Hepatocellular carcinoma (HCC) is a leading cause of death in both Africa and Asia. It is multifactorial in aetiology and complex in its pathogenesis. Genes that might affect tumour progression, invasion, and metastasis are good candidates to investigate in attempting to understand the transformation process. The p53, RBI, BRCA1, BRCA2, WT1 and Ecadherin genes were analysed for allelic imbalance/loss of heterozygosity (LOH), polymorphisms, and mutations. Tumour and non-tumorous liver tissue from 25 southern African blacks were examined, using polymerase chain reaction restriction fragment length polymorphisms (PCR-RFLP) and PCR-single stranded conformational polymorphisms (SSCP), sequencing, and Southern blotting techniques. Allele frequencies for polymorphisms at the WEI, D13S137, D13S120, D13S127, D17S855, D16S301, and D16S260 loci were determined in 20 random African blacks using microsatellite analysis to determine allele frequencies, polymorphism information content (PIC) and diversity (H) values. To our knowledge this has not been done previously for these loci in this population. The chromosomal region l i p 13, containing the VV77 gene, and the gene itself has been reported to be deleted in 4.5% of HCCs. LOH was detected at the WT1 locus for 1/13 HCCs (8%) in this study. The RBI gene has been described to be mutated in 32.4% (China), 33.3% (Korea), 29% and 50% tJapan), and 27% (Australia), of advanced stage HCCs. In our study LOH at this locus was found in 3/19 HCCs (16%). Our finding of LOH at the BRCA2 locus in 2/20 HCCs (10%) supports the previously proposed notion that BRCA2 may function as a tumour suppressor gene in a hormone-related pathway in the liver, and that it may in some way be involved in HCC. No conclusive findings were made for any o f the other loci. Microsatellite instability was detected in 3/22 (14%) individuals. We propose that microsatellite/genomic instability may play a role in a subset of HCCs only. O f this population, 27 % had the specific p53 codon 249 AGG-AGT mutation in some tumour and non-tumorous liver. This was expected as the great majority of the individuals were from Mozambique, a country where heavy aflatoxin exposure is prevalent. All the loci examined in the allele frequency studies proved to be highly informative, showing high PIC and ED values, and should therefore be useful in population studies.

by Hiu-Ming Li. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (p. 176-198). / 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 Wai-Tong Leung. / Thesis (M.D.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 282-315). / Title Page --- p.i / Dedication --- p.ii / Table of Contents --- p.iii / Precis to the thesis --- p.7 / Glossary of abbreviation used in the thesis --- p.20 / List of Figures and Pictures --- p.22 / List of Tables --- p.26 / Acknowledgments --- p.30 / Statement of Originality --- p.32 / Chapter PART ONE --- Introduction / Chapter Chapter 1 --- Background for Hepatocellular Carcinoma / Chapter 1. --- History --- p.33 / Chapter 2. --- "Epidemiology - World wide, China,Hong Kong" --- p.36 / Chapter 3. --- Pathology --- p.55 / Chapter 4. --- Aetiology --- p.62 / Chapter 5. --- Clinical Manifestation and Diagnosis --- p.68 / Chapter 6. --- Natural History --- p.74 / Chapter 7. --- Conventional Treatment --- p.76 / Chapter 8. --- Prognosis --- p.85 / Chapter Chapter 2 --- Hepatocellular Carcinoma in Hong Kong / Chapter 1. --- Clinical