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Immunoglobulin gene translocations in gastric lymphomaYip, Bon-ham. January 2006 (has links)
Thesis (M. Phil.)--University of Hong Kong, 2006. / Title proper from title frame. Also available in printed format.
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Development of antigenic tumors in tumor progression and endogenous IFN[Greek letter gamma] pathway in suppression of tumor growth by TNF /Wu, Terry Hung-Ta. January 2001 (has links)
Thesis (Ph. D.)--University of Chicago, Dept. of Pathology, December 2001. / Includes bibliographical references. Also available on the Internet.
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Epigenetic regulation of gene expression of cystatin 6, CST6, in hepatocellular carcinomaMa, Ka-li, Marcella, 馬嘉莉 January 2005 (has links)
published_or_final_version / Medical Sciences / Master / Master of Medical Sciences
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NotI microarrays for identification of chromosome 3 methylation signatures in nasopharyngeal carcinoma (NPC) and esophageal squamouscell carcinoma (ESCC)Law, Wai-lok., 羅韋洛. January 2010 (has links)
published_or_final_version / Clinical Oncology / Master / Master of Philosophy
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Identification and characterization of tumor suppressive gene and microRNA in esophageal squamous cell carcinomaKong, Kar-lok., 江家樂. January 2011 (has links)
published_or_final_version / Clinical Oncology / Doctoral / Doctor of Philosophy
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Promoter DNA methylation of tumour suppressor microRNA genes in multiple myelomaWong, Kwan-yeung., 黃君揚. January 2011 (has links)
Multiple myeloma (MM) is an incurable haematological malignancy. It is
characterized clinically by an asymptomatic precursor stage, known as monoclonal
gammopathy of undetermined significance (MGUS), which will transform into
symptomatic MM at a rate of 1% per year. Gene promoter hypermethylation by
catalytic conversion of cytosine into 5?methylcytosine at promoter?associated CpG
island is an alternative mechanism of gene inactivation. MicroRNA (miRNA) is a class of
short, single?stranded, non?coding RNA molecules, which will repress the expression of
target protein by sequence?specific binding to the three prime untranslated region of
the corresponding messenger RNA. In carcinogenesis, miRNA can be either oncogenic
when tumour suppressor genes are targeted, or tumour suppressive when oncogenes
are targeted. Despite reports of hypermethylation of multiple protein?coding tumour
suppressor genes, little is known about DNA methylation of non?coding tumour
suppressor miRNA genes in MM.
This thesis aimed to investigate the role of promoter hypermethylation of tumour
suppressor miRNA genes in MM using a candidate miRNA approach. Moreover, the
prognostic significance of tumour suppressor miRNA hypermethylation was studied in
a uniformly?treated cohort of MM patients.
The role of DNA methylation at the promoter of miR?203, miR?34a, miR?34b/c,
miR?124?1, miR?129?2 and miR?224 were studied in MM. The tumour suppressor role
of miR?34b/c, miR?124?1, miR?203 and miR?224 were demonstrated in human
myeloma cell lines (HMCLs). In particular, restoration of miR?203 in MM cells was
shown to inhibit cellular proliferation via targeting and hence direct downregulation of
a proto?oncogene, cyclic AMP responsive element binding protein. There are several
observations in primary MM samples. First, there was frequent methylation of
miR?129?2, miR?203 and miR?224 but infrequent methylation of miR?34a, miR?34b/c
and miR?124?1 in MM at diagnosis. Second, tumour?specific hypermethylation of each
of the miR?203 and miR?224 promoters was detected at comparable frequencies in
MGUS, diagnostic and relapsed/progressed MM, and hence implicated as an early
event in myelomagenesis. Thirdly, miR?129?2 methylation was more frequent in
diagnostic MM than MGUS, and hence implicated in MGUS progression to MM. On the
other hand, despite rare miR?34b/c methylation at diagnosis, miR?34b/c methylation
was frequent at relapse/progression, thereby implicating miR?34b/c methylation in
MM relapse/progression. Fourthly, despite frequent miR?124?1 methylation in HMCLs,
miR?124?1 methylation was rare in both diagnostic and relapsed MM marrow samples,
suggesting that miR?124?1 methylation was acquired during in vitro cell culture.
