-derived organoids (tumoroids) recapitulate the original tumour histology and genetic alterations and are also able to generate tumours in an in vivo xenograft mouse model after long-term expansion. Furthermore, we have shown that tumoroids can also be successfully used for drug testing, suggesting their use to devise new targeted therapy as well as personalised treatment strategies. Current models to investigate the role of genes in cancer rely mostly on animal studies, which can be very time consuming and cost demanding, especially if resulting in negative outcomes. To overcome this issue, I have set up a protocol for introducing mutations in healthy human liver organoids using the CRISPR-Cas9 technology. Interestingly, after mutating TP53, RNF43 and ZNRF3 either alone or in combination, human organoids undergo genetic alterations and phenotypic changes that partially resemble the ones observed in tumoroids. This data suggests that this system could be used as a screening platform to study gene function before using animal models. In the last part, I have further explored the role of RNF43 and ZNRF3 (R&Z) - two newly identified WNT pathway negative regulators mutated in many cancer types - in the liver using an in vivo mouse model. Interestingly, conditional deletion of R&Z specifically in adult mouse hepatocytes results metabolic changes that eventually lead to extensive liver damage. However, when the liver is challenged to regenerate in a chronic damage model, R&Z mutated livers fail to fully repair and show presence of multiple regenerative nodules. Later, livers develop either focal nodular hyperplasia and/or early hepatocellular carcinoma. These data suggest that R&Z have an important role in both liver metabolic homeostasis and liver regeneration and that their alteration can eventually lead to cancer formation.

Subjects/Keywords: 616.99; Rnf43; Znrf3; Liver cancer model; liver; crispr; organoids; tumoroids

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APA (6^th Edition):

Mastrogiovanni, G. (2018). Establishment of new human and mouse liver cancer models and their use to uncover the role of RNF43 and ZNRF3 in liver homeostasis and repair. (Doctoral Dissertation). University of Cambridge. Retrieved from https://doi.org/10.17863/CAM.20368 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.745022

Chicago Manual of Style (16^th Edition):

Mastrogiovanni, Gianmarco. “Establishment of new human and mouse liver cancer models and their use to uncover the role of RNF43 and ZNRF3 in liver homeostasis and repair.” 2018. Doctoral Dissertation, University of Cambridge. Accessed January 15, 2021. https://doi.org/10.17863/CAM.20368 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.745022.

MLA Handbook (7^th Edition):

Mastrogiovanni, Gianmarco. “Establishment of new human and mouse liver cancer models and their use to uncover the role of RNF43 and ZNRF3 in liver homeostasis and repair.” 2018. Web. 15 Jan 2021.

Vancouver:

Mastrogiovanni G. Establishment of new human and mouse liver cancer models and their use to uncover the role of RNF43 and ZNRF3 in liver homeostasis and repair. [Internet] [Doctoral dissertation]. University of Cambridge; 2018. [cited 2021 Jan 15]. Available from: https://doi.org/10.17863/CAM.20368 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.745022.

Council of Science Editors:

Mastrogiovanni G. Establishment of new human and mouse liver cancer models and their use to uncover the role of RNF43 and ZNRF3 in liver homeostasis and repair. [Doctoral Dissertation]. University of Cambridge; 2018. Available from: https://doi.org/10.17863/CAM.20368 ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.745022

NSYSU

25. Wu, Cian-rong. The relationship between C-reactive protein and hepatoma-derived growth factor in hepatoma carcinoma cell lines.

Degree: Master, Biological Sciences, 2014, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0726114-095757

► Hepatocellular carcinoma (HCC) is one of the most common malignancy and known as country disease in Taiwan. Hepatoma-derived growth factor (HDGF), a mitogen for various… (more)

Subjects/Keywords: HDGF; Liver cancer; nucleolin; CRP; CD64

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

APA (6^th Edition):

Wu, C. (2014). The relationship between C-reactive protein and hepatoma-derived growth factor in hepatoma carcinoma cell lines. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0726114-095757

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

Chicago Manual of Style (16^th Edition):

Wu, Cian-rong. “The relationship between C-reactive protein and hepatoma-derived growth factor in hepatoma carcinoma cell lines.” 2014. Thesis, NSYSU. Accessed January 15, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0726114-095757.