Study of 1119 cases of Hepatocellular Carcinoma --- p.88 / Chapter PART TWO --- Conventional Treatment for Hepatocellular Carcinoma / Chapter Chapter 3 --- Chemotherapy for Hepatocellular Carcinoma / Chapter 1. --- Review of the Literature in Systemic Chemotherapy --- p.108 / Chapter 2. --- Phase II Trials of Systemic Chemotherapy --- p.114 / Chapter a. --- VP16-213 --- p.115 / Chapter b. --- Low Dose 4'-Epidoxorubicin --- p.116 / Chapter c. --- High Dose 4'-Epidoxorubicin --- p.117 / Chapter d. --- 5_FU and High Dose Folinic Acid --- p.119 / Chapter e. --- High Dose Ifosfamide --- p.122 / Chapter 3. --- Review of the Literature in Intra-Arterial Chemotherapy --- p.125 / Chapter 4. --- Intra-Arterial Chemotherapy Trial Performed in PWH --- p.131 / Chapter a. --- An Early Phase II Trial on Treatment of Inoperable Hepatocellular Carcinoma by Intrahepatic Arterial Chemotherapy with Lipiodol and 4'-Epidoxorubicin --- p.131 / Chapter b. --- "Phase II Trial of Treatment of Inoperable Hepatocellular Carcinoma by Intra-Arterial Lipiodol and High Dose 4'-Epidoxorubicin, a Comparison with Intravenous 4'-Epidoxorubicin" --- p.137 / Chapter PART THREE --- Novel Treatment for Hepatocellular Carcinoma / Chapter Chapter 4 --- Selective Internal Radiation Treatment for Hepatocellular Carcinoma / Chapter 1. --- Review of the Literature in Radiotherapy for Liver Tumours --- p.145 / Chapter 2. --- Selective Internal Radiation with 131Iodine-Lipiodol in HCC / Chapter a. --- Background and Review of the Literature --- p.151 / Chapter b. --- Physical Aspects of 131Iodine-Lipiodol --- p.154 / Chapter c. --- Bio-distribution of 131I-L in one HCC Patient --- p.156 / Chapter d. --- Clinical Study on the Use of131I-Lipiodol in the Treatment of Inoperable HCC --- p.168 / Chapter 3. --- Selective Internal Radiation with 90Yttrium-Microspheres in HCC / Chapter a. --- Background and Review of the Literature --- p.182 / Chapter b. --- Physical Aspects of 90Yttrium-Microspheres --- p.187 / Chapter c. --- Treatment of Inoperable Hepatocellular Carcinoma with Intrahepatic-Arterial 90Yttrium Microspheres - An Early Phase II Study --- p.195 / Chapter d. --- Treatment of Inoperable Hepatocellular Carcinoma with Intrahepatic-arterial 90Yttrium Microspheres through Hepatic Angiography --- p.214 / Chapter 4. --- Selection of Patients for 90Yttrium -Microspheres Treatment --- p.230 / Chapter a. --- Diagnostic Scintigraphy with Hepatic Intra-Arterial Technetium-99m Macroaggregated Albumin in the Determination of Tumour to Non-Tumour Uptake Ratio in Hepatocellular Carcinoma --- p.230 / Chapter b. --- Measuring Lung Shunting in Hepatocellular Carcinoma with Intrahepatic-Arterial Technetium-99m Macroaggregated Albumin Scan --- p.245 / Chapter c. --- Correlation of Tumour Vascularity Grading by Selective Hepatic Angiography with T/N Ratio from Tc-MAA Scanin Hepatocellular Carcinoma --- p.260 / Chapter d. --- Pulmonary Complications from 90Yttrium-Microspheres Treatment --- p.266 / Conclusion of the Thesis --- p.280 / References to Chapter1 --- p.282 / References to Chapter2 --- p.296 / References to Chapter3 --- p.297 / References to Chapter4 --- p.308 / Appendix: / Chapter 1. --- Recommendations for Grading of Acute and Subacute Toxicityin Cancer Treatment --- p.316 / Chapter 2. --- Recommendations for Grading of Response Criteria --- p.318 / Selected Publications by the Author Relevant to the Thesis --- p.319

