Lin Kwok Yin. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 116-124). / Abstracts in English and Chinese. / ACKNOWLEDGMENT --- p.i / ABSTRACT --- p.ii / LIST OF CONTENTS --- p.vii / LIST OF APPENDIX --- p.x / LIST OF TABLES --- p.xi / Chapter CHAPTER 1 --- INTRODUCTION --- p.1 / Chapter CHAPTER 2 --- LITERATURE REVIEW --- p.3 / Introduction --- p.3 / Impact of childhood cancer on the family in general --- p.4 / Impact of childhood cancer on children with the disease --- p.10 / Impact of childhood cancer on the well siblings --- p.16 / Impact of childhood cancer on parents --- p.21 / Impact on families with terminally ill children --- p.25 / Impact of the disease on families who have lost children with cancer --- p.29 / Summary of literature review --- p.32 / Chapter CHAPTER 3 --- OBJECTIVES AND METHODOLOGY --- p.35 / Aim and objectives --- p.35 / Methodology and research design --- p.35 / Subjects for study --- p.36 / Data collection method --- p.38 / Data collection procedure --- p.42 / Data analysis --- p.45 / Validity --- p.47 / Reliability --- p.48 / Pilot study --- p.50 / Ethics --- p.51 / Chapter CHAPTER 4 --- FINDINGS AND DISCUSSION --- p.54 / Introduction --- p.54 / Parents --- p.55 / Summary of the findings obtained from parents' data --- p.75 / Children with cancer --- p.76 / Summary of the findings obtained from children's data --- p.85 / Siblings --- p.86 / Summary of the findings obtained from siblings' data --- p.98 / A comparison of the findings obtained from parents' and children's data --- p.99 / Chapter CHAPTER 5 --- CONCLUSION --- p.104 / Limitations --- p.104 / Implications for nursing practice --- p.107 / Recommendations for nursing practice and further research --- p.112 / Conclusion --- p.114 / REFERENCES --- p.116 / APPENDIX --- p.125

by Cheung Yuk Lung. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 95-111). / Abstracts in English and Chinese; questionnaires in Chinese. / Acknowledgements --- p.i-ii / 摘要 --- p.iii-iv / Abstract --- p.v-vi / Table of Contents --- p.vii-viii / List of Tables --- p.ix / List of Figures --- p.x / Chapter Chapter 1. --- Introduction --- p.1 / Chapter Chapter 2. --- Literature Review / Anxiety --- p.3 / Quality of Life --- p.8 / Quality of Life for Stoma Patients --- p.19 / Progressive Muscle Relaxation in Reducing Anxiety and Promoting Quality of Life --- p.24 / The Rationale of Using PMRT in Reducing Anxiety and Promoting Quality of Life --- p.35 / Summary of Literature Review --- p.38 / Chapter Chapter 3. --- Methods / Research Design --- p.40 / Aim and Objectives --- p.41 / Hypotheses --- p.42 / Operational Definitions --- p.43 / Ethical Consideration --- p.44 / Sample --- p.45 / Intervention --- p.47 / Instruments --- p.49 / Data Collection and Randomization --- p.54 / Pilot Study --- p.56 / Method of Data Analysis --- p.57 / Chapter Chapter 4. --- Results / Internal Consistency of the Instruments --- p.59 / Subjects' Characteristics --- p.60 / "Baseline Assessment of State-Anxiety, Trait-Anxiety, QoL-Colostomy and WHO-QoL Scores " --- p.64 / Effect of PMRT on the State-Anxiety and Quality of Life --- p.65 / The Frequency of Practicing PMRT --- p.71 / Chapter Chapter 5. --- Discussion and Conclusion / Discussion --- p.75 / Limitations --- p.84 / Recommendations and Implications for Future Studies --- p.88 / Conclusion --- p.93 / References --- p.95 / Appendixes / Chapter 1 . --- Letters of Ethical Approval / Chapter 2. --- Letter of Request for Access Aapproval / Chapter 3. --- Informed Consent / Chapter 4. --- Questionnaires / Chapter 5. --- Content Validity Index of Chinese Version of QoL-Colostomy