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

MLA Handbook (7^th Edition):

Wu, Cian-rong. “The relationship between C-reactive protein and hepatoma-derived growth factor in hepatoma carcinoma cell lines.” 2014. Web. 15 Jan 2021.

Vancouver:

Wu C. The relationship between C-reactive protein and hepatoma-derived growth factor in hepatoma carcinoma cell lines. [Internet] [Thesis]. NSYSU; 2014. [cited 2021 Jan 15]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0726114-095757.

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

Council of Science Editors:

Wu C. The relationship between C-reactive protein and hepatoma-derived growth factor in hepatoma carcinoma cell lines. [Thesis]. NSYSU; 2014. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0726114-095757

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

University of Hong Kong

26. Tsang, Ho-ching, Felice. Identification of ankyrin repeats and SOCS box protein 4 (ASB4) as oncogenic biomarker in liver cancer.

Degree: 2008, University of Hong Kong

URL: http://hdl.handle.net/10722/52077

Subjects/Keywords: Liver - Cancer.; Carcinogens.

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

APA (6^th Edition):

Tsang, Ho-ching, F. (2008). Identification of ankyrin repeats and SOCS box protein 4 (ASB4) as oncogenic biomarker in liver cancer. (Thesis). University of Hong Kong. Retrieved from http://hdl.handle.net/10722/52077

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

Chicago Manual of Style (16^th Edition):

Tsang, Ho-ching, Felice. “Identification of ankyrin repeats and SOCS box protein 4 (ASB4) as oncogenic biomarker in liver cancer.” 2008. Thesis, University of Hong Kong. Accessed January 15, 2021. http://hdl.handle.net/10722/52077.

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

MLA Handbook (7^th Edition):

Tsang, Ho-ching, Felice. “Identification of ankyrin repeats and SOCS box protein 4 (ASB4) as oncogenic biomarker in liver cancer.” 2008. Web. 15 Jan 2021.

Vancouver:

Tsang, Ho-ching F. Identification of ankyrin repeats and SOCS box protein 4 (ASB4) as oncogenic biomarker in liver cancer. [Internet] [Thesis]. University of Hong Kong; 2008. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/10722/52077.

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

Council of Science Editors:

Tsang, Ho-ching F. Identification of ankyrin repeats and SOCS box protein 4 (ASB4) as oncogenic biomarker in liver cancer. [Thesis]. University of Hong Kong; 2008. Available from: http://hdl.handle.net/10722/52077

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

University of Rochester

27. Alexander, William B. Oncogenic Mutations and Injury in the Mouse Liver.

Degree: PhD, 2018, University of Rochester

URL: http://hdl.handle.net/1802/34355

► Chronic injury and inflammation are among the most established determinants of cancer risk, and the myriad of factors that contribute to this association is an… (more)

▼ Chronic injury and inflammation are among the most established determinants of cancer risk, and the myriad of factors that contribute to this association is an active area of investigation. A key aspect of injury is the consequent regenerative and proliferative response. Understanding the mechanisms which restrain these proliferative processes and how these controls can be bypassed may shed light on the processes that drive early cancer development. Focusing on the mouse liver as a model tissue, we sought to determine how common oncogenic mutations impact the ductular reaction, the liver’s response to injury and one of the earliest events in cholangiocarcinoma development. Here we identify, among the most commonly mutated genes in cholangiocarcinoma, a uniquely critical role for the tumor suppressor Smad4 in restraining proliferation of ductular reactive cells, the biliary/epithelial compartment of the ductular reaction. Experiments testing the tumor suppressive role of Smad4 in mouse liver revealed a complex role as a suppressor of hepatocellular carcinoma, cholangiocarcinoma, and biliary cyst development. Focusing on Smad4’s role in the ductular reaction, we identify an IGF activation signature in Smad4-perturbed ductular reactive cells and in SMAD4-mutant cancers that is potentially mediated by SMAD4-regulated transcription of IGF binding proteins, key inhibitors of IGF signaling. This study therefore importantly links a key tumor suppressive pathway to regulation of the injury response, thereby shedding light on the earliest events in cancer development. In a related project, we sought to understand the cellular origins of cholangiocarcinoma. Hepatocytes and biliary epithelial cells may both be potential cells of origin for cholangiocarcinoma, although the contexts in which this has been demonstrated are limited. For example, although hepatocytes can be cells of origin in the setting of active Notch signaling, a key driver of biliary differentiation, Notch pathway mutations are not common events in human cases; therefore, it remains unknown if common genetic lesions identified in human cholangiocarcinoma are sufficient to promote hepatocyte-derived cholangiocarcinoma. To shed light on these matters, we demonstrate that targeting Kras and Tp53 mutations, two of the most common mutations in human cholangiocarcinoma, to the SOX9+ biliary compartment promotes cholangiocarcinoma development. Similarly, targeting these mutations to the hepatocyte compartment can lead to cholangiocarcinoma development in the setting of injury. We further establish that Tp53 in particular has a critical function in restricting reprogramming of hepatocytes to biliary epithelial cells, a role that likely enables hepatocyte-derived iCCA when it is mutated. Finally, mirroring what has been observed in other biliary tract-derived models, we observed active Notch and Wnt signaling in our hepatocyte-derived model, suggesting hepatocyte-derived cholangiocarcinoma may have similar programming regarding these important targetable pathways.…

