by Ho King Wah Stephen. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1996. / Includes bibliographical references (leaves 251-304). / Title Page --- p.1 / Table of Contents --- p.2 / Summary --- p.3 / Glossary of abbreviations used in the thesis --- p.10 / List of Figures --- p.12 / List of Tables --- p.20 / Acknowledgments --- p.24 / Chapter Chapter 1 --- Hepatic Cancer - Review of the Medical Literature --- p.25 / Chapter Chapter 2 --- Selective Internal Radiation Therapy - Review of the Medical Literature --- p.47 / Chapter Chapter 3 --- The Background In Physics --- p.76 / Chapter Chapter 4 --- Hypothesis and Testing the Hypothesis --- p.88 / Chapter Chapter 5 --- Parameters Required in the Partition Model --- p.98 / Chapter Chapter 6 --- Prediction of Radiation Dose and Verification of the Partition Model --- p.143 / Chapter Chapter 7 --- Clinical Evaluation of the Partition Model --- p.181 / Chapter Chapter 8 --- Conclusions and Future Development --- p.248 / References --- p.251

Ovarian carcinoma is considered to be the most deadly of the gynaecological malignancies which in its earliest stages is usually asymptomatic. The unsatisfactory survival rates of patients on conventional chemotherapy regimens, necessitates vehicles capable of carrying cytotoxic agents directly to the malignant cells. This mode of targeted delivery allows for efficient tumour cell kill whilst sparing surrounding normal tissue and substantially reducing side-effects. This project examined the possible therapeutic role of a targetable sustained drug delivery system, albumin immunomicrospheres containing the chemotherapeutic agents, cisplatin and 5-fluorouracil, for the treatment of ovarian adenocarcinoma. A rodent cell line, as a model, has proved to be similar to its human counterpart and also has shown to be transplantable from one animal to another. Such a model could therefore be useful for performing experiments relating to drug delivery targetability and therapeutic trials, as well as survival studies, in cases of ovarian adenocarcinoma. In particular, this project examines the efficacy of the immunospecific microspheres containing the drugs in a highly concentrated form, administered intraperitoneally and targeted to an ovarian adenocarcinoma, in an attempt to enhance tumour cell kill whilst largely sparing surrounding normal tissue. It is widely recognized that the effectiveness of most chemotherapeutic drugs would be enhanced if they were to act selectively where they are needed. In order to achieve a therapeutically relevant dose in tumour cells, the amount of drug required usually proves also to be highly toxic to normal tissues. It was postulated that, to overcome the above, it may be feasible to develop a sustained immunospecific drug delivery system to optimize the action of cisplatin and 5-fluorouracil at the target site. With the attainment of the above, it was further postulated that higher doses of drugs could be delivered to the target area effecting higher tumour cell kill, that less normal tissue damage should occur and that toxic side effects of the drugs should be reduced. The rationale for selecting combination therapy of cisplatin and 5-fluorouracil is that, although it has been inferred that DNA intrastrand and interstrand cross-links produced by the cisplatin often repair, this repair can be blocked by 5-fluorouracil by inhibition of thymidylate synthetase, thus preventing DNA strand repair. Albumin immunomicrospheres are relatively innocuous in terms of toxicity, non-antigenic and are capable of accommodating chemotherapeutic agents in a non-specific fashion. We showed that they were capable of a 0. 94% entrapment of 5-fluorouracil and 1.23% cisplatin. Delivery of these drugs at a target site, and at these concentrations, should effect extensive cell kill. As the microspheres are chemically stable and can be manipulated to offload the entrapped drugs satisfactorily, in vitro drug release profiles were performed employing immunospecific microspheres directed towards its target cells. Slow degradation of the drug- containing albumin immunomicrospheres showed that 0.283 μg cisplatin/ml plasma and 0. 799 μg 5-fluorouracil/ml plasma could be made available at the target site over a 14-day period. These concentrations could be maintained over at least another 14 days and effect tumour cell kill satisfactorily. In order to assess the tumour cell kill, we performed clonogenic assays, cell survival growth curves, MTT cytotoxicity assays and assessed the induction of micronuclei in the tumour cells. The synergism between 5-fluorouracil and cisplatin showed a modulation of cisplatin cytotoxicity and total tumour cell kill was achieved at concentrations of 0.5 μg/ml 5-fluorouracil and 0.1 μg/ml cisplat in at the target site. The above-mentioned evidence of effective targeting of the drugs was then investigated in female Wistar rats with ovarian adenocarcinoma to assess comparative survival times when treated with free drugs or immunospecific albumin microspheres containing the drugs. Animals given a free drug dose of 5 mg/kg cisplatin and 20mg/kg 5-fluorouracil, followed by a repeat dose at the same concentrations 7 days later showed that only 14% of the animals survived a 90-day trial period. Animals given an intraperitoneal bolus dose of immunomicrospheres at a dose of 1 O mg/kg cisplatin and 40 mg/kg 5-fluorouracil showed that 60% of the animals survived the 90-day trial period. This data indicated to us that the survival probability of animals treated with drug-containing immunomicrospheres was substantially superior to other protocols employed in this study.