Tse Lap-Ah. / "July 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. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Yu, Kai Shing. / "November 2010." / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 103-114). / Abstracts in English and Chinese. / Abstract --- p.2 / 中文摘要 --- p.6 / List of Contents --- p.9 / List of Table --- p.12 / Abbreviation --- p.13 / Acknowledgement --- p.14 / Chapter Chapter 1: --- Introduction --- p.15 / Chapter 1.1 --- Epidemiology of lung cancer --- p.15 / Chapter 1.2 --- Overview of significant prognostic factors for patients with NSCLC --- p.18 / Chapter 1.2.1 --- Tumor related factors --- p.19 / Chapter 1.2.2 --- Patient related factors --- p.21 / Chapter 1.3 --- Overview of significant prognostic factors for SCLC patients --- p.22 / Chapter Chapter 2: --- Literature Review --- p.25 / Chapter 2.1 --- Prevalence of co-morbidity among lung cancer patients --- p.25 / Chapter 2.2 --- Impact of co-morbidity on non small cell lung cancer patients --- p.28 / Chapter 2.3 --- Impact of co-morbidity on small cell lung cancer patients --- p.36 / Chapter 2.4 --- Summary of evidence from literature review --- p.40 / Chapter Chapter 3: --- Aim and Objectives --- p.42 / Chapter 3.1 --- General aim --- p.42 / Chapter 3.2 --- Specific objectives --- p.42 / Chapter 3.3 --- Main hypothesis --- p.42 / Chapter Chapter 4: --- Methodology --- p.43 / Chapter 4.1 --- Research design --- p.43 / Chapter 4.2 --- Study population --- p.43 / Chapter 4.3 --- Sample size estimation --- p.45 / Chapter 4.4 --- Data collection --- p.47 / Chapter 4.4.1 --- Demographic information --- p.47 / Chapter 4.4.2 --- Co-morbidity --- p.51 / Chapter 4.4.3 --- Adverse symptoms --- p.51 / Chapter 4.4.4 --- Disease characteristics --- p.52 / Chapter 4.4.5 --- Baseline laboratory findings --- p.53 / Chapter 4.4.6 --- Treatment data --- p.53 / Chapter 4.4.7 --- Follow up --- p.53 / Chapter 4.5 --- Statistical analyses --- p.54 / Chapter Chapter 5: --- Results --- p.56 / Chapter 5.1 --- Description of cohort --- p.56 / Chapter 5.2 --- Baseline characteristics --- p.58 / Chapter 5.3 --- Symptom presentation --- p.62 / Chapter 5.4 --- Histological characteristics --- p.64 / Chapter 5.5 --- Treatment characteristics --- p.67 / Chapter 5.6 --- Haematological characteristics of study population --- p.69 / Chapter 5.7 --- Prevalence of co-morbidity --- p.71 / Chapter 5.8 --- Overall survival --- p.74 / Chapter 5.8.1 --- Univariate and multivariate survival analysis for SCLC patients --- p.75 / Chapter 5.8.2 --- Univariate and multivariate survival analysis for NSCLC patients --- p.77 / Chapter 5.8.3 --- In-depth analyses for the Impact of co-morbidity on lung cancer survival --- p.79 / Chapter 5.8.4 --- Selected underlying causes of death --- p.84 / Chapter Chapter 6: --- Discussion --- p.85 / Chapter 6.1 --- Prognostic factors --- p.85 / Chapter 6.2 --- Prevalence of co-morbidity --- p.89 / Chapter 6.3 --- Impact of co-morbidity on lung cancer survival --- p.92 / Chapter 6.4 --- Strengths and limitations of this study --- p.97 / Chapter Chapter 7: --- Conclusions --- p.101 / Chapter Chapter 8: --- Implications and Recommendations for medial practice --- p.102 / References --- p.103

Cancer is the leading cause of death in Hong Kong (21,300 new cases and 11,500 deaths in 2003), with nasopharyngeal carcinoma (NPC), esophageal cancer (ESCC), and colorectal cancer (CRC) among the common ones. For these tumors, most patients present with advanced stage disease and poor treatment outcome, with an urge of early detection. Epigenetic inactivation of tumor suppressor genes (TSG) by CpG methylation represents an important mechanism of tumorigenesis, in addition to genetic abnormalities. Tumor-specific methylation can also be used as biomarkers for the identification of novel TSGs and for cancer early diagnosis and prognosis prediction. / Finally, for the purpose of development of epigenetic biomarker for cancer molecular diagnosis, I screened gene methylation in the serum samples. Aberrant methylation of PCDH10 and DLC1 was detected in serum samples (2/14 (14%) and 4/14 (29%) respectively) from tumor