Dong Zhiqian. / "June 2003." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2003. / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

by Tong Yuen Kwan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 124-141). / Abstract also in Chinese. / acknowledgements --- p.i / Abstract (English/Chinese) --- p.ii / contents --- p.vi / list of tables --- p.viii / ost of figures --- p.x / Chapter I. --- introduction --- p.1 / Chapter I.1. --- Tumors of the Central Nervous System --- p.1 / Chapter I.2. --- Histopathological Classification of Human Glial Tumors --- p.3 / Chapter I.2.1. --- Histopathology of Astrocytic Gliomas --- p.3 / Chapter I.2.1.1. --- Diffuse Astrocytomas --- p.3 / Chapter I.2.1.2. --- Others --- p.6 / Chapter I.2.2. --- Histopathology of Non-Astrocytic Gliomas --- p.6 / Chapter I.2.2.1. --- Oligodendroglial Tumors --- p.6 / Chapter I.2.2.2. --- Ependymal Tumors --- p.9 / Chapter I.3. --- Tumor Suppressor Genes --- p.14 / Chapter I.3.1. --- p53 --- p.14 / Chapter I.3.1.1. --- Historical Perspectives --- p.14 / Chapter I.3.1.2. --- Structure of p53 Gene and Protein --- p.15 / Chapter I.3.1.3. --- Functions of Wild-Type p53 Protein --- p.18 / Chapter I.3.1.4. --- Regulation and Modulation of the Functions of p53 --- p.21 / Chapter I.3.1.5. --- Mechnism of p53 Inactivation --- p.23 / Chapter I.3.1.6. --- p53 Mutation Profiles in Human Tumors --- p.25 / Chapter I.3.2. --- Novel Genes --- p.28 / Chapter I.3.2.1. --- PTEN/MMAC1 --- p.28 / Chapter I.3.2.2. --- DMBT1 --- p.31 / Chapter I.4. --- Cytogenetic and Molecular Genetic Studies in Gliomas --- p.34 / Chapter I.4.1. --- Astrocytic Gliomas --- p.34 / Chapter I.4.2. --- Non-Astrocytic Gliomas --- p.39 / Chapter I.4.2.1. --- Oligodendroglial Tumors --- p.39 / Chapter I.4.2.2. --- Ependymal Tumors --- p.46 / Chapter II. --- objectives of study --- p.49 / Chapter III. --- materials and methods --- p.52 / Chapter III.l. --- Patients and Materials --- p.52 / Chapter III.2. --- Collection of Samples --- p.57 / Chapter III.3. --- DNA Extraction --- p.58 / Chapter III.3.1. --- Extraction of Genomic DNA from Formalin-Fixed Paraffin Embedded Tissues --- p.58 / Chapter III.3.2. --- Extraction of Genomic DNA from Blood --- p.60 / Chapter III.4. --- Loss of Heterozygosity (LOH) Analysis on Chromosome 10q --- p.61 / Chapter III.4.1. --- Microsatellite Markers --- p.62 / Chapter III.4.2. --- Amplification of Target Sequences by PCR --- p.63 / Chapter III.4.3. --- Denaturing Polyaerylamide Gel Electrophoresis --- p.64 / Chapter III.4.4. --- Detection of Loss of Heterozygosity (LOH) --- p.64 / Chapter III.5. --- Mutational Analysis of p53 and PTEN/MMAC1 --- p.66 / Chapter III.5.1. --- Polymerase Chain Reaction-Single Strand Conformation Polymorphism (PCR-SSCP) Analysis --- p.66 / Chapter III.5.1.1. --- PCR Primers --- p.66 / Chapter III.5.1.2. --- PCR Amplification of Target Sequences --- p.68 / Chapter III.5.1.3. --- Non-denaturing Polyacrylamide Gel Electrophoresis --- p.71 / Chapter III.5.2. --- Direct DNA Sequencing Analysis --- p.72 / Chapter III.5.2.1. --- Cycle Sequencing --- p.72 / Chapter III.5.2.2. --- Denaturing Gel Electrophoresis --- p.73 / Chapter III.6. --- Differential PCR for Detection of MDM2 Amplification --- p.74 / Chapter III.6.1. --- DNA Amplification by PCR --- p.74 / Chapter III.6.2. --- Polyacrylamide Gel Electrophoresis --- p.75 / Chapter III.6.3. --- Detection of Gene Amplification --- p.75 / Chapter IV. --- Results --- p.77 / Chapter IV.1. --- LOH Analysis of Chromosome l0q --- p.77 / Chapter IV.2. --- Mutational Analysis ofp53 and PTEN/MMAC1 --- p.92 / Chapter IV.3. --- Differential PCR Analysis of MDM2 Amplification --- p.103 / Chapter V. --- discussion --- p.109 / Chapter V.l. --- p53 Gene Inactivation Studies --- p.110 / Chapter V.2. --- Molecular Genetic Studies on Chromosome l0q --- p.113 / Chapter V.3. --- Microsatellite Instability in Non-Astrocytic Gliomas --- p.117 / Chapter V.4. --- Significance of This Study --- p.118 / Chapter V.5. --- Limitations of This Study --- p.119 / Chapter V.6. --- Future Studies --- p.122 / Chapter VI. --- REFERENCES --- p.124