Subjects/Keywords: Liver; Injury; Cancer; Cholangiocarcinoma; SMAD4; TP53

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

APA (6^th Edition):

Alexander, W. B. (2018). Oncogenic Mutations and Injury in the Mouse Liver. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/34355

Chicago Manual of Style (16^th Edition):

Alexander, William B. “Oncogenic Mutations and Injury in the Mouse Liver.” 2018. Doctoral Dissertation, University of Rochester. Accessed January 15, 2021. http://hdl.handle.net/1802/34355.

MLA Handbook (7^th Edition):

Alexander, William B. “Oncogenic Mutations and Injury in the Mouse Liver.” 2018. Web. 15 Jan 2021.

Vancouver:

Alexander WB. Oncogenic Mutations and Injury in the Mouse Liver. [Internet] [Doctoral dissertation]. University of Rochester; 2018. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1802/34355.

Council of Science Editors:

Alexander WB. Oncogenic Mutations and Injury in the Mouse Liver. [Doctoral Dissertation]. University of Rochester; 2018. Available from: http://hdl.handle.net/1802/34355

University of Alberta

28. Pant, Asha. Alteration of liver fat metabolism following irinotecan plus 5-fluorouracil treatment.

Degree: MS, Department of Agricultural, Food and Nutritional Science, 2011, University of Alberta

URL: https://era.library.ualberta.ca/files/qj72p851d

► This study determined how chemotherapy treatment for colorectal cancer alters hepatic fat metabolism. Livers were isolated from tumor-bearing animals after one and two cycles of… (more)

Subjects/Keywords: liver fat metabolism; chemotherapy; colorectal cancer

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

APA (6^th Edition):

Pant, A. (2011). Alteration of liver fat metabolism following irinotecan plus 5-fluorouracil treatment. (Masters Thesis). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/qj72p851d

Chicago Manual of Style (16^th Edition):

Pant, Asha. “Alteration of liver fat metabolism following irinotecan plus 5-fluorouracil treatment.” 2011. Masters Thesis, University of Alberta. Accessed January 15, 2021. https://era.library.ualberta.ca/files/qj72p851d.

MLA Handbook (7^th Edition):

Pant, Asha. “Alteration of liver fat metabolism following irinotecan plus 5-fluorouracil treatment.” 2011. Web. 15 Jan 2021.

Vancouver:

Pant A. Alteration of liver fat metabolism following irinotecan plus 5-fluorouracil treatment. [Internet] [Masters thesis]. University of Alberta; 2011. [cited 2021 Jan 15]. Available from: https://era.library.ualberta.ca/files/qj72p851d.