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Li Ching-wan. / Thesis submitted in: November 2001. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (leaves 104-130). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABSTRACTS (ENGLISH/CHINESE) --- p.iii / LIST OF FIGURES --- p.xi / LIST OF TABLES --- p.xiii / LIST OF ABBREVIATIONS --- p.xiv / Chapter CHAPTER1 --- INTRODUCTION / Chapter 1.1. --- Liver Cancer --- p.1 / Chapter 1.2. --- Hepatocellular Carcinoma --- p.1 / Chapter 1.2.1. --- Types of Liver Cancer --- p.1 / Chapter 1.2.2. --- Epidemiology --- p.4 / Chapter 1.2.2.1. --- Geographical Distribution --- p.4 / Chapter 1.2.2.2. --- Age and Gender Distribution --- p.8 / Chapter 1.2.3. --- Etiologic Factors --- p.9 / Chapter 1.2.3.1. --- Chronic Infection with Hepatitis B (HBV) and C (HCV) Viruses --- p.9 / Chapter 1.2.3.2. --- Aflatoxin B1 --- p.11 / Chapter 1.2.3.3. --- Alcohol --- p.12 / Chapter 1.2.3.4. --- Summary --- p.12 / Chapter 1.3. --- HCC in Hong Kong --- p.14 / Chapter 1.4. --- Role of Viral Hepatitis B in HCC --- p.17 / Chapter 1.4.1. --- HBV Genome --- p.17 / Chapter 1.4.2. --- Consequences of HBV DNA Integration --- p.17 / Chapter 1.4.2.1. --- HBV Integration --- p.17 / Chapter 1.4.2.2. --- Transactivation of Cellular Genes by HBV DNA --- p.19 / Chapter 1.4.2.3. --- Chromosomal DNA Instability --- p.20 / Chapter 1.5. --- Genetic Alterations in HCC --- p.21 / Chapter 1.5.1. --- Tumor Suppressor Gene --- p.21 / Chapter 1.5.2. --- Proto-oncogene --- p.23 / Chapter 1.5.3. --- Genetic Studies in HCC --- p.23 / Chapter 1.5.3.1. --- Loss of Heterozygosity (LOH) --- p.25 / Chapter 1.5.3.2. --- Comparative Genomic Hybridization (CGH) --- p.26 / Chapter 1.5.3.3. --- Array CGH --- p.26 / Chapter 1.5.4. --- Large-Scale Genetic Analysis in HCC --- p.27 / Chapter CHAPTER2 --- RATIONALE IN THIS STUDY --- p.35 / Chapter CHAPTER3 --- MATERIALS AND METHODS / Chapter 3.1. --- Patients and Materials --- p.38 / Chapter 3.1.1. --- DNA Extraction --- p.40 / Chapter 3.2. --- Loss of Heterozygosity Analysis on Chromosome 4q --- p.40 / Chapter 3.2.1. --- Microsatellite Markers --- p.41 / Chapter 3.2.2. --- Amplification of Target Sequences by PCR --- p.42 / Chapter 3.2.2.1. --- 5-end Labeling Primers --- p.42 / Chapter 3.2.2.2. --- Amplification of Target Sequences --- p.42 / Chapter 3.2.3. --- Denaturing Polyacrylamide Gel --- p.44 / Chapter 3.2.3.1. --- Electrophoresis --- p.44 / Chapter 3.2.4. --- Detection of Loss of Heterozygosity (LOH) --- p.45 / Chapter 3.2.5. --- Duplex PCR Analysis of Homozygous Deletion --- p.45 / Chapter 3.3. --- Amplification Analysis by Array-CGH --- p.46 / Chapter 3.3.1. --- Nick-Translation --- p.49 / Chapter 3.3.2. --- Hybridization --- p.49 / Chapter 3.3.3. --- Imaging and Data Analysis --- p.50 / Chapter 3.3.4. --- Determination of Normal Range for All Cases --- p.51 / Chapter 3.3.5. --- Assessment of Data Quality --- p.51 / Chapter 3.4. --- Statistical Analysis --- p.52 / Chapter CHAPTER4 --- RESULTS / Chapter 4.1. --- Loss of Heterozygosity Analysis on Chromosome 4q --- p.53 / Chapter 4.1.1. --- Region I of Smallest Common Deletion Region --- p.54 / Chapter 4.1.2. --- Region II of Smallest Common Deletion Region --- p.54 / Chapter 4.2. --- Amplification Analysis by Array-CGH --- p.62 / Chapter CHAPTER5 --- DISCUSSION / Chapter 5.1. --- LOH Analysis on Chromosome 4q --- p.73 / Chapter 5.1.1. --- LOH of Chromosome 4q in Various Cancers --- p.74 / Chapter 5.1.1.1. --- Hepatocellular Carcinomas --- p.74 / Chapter 5.1.1.2. --- Other Neoplasia --- p.76 / Chapter 5.1.2. --- Functional Studies on Chromosome 4 --- p.76 / Chapter 5.1.3. --- Putative Tumor Suppressors on Chromosome 4q --- p.80 / Chapter 5.1.3.1. --- Region I (4q27-q28.1) --- p.80 / Chapter 5.1.3.1.1. --- MAD2L1 (4q27) --- p.80 / Chapter 5.1.3.2. --- Region II (4q35.2) --- p.81 / Chapter 5.1.3.2.1. --- INGlL(4q35.1) --- p.81 / Chapter 5.1.3.2.2. --- FAT (4q34-q35) --- p.81 / Chapter 5.1.3.2.3. --- Caspase 3 (4q35) --- p.82 / Chapter 5.1.4. --- Limitation of this Study --- p.83 / Chapter 5.1.4.1. --- Markers --- p.83 / Chapter 5.1.4.1.1. --- Limitation of the Markers --- p.83 / Chapter 5.1.4.1.2. --- Location of the Microsatellite Markers --- p.83 / Chapter 5.1.4.2. --- Tissue Samples --- p.84 / Chapter 5.1.4.2.1. --- Normal Reference --- p.84 / Chapter 5.1.4.2.2. --- Pathologic Characterization --- p.85 / Chapter 5.1.5. --- Future Studies --- p.85 / Chapter 5.1.5.1. --- Improvement of the Experiment --- p.85 / Chapter 5.1.5.2. --- Extension of the Present Study --- p.86 / Chapter 5.2. --- Amplification Analysis by Array-CGH --- p.88 / Chapter 5.2.1. --- Amplicons Showing Amplification in HCC --- p.89 / Chapter 5.2.1.1. --- Locus of 17q23 --- p.89 / Chapter 5.2.1.1.1. --- D17S1670 --- p.89 / Chapter 5.2.1.1.2. --- RPS6KB1 --- p.91 / Chapter 5.2.1.2. --- Locus of 1q25-q31 --- p.92 / Chapter 5.2.1.2.1. --- LAMC2 --- p.92 / Chapter 5.2.1.3. --- Locus of 3q26.3 --- p.93 / Chapter 5.2.1.3.1. --- PIK3CA --- p.93 / Chapter 5.2.1.4. --- Locus of 8p22 --- p.94 / Chapter 5.2.1.4.1. --- CTSB --- p.94 / Chapter 5.2.1.5. --- Locus of 6q22 --- p.95 / Chapter 5.2.1.5.1. --- MYB --- p.95 / Chapter 5.2.1.6. --- Locus of 20ql3 --- p.96 / Chapter 5.2.1.6.1. --- CSE1L --- p.96 / Chapter 5.2.1.7. --- Locus of Ip36.2-p35.1 --- p.97 / Chapter 5.2.1.7.1. --- FGR --- p.97 / Chapter 5.2.1.8. --- Locus of 7q21.1 --- p.98 / Chapter 5.2.1.8.1. --- PGY1 --- p.98 / Chapter 5.2.2. --- Amplicons Showing Deletion in HCC --- p.99 / Chapter 5.2.2.1. --- Loss at 11ql3 and 14q32.3 --- p.99 / Chapter 5.2.3. --- Limitation of the Study --- p.100 / Chapter 5.2.3.1. --- Samples and Materials --- p.100 / Chapter 5.2.4. --- Further Study --- p.101 / Chapter 5.2.4.1. --- Confirmation of the Result in Various Levels --- p.101 / Chapter 5.2.4.2. --- Assessment of the Significant Losses on Chromosomes 11ql3 and 14ql3 --- p.101 / Chapter 5.2.5. --- Application of Microarray in Genetic Studies --- p.102 / Chapter 5.2.5.1. --- Deletion Analysis --- p.102 / Chapter 5.2.5.2 --- Tissue Microarray --- p.103 / Chapter 5.2.5.3. --- cDNA Microarray --- p.103 / Chapter chapter6 --- references --- p.104

Being a dissertation presented in fulfilment of the requirements governing the degree of Masters of Science in the Faoulty of Medicine, University of the Witwatersrand / Recent investigations have shown enhanced or aberrant expression of major histocompatibility system (MHC) antigens on cells lines derived from human hepatocellular carcinoma (HCC) in vitro and HCC in vivo. ( Abbreviation abstract ) / AC2017

Chen, Juan. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 124-154). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