Ng Yeung Lam. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 180-209). / Abstracts in English and Chinese. / acknowledgements --- p.i / abstract --- p.ii / abstract in chinese --- p.vi / table of contents --- p.ix / list of tables --- p.xiii / list of figures --- p.xi v / list of abbreviations --- p.xvi / Chapter 1 --- chapter1 introduction and literature review --- p.1 / Chapter 1.1 --- Introduction of brain tumors --- p.1 / Chapter 1.2 --- Oligodendroglial tumors (OTs) --- p.3 / Chapter 1.2.1 --- Oligodendroglioma (OD) and anaplastic oligodendroglioma (AOD) --- p.3 / Chapter 1.2.1.1 --- WHO's definition and grading --- p.3 / Chapter 1.2.1.2 --- "Incidence, age, sex distribution, tumor location and survival rate" --- p.3 / Chapter 1.2.1.3 --- Clinical presentation --- p.4 / Chapter 1.2.1.4 --- Macroscopy and histopathology --- p.4 / Chapter 1.2.1.5 --- Immunohistochemistry --- p.5 / Chapter 1.2.1.6 --- Treatment --- p.6 / Chapter 1.2.2 --- Oligoastrocytoma (OA) and anaplastic oligoastrocytoma (AOA) --- p.11 / Chapter 1.2.2.1 --- WHO's definition and grading --- p.11 / Chapter 1.2.2.2 --- "Incidence, age, sex distribution, tumor location and survival rate" --- p.12 / Chapter 1.2.2.3 --- Clinical features --- p.12 / Chapter 1.2.2.4 --- Macroscopy and histopathology --- p.12 / Chapter 1.3 --- Overview of Genetic and Epigenetic Aberrations of OTs --- p.14 / Chapter 1.3.1 --- Chromosomal and genetic aberrations in OTs --- p.14 / Chapter 1.3.2 --- Candidate regions and genes on 1 p --- p.15 / Chapter 1.3.3 --- Candidate regions and genes on 19q --- p.20 / Chapter 1.3.4 --- Other aberrations in WHO grade II OTs --- p.24 / Chapter 1.3.5 --- Progression-associated aberrations in ODs --- p.25 / Chapter 1.3.6 --- Chromosomal and genetic aberrations in OAs --- p.29 / Chapter 1.4 --- Correlation of genetic alterations with response to therapy and survival --- p.31 / Chapter 1.4.1 --- Response to PCV chemotherapy correlates with lp and combined lp/19q status in patients with AODs --- p.31 / Chapter 1.4.2 --- Survival of patients with AODs correlates with lp/19q status --- p.32 / Chapter 1.4.3 --- WHO grade II ODs behavior and lp/19q status --- p.32 / Chapter 1.4.4 --- Response to other therapies (temozolomide and radiotherapy) and lp/19q status in patients with ODs --- p.33 / Chapter 1.4.5 --- lp and 19q loss in OAs and diffuse astrocytomas --- p.34 / Chapter 1.5 --- Microarray-based expression profiling of OTs --- p.35 / Chapter 1.6 --- Description of p73 protein --- p.37 / Chapter 1.6.1 --- Introduction of p73 --- p.37 / Chapter 1.6.2 --- p73: gene structure and splicing variants --- p.37 / Chapter 1.6.3 --- Signaling in p73 --- p.40 / Chapter 1.6.4 --- Regulation ofp73 protein stability and transcriptional activity --- p.43 / Chapter 1.6.4.1 --- Regulation by DNA damage --- p.43 / Chapter 1.6.4.2 --- Regulation by oncogenes --- p.44 / Chapter 1.6.4.3 --- Interaction with viral proteins --- p.44 / Chapter 1.6.5 --- Role of p73 in the nervous system --- p.45 / Chapter 1.6.6 --- p73 in cancer --- p.45 / Chapter 1.6.6.1 --- p73 knockout mice --- p.45 / Chapter 1.6.6.2 --- Alteration of p73 expression in human cancers --- p.46 / Chapter 1.6.7 --- p73 and chemosensitivity --- p.50 / Chapter CHAPTER2 --- AIMS OF STUDY --- p.51 / Chapter CHAPTER3 --- MATERIALS AND METHODS --- p.53 / Chapter 3.1 --- Tumor and blood samples --- p.53 / Chapter 3.2 --- Cell culture --- p.53 / Chapter 3.3 --- DNA extraction from frozen tissues and blood samples --- p.54 / Chapter 3.4 --- Detection of allelic loss of chromosome lp --- p.58 / Chapter 3.4.1 --- LOH analysis --- p.58 / Chapter 3.4.2 --- Fluorescence in situ Hybridization (FISH) analysis on Paraffin and Frozen Sections --- p.60 / Chapter 3.6 --- DNA sequencing analysis --- p.62 / Chapter 3.7 --- Analysis of Methylation --- p.63 / Chapter 3.7.1 --- Bisulfite sequencing --- p.63 / Chapter 3.7.2 --- Methylation-specific polymerase chain reaction (MSP) --- p.66 / Chapter 3.8 --- Northern Blot analysis --- p.68 / Chapter 3.9 --- RNA isolation and cDNA preparation --- p.70 / Chapter 3.10 --- Laser microdissection and RNA extraction from microdissected tumor cells --- p.71 / Chapter 3.10.1 --- Conventional RT-PCR --- p.71 / Chapter 3.11 --- Primer design for TP73 and its isoforms --- p.74 / Chapter 3.12 --- Real-time RT-PCR --- p.77 / Chapter 3.12.1 --- Real-time RT-PCR for TP73 and its isoforms --- p.78 / Chapter 3.12.2 --- Real-time RT-PCR for KIAA0495 --- p.79 / Chapter 3.13 --- Statistical analyses --- p.81 / Chapter CHAPTER4 --- RESULTS --- p.82 / Chapter 4.1 --- Genes annotated in the minimally deleted regions --- p.82 / Chapter 4.2 --- Expression analyses of TP73 and its isoforms in ODs by quantitative real-time RT-PCR --- p.85 / Chapter 4.3 --- Methylation analysis of TP73 in ODs by methylation sensitive PCR (MSP) --- p.97 / Chapter 4.4 --- A rapid screen of candidate genes for aberrant expression in microdissected tumors --- p.100 / Chapter 4.5 --- Quantitative real-time RT-PCR of KIAA0495 gene --- p.103 / Chapter 4.6 --- Mutation analysis of KIAA0495 gene --- p.110 / Chapter 4.7 --- Methylation analysis of KIAA0495 in ODs by bisulfite sequencing…… --- p.112 / Chapter 4.8 --- Detection of allelic loss of lp by LOH analysis and interphase FISH --- p.121 / Chapter 4.9 --- Two-hit inactivation of KIAA0495 gene in ODs --- p.126 / Chapter 4.10 --- Tissue distribution of KIAA0495 gene --- p.130 / Chapter 4.11 --- Bioinformatics of KIAA0495 --- p.133 / Chapter CHAPTER5 --- DISCUSSION --- p.146 / Chapter 5.1 --- Expression analysis of TP73 and its isoforms in ODs by isoform-specific RT-PCR --- p.148 / Chapter 5.2 --- Methylation status ofTP73 in ODs --- p.153 / Chapter 5.3 --- A rapid screening of candidate genes for aberrant expressionin microdissected tumors --- p.156 / Chapter 5.4 --- Expression pattern of KIAA0495 mRNA in a large cohort of ODs --- p.157 / Chapter 5.5 --- No somatic mutation in coding region of KIAA0495 --- p.158 / Chapter 5.6 --- Methylation status of putative promoter region of KIAA0495 in ODs --- p.159 / Chapter 5.7 --- Status of chromosome lp in ODs --- p.161 / Chapter 5.8 --- Two-hit inactivation of KIAA0495 gene in ODs by promoter hypermethylation and allelic loss of lp --- p.162 / Chapter 5.9 --- Evaluation of expression of KIAA0495 gene as a marker for the response to chemotherapy and prognostic marker in patients with OTs --- p.164 / Chapter 5.10 --- Tissue distribution of KIAA0495 --- p.166 / Chapter 5.11 --- "KIAA0495 cDNA sequence, protein sequence and potential functional features" --- p.167 / Chapter 5.12 --- Candidate tumor suppressor genes on lp in other type of tumors with loss of lp --- p.171 / Chapter CHAPTER6 --- CONCLUSIONS --- p.174 / Chapter CHAPTER7 --- FUTURE STUDIES --- p.177 / Chapter CHAPTER8 --- REFERENCES --- p.180

Dong Shumin. / "February 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 187-220). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.