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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.

Characterization of phospholipid transfer protein (PLTP) in hepatocellular carcinoma

盧家健, Lo, Ka-kin. January 2007 (has links)
published_or_final_version / abstract / Surgery / Master / Master of Philosophy

The effect of AMN107 on hepatocellular carcinoma

Lui, Lik-hang, Eric, 雷力恆 January 2007 (has links)
published_or_final_version / abstract / Surgery / Master / Master of Philosophy

Novel role of drug-induced non homologous end joining factor 1 in the chemoresistance of hepatocellular carcinoma

Yang, Sitian, 楊斯恬 January 2015 (has links)
abstract / Surgery / Doctoral / Doctor of Philosophy

The role of GEP on chemotherapy induced alterations in hepatocellular carcinoma

Wong, Chung-lim, 黃仲廉 January 2013 (has links)
Hepatocellular carcinoma (HCC) is the fifth most common malignancy and the third leading cause of cancer related death worldwide. Chemo-therapy has been commonly used to treat unresectable HCC but with limited efficacy. Therefore, there is an urgent demand for the development of better therapeutic approaches. Granulin-epithelin precursor (GEP) is a novel growth factor with over-expression in more than 70% of HCCs and has been demonstrated as potential therapeutic target. The aims of this study are to examine the role of GEP in chemo-resistance and the therapeutic potential of GEP antibody therapy in combination with chemo-therapy in HCC. The role of GEP in HCC chemo-resistance has been examined by HCC in vitro models in the first part of the study and by in vivo human HCC xenograft models in immunocompromised mice in the second part of the study. It was shown that the chemo-therapeutic agents selected HCC cells in vitro and in vivo resulted in increased cellular expression of GEP, ABCB5, hepatic cancer stem cell (CSC) marker CD133/EpCAM positive populations and demonstrated enhanced CSCs properties including colony formation ability and chemo-resistance. Over-expression and knockdown of GEP expressions respectively demonstrated that GEP levels were important in conferring resistance to the chemo-therapeutic agents and the drug-induced apoptosis. GEP antibody therapy not only sensitized the parental HCC populations but also the chemo-resistant subpopulations to chemo-therapy induced apoptosis. Importantly, combination of GEP antibody therapy with chemo-therapy inhibited the chemo-therapy induced GEP, ABCB5 and heaptic CSCs marker over-expression through neutralization of the secretary GEP levels in the culture supernatant, and the serum GEP levels in the HCC orthotopic mice model. In human HCC xenograft models, GEP antibody treatment alone is consistently able to inhibit the tumor growth, but is unable to eliminate the established intrahepatic tumor. Cisplatin treatment, low and high dose respectively, was only able to eradicate a fraction of the intrahepatic tumor and the residual tumors grew aggressively after chemo-drug withdrawal. Combination of GEP antibody with low dose of cisplatin resulted in significant proliferation inhibition and apoptosis induction respectively. Importantly, combination of GEP antibody with high dose of cisplatin resulted in eradication of all established intrahepatic tumor. In addition, chemo-therapy induced the Akt/PKB and MEK/ERK prosurvival pathways, disturbed the balanced between the ratio of pro-apoptotic (Bax) to anti-apoptotic (Bcl-2) member through the induction of Bcl-2. Nonetheless, combination GEP antibody therapy suppressed the chemo-therapy induced phosphorylation of PDK1, Akt, MEK, ERK, and Bcl-2 levels. It was shown that Wortmannin, the PI3K/Akt inhibitor, suppressed the expression of ABCB5 and Bcl-2 induced by chemo-therapy but showed no effect on GEP expression levels. In summary, the study demonstrated the chemo-therapy treatment alone induced the expression of growth factor GEP, drug transporter ABCB5, hepatic cancer stem cell markers expressions, and the residual cancer cells showed enhanced CSCs properties. Combination treatment with GEP antibody reversed the signaling and cancer stem cell properties induced by chemo-therapy alone. Therefore, further investigations of this combination treatment approach may lead to the development of novel therapeutic approach for the clinical treatment of chemo-resistant HCC. / published_or_final_version / Surgery / Doctoral / Doctor of Philosophy

Signaling pathways modulated by gold-1A in its anti-tumour effects against hepatocellular carcinoma

Li, Hoi-yee., 李凱怡. January 2006 (has links)
published_or_final_version / abstract / Chemistry / Master / Master of Philosophy

Study of mammalian target of rapamycin (mTOR) signaling and the effects of its specific inhibitors in hepatocellular carcinoma

Hui, Chun-fai, Ivan., 許振輝. January 2007 (has links)
published_or_final_version / abstract / Pathology / Master / Master of Philosophy

Targeting mTOR as a novel therapeutic strategy for hepatocellular carcinoma

Tam, Ka-ho, Chris, 譚家豪 January 2006 (has links)
published_or_final_version / Surgery / Master / Master of Philosophy

FTY720, a novel pharmaceutical therapy for hepatocellular carcinoma

Lee, Kin-wah, Terence, 李建華 January 2004 (has links)
published_or_final_version / abstract / toc / Molecular Biology / Doctoral / Doctor of Philosophy

Blockade of hypoxia inducible factor-1α sensitizes hepatocellular carcinoma to hypoxia and chemotherapy

Lau, Chi-keung, 劉智強 January 2008 (has links)
published_or_final_version / abstract / Surgery / Doctoral / Doctor of Philosophy

The role of proline rich tyrosine kinase 2 (Pyk2) on cisplatin resistance in HCC

Geng, Wei, 耿瑋 January 2009 (has links)
published_or_final_version / Surgery / Master / Master of Philosophy

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