by Chan Ka Kui. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 104-113). / Abstracts in English and Chinese. / ABSTRACT --- p.1 / Chapter 1 --- INTRODUCTION --- p.5 / Chapter 1.1 --- Incidence rate of breast cancer in Hong Kong --- p.5 / Chapter 1.2 --- Estrogen and breast cancer --- p.6 / Chapter 1.3 --- The relation between glucose transporters and breast cancer --- p.7 / Chapter 1.4 --- Antisense oligonucleotide --- p.10 / Chapter 1.5 --- Action mechanisms of antisense oligonucleotide --- p.11 / Chapter 1.6 --- Modification of the oligonucleotide --- p.13 / Chapter 1.7 --- Length --- p.16 / Chapter 1.8 --- Sequence selection of the antisense oligonucleotide --- p.16 / Chapter 1.9 --- Delivery means in antisense oligonucleotide --- p.18 / Chapter 1.10 --- The therapeutic role of antisense oligonucleotide --- p.19 / Chapter 1.11 --- Objective of the project --- p.21 / Chapter 2 --- MATERIAL AND METHODS --- p.23 / Chapter 2.1 --- Materials --- p.23 / Chapter 2.2 --- Methods --- p.26 / Chapter 3 --- RESULTS --- p.37 / Chapter 3.1 --- The characteristics of MCF-7 and MDA-MB-231 cells --- p.37 / Chapter 3.2 --- Trend of uptake of antisense oligonucleotides in MCF-7 and MDA- MB-231 cells --- p.41 / Chapter 3.3 --- The integrity of the oligonucleotide in serum-free medium during transfection --- p.48 / Chapter 3.4 --- Detection of effects of Glut5 antisense oligonucleotides of breast tumor cells-MTT assay --- p.50 / Chapter 3.5 --- Detection of the antiproliferative effect by trypan blue exclusion assay and thymidine incorporation --- p.56 / Chapter 3.6 --- Cell cycle analysis and DNA extraction --- p.61 / Chapter 3.7 --- Suppression of Glut5 mRNA detected by RT-PCR --- p.66 / Chapter 3.8 --- Suppression of translation of Glut5 proteins as indicated by Western blotting --- p.73 / Chapter 3.9 --- Measurement of the fructose and glucose uptake in MCF-7 and MDA -MB-231 cells after antisense treatment --- p.76 / Chapter 3.10 --- Change of the phosphofructokinase-1 (PFK-1) activities in MDA- MB-231 cells --- p.82 / Chapter 3.11 --- Measurement of the change in the intracellular pH of the breast tumor cells --- p.84 / Chapter 4 --- DISCUSSION --- p.89 / Chapter 4.1 --- The insights of Glut5 antisense oligonucleotide into cancer therapy --- p.89 / Chapter 4.2 --- The uptake pattern of Glut5 antisense oligonucleotides in breast tumor cells --- p.90 / Chapter 4.3 --- Stability of antisense oligonucleotide during transfection --- p.92 / Chapter 4.4 --- Effects of Glut5 antisense oligonucleotide on MCF-7 and MDA-MB- 231cells --- p.93 / Chapter 4.5 --- Proofs of undergoing antisense action mechanism --- p.95 / Chapter 4.6 --- Physiological changes in breast tumor cells after antisense treatment --- p.97 / Chapter 5 --- CONCLUSION --- p.103 / Chapter 6 --- References --- p.104

by Chan Chi Wai, Angus. / "Submitted in Jan 1999, revised in Jan 2000." / Thesis (M.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 262-294). / 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.