Council of Science Editors:

Pant A. Alteration of liver fat metabolism following irinotecan plus 5-fluorouracil treatment. [Masters Thesis]. University of Alberta; 2011. Available from: https://era.library.ualberta.ca/files/qj72p851d

Drexel University

29. Shah, Arpit. Elucidating the Effects of Interstitial Fluid Flow on Hepatocellular Carcinoma Invasion.

Degree: 2017, Drexel University

URL: http://hdl.handle.net/1860/idea:7584

► Over the last two decades with advancements in research, detection, and treatment of all cancer types in the United States, resulting in an overall 23%… (more)

▼ Over the last two decades with advancements in research, detection, and treatment of all cancer types in the United States, resulting in an overall 23% decrease in cancer related deaths, liver cancer has gone against this trend possessing an increased death rate. Globally, hepatocellular carcinoma (HCC), the most common form of liver cancer, ranks as the second leading cause of cancer related deaths with approximately 788,000 deaths annually. In recent years much emphasis has been placed on understanding the process of HCC cell invasion; however, it has become apparent that the progression of this disease is not solely dependent on just the cancer cells or biological factors, but also their interaction with the tumor microenvironment. A significant number of studies have shown that changes in biomechanical forces within the tumor microenvironment can alter cancer progression. Previous research has demonstrated that interstitial fluid flow (IFF), one of the biomechanical forces that is altered during tumor growth, can promote cancer cell invasion. The findings in this work elucidate the effects of IFF in HCC cell invasion. Using our 3D in vitro flow invasion assay, we demonstrate that IFF increases cellular invasion through autologous gradient formation of chemokines (CXCR4/CXCL12) that promote migration, a mechanism known as autologous chemotaxis. We also demonstrated that MEK/ERK signaling affects IFF-induced invasion; however, this pathway was separate from CXCR4/CXCL12 signaling. Increased matrix metalloproteinase (MMP) expression is a hallmark for cancer progression and poor prognosis. Biomechanical forces have been observed to increase the secretion of these proteolytic enzymes, which promote extracellular matrix degradation and tumor cell invasion. We observed an increase in MMP-9 and MMP-2 activity in HCC cells exposed to IFF. In total these findings indicate multiple mechanisms are at play in HCC flow-induced invasion, further emphasizing the significance biomechanical forces play in disease progression. Finally, by modifying our 3D in vitro flow invasion assay, we examined IFF in a relevant cell-based disease model where HCC cells are embedded in a stiff matrix. The increase in matrix stiffness is a result of tumor growth, shown to disturb the mechanical forces and biochemical signaling that occurs in the microenvironment, effectively promoting disease progression. HCC also possesses a very unique disease profile and risk factors; nearly 80% of HCCs occur from patients who suffer from chronic fibrosis or cirrhosis, where inflammation and hepatic wound-healing response attributes to the hepatocarcinogenesis. Many studies have observed cellular behavior of hepatocytes and HCC cells in a stiff matrix; however, none have observed the effect of IFF and a stiff microenvironment in HCC cells. The findings in this chapter confirm a synergistic relationship between IFF and matrix stiffness on HCC cell invasion. Ultimately the findings in this study provide a better foundational and mechanistic understanding of IFF… Advisors/Committee Members: Shieh, Adrian, School of Biomedical Engineering, Science, and Health Systems.

Subjects/Keywords: Biomedical engineering; Biomechanics; Liver – Cancer; Extracellular fluid

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

APA (6^th Edition):

Shah, A. (2017). Elucidating the Effects of Interstitial Fluid Flow on Hepatocellular Carcinoma Invasion. (Thesis). Drexel University. Retrieved from http://hdl.handle.net/1860/idea:7584

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

Chicago Manual of Style (16^th Edition):

Shah, Arpit. “Elucidating the Effects of Interstitial Fluid Flow on Hepatocellular Carcinoma Invasion.” 2017. Thesis, Drexel University. Accessed January 15, 2021. http://hdl.handle.net/1860/idea:7584.

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

MLA Handbook (7^th Edition):

Shah, Arpit. “Elucidating the Effects of Interstitial Fluid Flow on Hepatocellular Carcinoma Invasion.” 2017. Web. 15 Jan 2021.

Vancouver:

Shah A. Elucidating the Effects of Interstitial Fluid Flow on Hepatocellular Carcinoma Invasion. [Internet] [Thesis]. Drexel University; 2017. [cited 2021 Jan 15]. Available from: http://hdl.handle.net/1860/idea:7584.

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

Council of Science Editors:

Shah A. Elucidating the Effects of Interstitial Fluid Flow on Hepatocellular Carcinoma Invasion. [Thesis]. Drexel University; 2017. Available from: http://hdl.handle.net/1860/idea:7584

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

Université Paris-Sud – Paris XI

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

APA (6^th 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 (16^th 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 (7^th 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

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Open Access Theses and Dissertations