by Kam-Ming Au. / Thesis (M.Sc.)--Chinese University of Hong Kong, 1990. / Bibliography: leaves 87-101. / LIST OF TABLES / LIST OF FIGURES / ACKNOWLEDGEMENTS / ABSTRACT / Chapter CHAPTER 1. --- INTRODUCTION --- p.1 / Chapter 1.1 --- Normal calcium homeostasis --- p.1 / Chapter 1.2 --- The incidence and common causes of hypercalcemia in hospital population --- p.6 / Chapter 1.3 --- Hypercalcemia in primary hyperparathyroidism --- p.10 / Chapter 1.4 --- Hypercalcemia of malignancy --- p.13 / Chapter 1.5 --- Pathophysiology of humoral hypercalcemia of malignancy --- p.16 / Chapter 1.6 --- Pathogenesis of humoral hypercalcemia of malignancy-evidence for a parathyroid hormone-related peptide --- p.20 / Chapter 1.7 --- Hypercalcemia in primary hepatocellular carcinoma --- p.27 / Chapter 1.8 --- Physiological role of cyclic adenosine monophosphate --- p.28 / Chapter 1.9 --- Aim of the present study --- p.29 / Chapter CHAPTER 2. --- MATERIALS AND METHODS --- p.30 / Chapter 2.1 --- Patients --- p.30 / Chapter 2.1.1 --- Hepatocellular carcinoma patients --- p.30 / Chapter 2.1.2 --- Cirrhotic patients --- p.30 / Chapter 2.2 --- Healthy control subjects --- p.30 / Chapter 2.3 --- Collection of blood and urine specimens --- p.32 / Chapter 2.4 --- Methods --- p.32 / Chapter 2.4.1 --- Routine chemistries --- p.32 / Chapter 2.4.2 --- Plasma and urine cyclic adenosine monophosphate --- p.33 / Chapter - --- commercial urine controls --- p.34 / Chapter - --- scintillation cocktail --- p.34 / Chapter - --- imprecision study --- p.34 / Chapter - --- accuracy study --- p.34 / Chapter 2.4.3 --- Nephrogenous cyclic adenosine monophosphate and total urinary cyclic adenosine monophosphate / 100 ml glomerular filtrate --- p.35 / Chapter 2.4.4 --- Total urinary cyclic adenosine monophosphate : creatinine ratio --- p.36 / Chapter 2.4.5 --- Components of hypercalcemia --- p.36 / Chapter 2.4.6 --- Urinary hydroxyproline : creatinine ratio --- p.37 / Chapter 2.4.7 --- Renal phosphate threshold --- p.37 / Chapter 2.4.8 --- Serum parathyroid hormone --- p.38 / Chapter 2.4.9 --- Serum parathyroid hormone-related peptide --- p.38 / Chapter 2.5 --- Statistical analysis --- p.39 / Chapter CHAPTER 3. --- RESULTS --- p.40 / Chapter 3.1 --- Method validation for cyclic adenosine monophosphate assay --- p.40 / Chapter 3.1.1 --- Standard curve of the cyclic adenosine monophosphate assay --- p.40 / Chapter 3.1.2 --- Results of imprecision study --- p.43 / Chapter 3.1.3 --- Results of accuracy study --- p.43 / Chapter 3.2 --- "Results of hypercalcemic and normocalcemic hepatocellular carcinoma patients, cirrhotic patients, and healthy control subjects" --- p.47 / Chapter 3.2.1 --- "Results of serum calcium, albumin adjusted calcium, serum albumin and serum alkaline phosphatase" --- p.47 / Chapter 3.2.2 --- "Results of serum phosphate, renal phosphate threshold and serum parathyroid hormone" --- p.51 / Chapter 3.2.3 --- Results of plasma cyclic adenosine monophosphate --- p.55 / Chapter 3.2.4 --- "Results of nephrogenous cyclic adenosine monophosphate , total urinary cyclic adenosine monophosphate / 100 ml glomerular filtrate and total urinary cyclic adenosine monophosphate : creatinine ratio 59" / Chapter 3.2.5 --- Results of urinary calcium : creatinine ratio and urinary hydroxyproline : creatinine ratio --- p.66 / Chapter 3.2.6 --- Factors contributing to hypercalcemia in hepatocellular carcinoma patients 71 / Chapter 3.2.7 --- Results of serum parathyroid hormone-related peptide --- p.75 / Chapter CHAPTER 4. --- DISCUSSION --- p.77 / REFERENCES --- p.87

Chi Tian-yi. / "July 2002." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (p. 213-257). / 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.

