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Studies of liver cancers in man and in rats, with special reference totheir fine structure as seen by electron microscopyMa, Tung, Lily., 馬童麗麗. January 1977 (has links)
published_or_final_version / Pathology / Doctoral / Doctor of Philosophy
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Mechanism of spontaneous rupture of hepatocellular carcinoma朱立新, Zhu, Lixin. January 1998 (has links)
published_or_final_version / Surgery / Doctoral / Doctor of Philosophy
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Radiofrequency ablation of hepatocellular carcinoma: identifying prognostic factors in long-term survivaloutcome張飛泉, Tzang, Fei-chuen. January 2008 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
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The impact of heat on hepatocellular carcinoma (HCC)龔衍峰, Kung, Hin-fung, Tony. January 2008 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
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The characterization of PAK 6 in liver cancerFung, Wai-yip, 馮偉業 January 2009 (has links)
published_or_final_version / Pathology / Master / Master of Medical Sciences
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Patho-biological prognostic factors in hepatocellular carcinoma /Ng, Oi-lin, Irene. January 1994 (has links)
Thesis (M.D.)--University of Hong Kong, 1994. / Includes bibliographical references (leaves 143-173).
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Patho-biological prognostic factors in hepatocellular carcinomaNg, Oi-lin, Irene. January 1994 (has links)
Thesis (M.D.)--University of Hong Kong, 1994. / Includes bibliographical references (leaves 143-173) Also available in print.
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Resection margin for hepatocellular carcinoma黎卓先, Lai, Cheuck-seen, Edward. January 1992 (has links)
published_or_final_version / abstract / Surgery / Master / Master of Surgery
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Identification and characterization of novel genetic alterations in the progression of hepatocellular carcinomaLiu, Ming, 劉銘 January 2013 (has links)
Hepatocellular carcinoma (HCC) is one of the most frequent human malignancies worldwide with very poor prognosis. It is generally believed that accumulation of irreversible alterations in critical oncogenes and tumor suppressor genes during the long-term inflammation finally leads to the hepatocellular pathogenesis. Although under intensive investigation, the molecular pathogenesis of HCC still remains to be further elucidated.
In this study, we aimed to identify novel genetic alterations critical to the pathogenesis of HCC, especially in hot regions with recurrent chromosomal instability. Amplification of broad regions of 8q is one of the most frequent genetic alterations in HCC, suggesting the existence of oncogenes in addition to MYC at 8q24. By screening the publicly available microarray database and clinical samples, we found frequent amplification and overexpression of Serum and Glucocorticoid Kinase 3 (SGK3) in clinical HCC specimens, and SGK3 genomic activation was significantly associated with poor outcome of HCC patients. Functional assays revealed that SGK3 could increase G1/S cell cycle progression, cell survival, clonogenicity, anchorage-independent growth, and tumor formation in nude mice. We provided evidences that SGK3 could promote HCC growth and survival through inactivating GSK3-β and BAD respectively. We also found that expression of SGK3, which like AKT is activated by PI3K/PDK1, has more significance than overexpression of AKT in predicting poor outcome of HCC patients. Our findings suggested the existence of an AKT-independent SGK3 pathway, which may function in parallel with AKT pathway in the pathogenesis of HCC. In addition to large chromosomal alterations, small changes in nucleotides may also make substantial contributions to carcinogenesis. Recent advances in high-throughput deep sequencing technology have provided a powerful tool to understand the whole cancer transcriptome and identify novel genetic alterations related to cancer progression. In this study, we identified a high proportion of allele imbalance in genes related to cellular stress response by sequencing the whole transcriptome of 3 paired HCC tissues. A novel nucleotide variation which resulted in a R438H amino acid change was identified in the coding region of the gene Oxidative Stress Induced Growth Inhibitor 1 (OSGIN1), and the variant 438H form of OSGIN1 was found to be specifically retained in the tumor tissues in a cohort of HCC patients. OSGIN1 was found to be closely associated with chemotherapeutic reagents and exhibited strong tumor suppressive function in HCC by directly inducing cell apoptosis. The wild type OSGIN1 was found to have stronger tumor suppressive function than the variant allele, and this might be due to their different ability to localize to mitochondria. The significantly decreased basal apoptotic index in HCC patients carrying OSGIN1 variant allele and their poor prognosis further suggested that the specific retention of 438H OSGIN1 might be important in HCC progression.
In summary, we found a frequently amplified oncogenic SGK3 signaling pathway, as well as the allele-specific imbalance of tumor suppressive OSGIN1 in the pathogenesis of HCC. Further characterization of their mechanisms in hepatocarcinogenesis may help provide novel prognostic biomarkers and therapeutic targets in HCC treatment. / published_or_final_version / Clinical Oncology / Doctoral / Doctor of Philosophy
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Patho-biological prognostic factors in hepatocellular carcinomaNg, Oi-lin, Irene., 呂愛蓮 January 1994 (has links)
published_or_final_version / Medicine / Master / Doctor of Medicine
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