patients but not in normal controls. It suggests that screening for PCDH10 and DLC1 methylation in sera could be a tumor-specific and non-invasive epigenetic biomarker for molecular diagnosis and prognostics. (Abstract shortened by UMI.) / In the second approach, 1-Mb array-based comparative genomic hybridization (aCGH) was carried out to detect DNA copy number aberrations, which contain potential TSG loci, in a panel of NPC and ESCC cell lines. Frequent deletions include: 1p36.3, 3p14-11, 4p16-15, 5p13-q12, 6p21-12, 8p22-cent, 9p, 9q22-31, 10p, 13q12, 14q32, 16q23-24, 17q11.2, 18q in NPC, and 1p21, 4q21, 7p21, 7q35, 8p22-23, 8q11, 10p11, 11q22, 13q31, 14q32, 18q11-23 in ESCC. Several deletions (3p14-11 and 16q23) were further investigated in detail in this study. More than 12 genes were identified to be frequently silenced by methylation in tumors, including FHIT (3p14), WNT5A (3p14), ADAMTS9 (3p14), FEZF2 (3p14), ROBO (3p12), CADM2 (3p12), EPHA3 (3p11), RAB (11q22), ADAMTS18 (16q23), and TUSC8 (16q23), while homozygous deletion of these genes was infrequently detected. Aberrant methylation of these genes was also frequently detected in primary tumors in a tumor-specific manner. The tumor suppressor functions of TUSC8, WNT5A, CADM2 and ROBO were further investigated and validated. Further experiment indicated that induction of tumor cell apoptosis may contribute to the tumor suppressor function of TUSC8. / Modified genomic methylation subtractive approaches using uracil-DNA glycosylase or combined with pharmacological demethylation were developed. GADD45G, PCDH10, ROR2, DLC1L1 were among a series of novel methylated targets identified by these approaches. Methylation-associated silencing of these genes was frequently detected in various types of tumor cell lines and primary tumors including NPC, ESCC and CRC, in a tumor-specific manner. Ectopic expression of these genes strongly suppressed tumor cell growth and colony formation of silenced tumor cells. Epigenetic inactivation of GADD45G is the major mechanism for the loss of its response to environmental stresses. Reintroduction of PCDH10 strongly suppressed tumor cell migration and invasion. Ectopic expression of DLC1L1 in silenced tumor cells resulted in a remarkable suppression of tumor cell clonogenicity, which depends on its GAP activity. Furthermore, DLC1L1, but not its inactivating mutants, inhibited Ras mediated oncogenic transformation. Thus, these identified genes are functional TSGs. / Ying Jianming. / "July 2007." / Adviser: Qian Tao. / Source: Dissertation Abstracts International, Volume: 69-01, Section: B, page: 0083. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (p. 147-173). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract in English and Chinese. / School code: 1307.

Ho, Ching Sze. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 142-160). / Abstracts in English and Chinese. / DECLARATION --- p.I / ACKNOWLEDGEMENTS --- p.II / ABSTRACT (ENGLISH VERSION) --- p.IV / ABSTRACT (CHINESE VERSION) --- p.VII / TABLE OF CONTENTS --- p.IX / LIST OF FUGURES --- p.XII / LIST OF TABLES --- p.XIII / LIST OF ABBREVIATIONS --- p.XV / Chapter CHAPTER 1: --- INTRODUCTION --- p.1 / Chapter 1.1 --- Biology of human papillomavirus --- p.2 / Chapter 1.1.1 --- History --- p.2 / Chapter 1.1.2 --- Classification --- p.3 / Chapter 1.1.3 --- Genome structure --- p.5 / Chapter 1.1.4 --- Life cycle --- p.9 / Chapter 1.2 --- Epidemiology of cervical cancer --- p.10 / Chapter 1.2.1 --- Cervical intraepithelial neoplasia and cervical cancer --- p.10 / Chapter 1.2.2 --- Spectrum of cervical neoplasia --- p.13 / Chapter 1.2.3 --- Incidence of cervical cancer --- p.15 / Chapter 1.2.4 --- Screening programme --- p.16 / Chapter 1.3 --- Risk factors for cervical cancer --- p.17 / Chapter 1.4 --- Oncogenic HPV infection --- p.20 / Chapter 1.4.1 --- Risk association --- p.21 / Chapter 