Chiu Hoi Shan Clarissa. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (leaves 110-126). / Abstracts in English and Chinese. / Abstract in English --- p.i / Abstract in Chinese --- p.iii / Acknowledgement --- p.iv / List of Abbreviations --- p.v / List of Tables --- p.vi / List of Figures --- p.viii / Introduction and Objectives / Hepatocellular Carcinoma / Epidemiology --- p.1 / Sex and Age --- p.1 / Geographic distibution --- p.2 / Risk factors of HCC --- p.2 / Mortality from liver cancer --- p.4 / Treatment for HCC --- p.4 / Tumor markers --- p.5 / Alpha-fetoprotein / Structure --- p.5 / Physiological Functions of AFP --- p.7 / Re-expression of AFP in Adult --- p.7 / Re-expression of AFP in HCC --- p.8 / Isoforms of AFP --- p.8 / Specific AFP isoform in HCC --- p.9 / Sialic Acid --- p.11 / Sialyltransferase / "Galβ 1,4GlcnAc α2,6-sialyitransferase" --- p.12 / "Characterization of ST2,6Gal I" --- p.12 / "Expression of ST2,6Gal I" --- p.12 / "General features of ST2,6Gal I Activity" --- p.15 / Relationship Between AFP isoforms and ST2，6Gal in Fetal Mouse Model --- p.15 / "Change in ST2,6GaI I Activity in Transgenic Mouse Models of HCC" --- p.16 / "Study of Activity of ST2,6Gal I in Colon Carcinoma" --- p.16 / Objective of the Project --- p.18 / Chapter Chapter 1 --- Formation of Monosialyated AFP by Hepatoma Cells / Chapter 1.1 --- Introduction --- p.21 / Chapter 1.2 --- Materials and Methods --- p.23 / Chapter 1.3 --- Results / Chapter 1.3.1 --- AFP obtained from cell culture --- p.34 / Chapter 1.3.2 --- IEF for AFP in cell culture medium --- p.34 / Chapter 1.3.3 --- SDS-PAGE analysis of AFP --- p.34 / Chapter 1.3.4 --- Stability of AFP isoforms after secreted to cell culture medium --- p.39 / Chapter 1.3.5 --- Comparison of the AFP isoforms between liver tissues and serum --- p.38 / Chapter 1.4 --- Discussion / Chapter 1.4.1 --- Origin of the extracellular msAFP - in vitro Model --- p.43 / Chapter 1.4.2 --- Origin of circulating msAFP - in vivo Model --- p.44 / Chapter 1.5 --- Conclusion --- p.46 / Chapter Chapter 2 --- "Presence of msAFP in the serum of HCC patient is a Consequence of Decrease in the Activity of ST2, / Chapter 2.1 --- Introduction --- p.47 / Chapter 2.2 --- Materials and Methods --- p.49 / Chapter 2.3 --- Results / Chapter 2.3.1 --- Semi-quantitation of msAFP --- p.61 / Chapter 2.3.2 --- Evaluation of the ST2，6Gal I Assay --- p.65 / Chapter 2.3.3 --- "Measurements and comparisons of the activity of ST2,6Gal I in non-tumor and tumor tissue" --- p.65 / Chapter 2.3.4 --- "Evaluation of the RT-PCR ELISA for semi-quantitation and comparisons of ST2,6Gal I mRNA levels" --- p.75 / Chapter 2.3.5 --- "Semi-quantitation and comparisons of ST2,6Gal I mRNA levels in the non-tumor and tumor tissues" --- p.84 / Chapter 2.3.6 --- Correlations between the markers --- p.87 / Chapter 2.4 --- Discussion / Chapter 2.4.1 --- "Overproduction of AFP, a possible cause for increased msAFP formation" --- p.99 / Chapter 2.4.2 --- "Decrease of ST2,Gal I activity, a possible cause for increased msAFP formation" --- p.100 / Chapter 2.4.3 --- "ST2,6Gal I activity in tumor is not regulated at transcriptional level" --- p.102 / General Discussion / Origin of blood stream msAFP --- p.103 / Physiological Mechanism for the formation of msAFP in HCC --- p.104 / Regulation of ST2，6Gal I activity in HCC --- p.105 / "Comparison between the ST2,6GaI I activities in human HCC and Colon Cancer" --- p.107 / Conclusion and Future studies / Conclusion --- p.108 / Future studies --- p.109 / References --- p.110