Finally, the prognostic significance of methylation of a panel of tumour
suppressor miRNAs was studied in a uniformly?treated cohort of MM patients, which
revealed that miR?224 hypermethylation as an independent favourable prognostic
factor for survival.
In conclusion, hypermethylation of tumour suppressor miRNAs is implicated in
the pathogenesis (miR?203, miR?129?2, miR?224), progression (miR?34b/c), and
prognostification (miR?224) of MM. / published_or_final_version / Medicine / Doctoral / Doctor of Philosophy
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The relationship between the repair of ultraviolet light induced DNA damage in human cells and the p53 tumour suppressor /McKay, Bruce C. January 1997 (has links)
Thesis (Ph.D.) -- McMaster University, 1998. / Includes bibliographical references (leaves 167-182). Also available via World Wide Web.
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Regulation of the human U6 small nuclear RNA transcription by the Retinoblastoma tumor suppressor proteinSelvakumar, Tharakeswari. January 2008 (has links)
Thesis (PH.D.)--Michigan State University. Cell and Molecular Biology, 2008. / Title from PDF t.p. (viewed on Aug. 11, 2009) Includes bibliographical references. Also issued in print.
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PTEN-PKB in endometriosis and related malignant transformation /Cheng, Wai-sheung. January 2005 (has links)
Thesis (M. Med. Sc.)--University of Hong Kong, 2005.
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Analysis of transcription factor binding specificity using ChIP-seq data.Kibet, Caleb Kipkurui January 2014 (has links)
Transcription factors (TFs) are key regulators of gene expression whose failure has been implicated in many diseases, including cancer. They bind at various sites at different specificity depending on the prevailing cellular conditions, disease, development stage or environmental conditions of the cell. TF binding specificity is how well a TF distinguishes functional sites from potential non-functional sites to form a useful regulatory network. Owing to its role in diseases, various techniques have been used to determine TF binding specificity in vitro and in vivo, including chromatin immuno-precipitation followed by massively parallel sequencing (ChIP-seq). ChIP-seq is an in vivo technique that considers how the chromatin landscape affects TF binding. Motif enrichment analysis (MEA) tools are used to identify motifs that are over-represented in ChIP-seq peak regions. One such tool, CentriMo, finds over-represented motifs at the center since peak calling software are biased to declaring binding regions centered at the TF binding site. In this study, we investigate the use of CentriMo and other MEA tools to determine the difference in motif enrichment attributed presence of Chronic Myeloid leukemia (CML)), treatment with Interferon (IFN) and Dexamethasone (DEX) compared to control based on Fisher’s exact test; using uniform peaks ChIP-seq data generated by the ENCODE consortium. CentriMo proved to be capable. We observed differential motif enrichment of TFs with tumor promoter activity: YY1, CEBPA, Egr1, Cmyc family, Gata1 and JunD in K562 while Stat1, Irf1, and Runx1 in Gm12878. Enrichment of CTCF in Gm12878 with YY1 as the immuno-precipitated (ChIP-ed) factor and the presence of significant spacing (SpaMo analysis) of CTCF and YY1 in Gm12878 but not in K562 could show that CTCF, as a repressor, helps in maintaining the required YY1 level in a normal cell line. IFN might reduce Cmyc and the Jun family of TFs binding via the repressive action of CTCF and E2f2. We also show that the concentration of DEX treatment affects motif enrichment with 50nm being an optimum concentration for Gr binding by maintaining open chromatin via AP1 TF. This study has demonstrated the usefulness of CentriMo for TF binding specificity analysis.
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