1.4.2 --- Geographical distribution --- p.23 / Chapter 1.4.3 --- Age distribution --- p.24 / Chapter 1.4.4 --- Oncogenic property of HPV --- p.25 / Chapter 1.4.5 --- Sequence variation --- p.28 / Chapter 1.5 --- Prevention by vaccination --- p.30 / Chapter 1.6 --- Objectives --- p.31 / Chapter CHAPTER 2: --- MATERIALS AND METHODS --- p.33 / Chapter 2.1 --- HPV type and prevalence distribution --- p.34 / Chapter 2.1.1 --- Study population --- p.34 / Chapter 2.1.2 --- Specimen and epidemiological data collection --- p.34 / Chapter 2.1.3 --- DNA extraction --- p.35 / Chapter 2.1.4 --- PCR amplification of DNA --- p.36 / Chapter 2.1.4.1 --- PCR for Beta-globin --- p.36 / Chapter 2.1.4.2 --- PCR for HPV DNA --- p.37 / Chapter 2.1.5 --- HPV typing by reverse line-blot hybridization --- p.39 / Chapter 2.1.6 --- Statistical method --- p.40 / Chapter 2.2 --- HPV 52 SEQUENCE VARIATION --- p.43 / Chapter 2.2.1 --- Study population --- p.43 / Chapter 2.2.2 --- Specimen processing --- p.43 / Chapter 2.2.3 --- DNA extraction --- p.44 / Chapter 2.2.4 --- PCR amplification for sequencing --- p.45 / Chapter 2.2.4.1 --- Optimization of gene-specific PCR --- p.45 / Chapter 2.2.4.2 --- Validation of type-specificity of gene-specific PCR --- p.46 / Chapter 2.2.4.3 --- PCR for HPV52 E6 and E7 --- p.46 / Chapter 2.2.4.4 --- PCR for LI gene --- p.47 / Chapter 2.2.4.5 --- PCR for long control region (LCR) --- p.48 / Chapter 2.2.5 --- Purification of PCR products --- p.49 / Chapter 2.2.6 --- Sequencing --- p.50 / Chapter 2.2.6.1 --- Preparation of template --- p.50 / Chapter 2.2.6.2 --- Purification of template --- p.50 / Chapter 2.2.6.3 --- Sequencer and data analysis --- p.51 / Chapter 2.2.7 --- Statistical methods --- p.51 / Chapter CHAPTER 3: --- RESULTS --- p.54 / Chapter 3.1 --- HPV TYPE AND PREVALENCE DISTRIBUTION --- p.55 / Chapter 3.1.1 --- Study population --- p.55 / Chapter 3.1.2 --- HPV prevalence --- p.59 / Chapter 3.1.2.1 --- Prevalence for HPV infection --- p.59 / Chapter 3.1.2.2 --- HPV age-specific prevalence --- p.68 / Chapter 3.1.3 --- Epidemiological risk profile --- p.73 / Chapter 3.1.3.1 --- Age-adjusted analyses --- p.73 / Chapter 3.1.3.2 --- Multivariate analyses --- p.76 / Chapter 3.2 --- HPV52 SEQUENCE VARIATION --- p.79 / Chapter 3.2.1 --- Study population --- p.79 / Chapter 3.2.2 --- Sequence variability of HPV52 --- p.79 / Chapter 3.2.3 --- HPV52 --- p.82 / Chapter 3.2.3.1 --- Sequence variation of E6 ORF --- p.82 / Chapter 3.2.3.2. --- HPV52 E6 variants and risk for cervical neoplasia --- p.86 / Chapter 3.2.4 --- HPV52 E7 --- p.89 / Chapter 3.2.4.1 --- Sequence variation of E7 ORF --- p.89 / Chapter 3.2.4.2 --- HPV52 E7 variants and risk for cervical neoplasia --- p.93 / Chapter 3.2.5 --- HPV52 LI --- p.95 / Chapter 3.2.5.1 --- Sequence variation of LI ORF --- p.95 / Chapter 3.2.5.2 --- HPV52 LI variants and risk for cervical neoplasia --- p.100 / Chapter 3.2.6 --- HPV52 long control region (LCR) --- p.104 / Chapter 3.2.6.1 --- Sequence variation of LCR --- p.104 / Chapter 3.2.6.2 --- HPV52 LCR variants and risk for cervical neoplasia --- p.110 / Chapter CHAPTER 4: --- DISCUSSION --- p.113 / Chapter 4.1 --- HPV PREVALENCE AND TYPE DISTRIBUTION --- p.114 / Chapter 4.1.1 --- HPV prevalence --- p.114 / Chapter 4.1.2 --- Age-specific prevalence --- p.116 / Chapter 4.1.3 --- Epidemiological risk profile --- p.121 / Chapter 4.1.4 --- Conclusions --- p.126 / Chapter 4.2 --- HPV 52 SEQUENCE VARIATION --- p.127 / Chapter 4.2.1 --- Sequence variability of HPV52 --- p.127 / Chapter 4.2.2 --- Sequence variation of E6 gene --- p.129 / Chapter 4.2.3 --- Sequence variation of E7 gene --- p.132 / Chapter 4.2.4 --- Sequence variation of LI gene --- p.134 / Chapter 4.2.5 --- Sequence variation of LCR --- p.135 / Chapter 4.2.6 --- Conclusions --- p.139 / Chapter 4.3 --- FURTHER STUDIES --- p.140 / REFERENCES --- p.142 / APPENDIXES --- p.A