Xu, Dandan. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 209-231). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

No description available.

Ma, Buig Yue Brigette. / Thesis M.D. Chinese University of Hong Kong 2014. / Includes bibliographical references (leaves 232-270). / Title from PDF title page (viewed on 18, November, 2016).

by Lui Chi Pang. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1992. / Includes bibliographical references (leaves 265-281). / Acknowledgements --- p.i / Abbreviations --- p.ii / Abstract --- p.iii / Table of contents --- p.vii / Introduction / Review of Literature --- p.2 / Chapter I. --- Cellular response of hyperthermia --- p.3 / Chapter A) --- Effects on macromolecules synthesis --- p.3 / Chapter B) --- Effects on glycolysis and respiration --- p.5 / Chapter C) --- "Effects on plasma membrane, intracellular ionic level and intracellular pH" --- p.6 / Chapter II. --- Physical aspects --- p.11 / Chapter A) --- Survival curves --- p.11 / Chapter B) --- Concept of thermal dose --- p.13 / Chapter III. --- Clinical thermal theraphy --- p.21 / Chapter A) --- Hyperthermia in vivo --- p.21 / Chapter B) --- Combination of hyperthermia and radiotheraphy --- p.29 / Chapter C) --- Combination of hyperthermia and chemotherapy --- p.37 / Chapter IV. --- Thermotolerance --- p.48 / Scope of study --- p.54 / Materials and Methods / Chapter I. --- Cytotoxicity tests of cells in vitro --- p.59 / Chapter II. --- Whole body hyperthermia on Ehrlich ascite tumour (EAT)-bearing mice --- p.63 / Chapter III. --- Combination of hyperthermia and drugs --- p.66 / Chapter IV. --- Measurement of intracellular pH --- p.68 / Chapter V. --- Assay for sialic acids in the plasma membrane --- p.72 / Chapter VI. --- Assays of nucleolar proteins --- p.76 / Chapter VII. --- Acetylation of nuclear proteins --- p.80 / Chapter VIII. --- Detection of 72-kD heat shock protein --- p.93 / Results and Discussion / Chapter I. --- Cytotoxicity of hyperthermia in vitro --- p.102 / Chapter II. --- Hyperthermia on EAT cells in vivo --- p.131 / Chapter III. --- Cytotoxicity of combination of hyperthermia and drugs --- p.148 / Chapter IV. --- Intracellular pH changes during hyperthermia --- p.162 / Chapter V. --- Modification of sialic acid level in plasma membrane --- p.180 / Chapter VI. --- Conformational changes of nucleolar proteins --- p.193 / Chapter VII. --- Hyperthermic effect on acetylation of nuclear proteins --- p.209 / Chapter VIII. --- Induction of 72-kD heat shock protein --- p.223 / General Discussion / Chapter A. --- Hyperthermic cytotoxicity --- p.249 / Chapter B. --- Effects on plasma membrane and control of intracellular pH --- p.253 / Chapter C. --- Effects on the nuclear proteins --- p.256 / Chapter D. --- Conclusion --- p.263 / Bibliography --- p.264

by Ng Ping-chung. / Thesis (Ph.D.)--Chinese University of Hong Kong, 1994. / Includes bibliographical references (leaves 161-179). / List of Abbreviation / Abstract / Acknowledgements / Table of contents / Chapter 1. --- Introduction / Chapter 1.1 --- Hormone and carcinogenesis --- p.1 / Chapter 1.2 --- Estrogen and carcinogenesis --- p.3 / Chapter 1.2.1 --- Carcinogenesis and endogenous sex hormone status --- p.3 / Chapter 1.2.2 --- Etiology of breast cancer --- p.3 / Chapter 1.2.2.1 --- Epidemiology --- p.3 / Chapter 1.2.2.2 --- Hormonal factors --- p.5 / Chapter 1.2.2.3 --- Genetic predisposition --- p.8 / Chapter 1.2.2.4 --- Influence of diet --- p.8 / Chapter 1.2.3 --- Hormonal therapy --- p.18 / Chapter 1.2.3.1 --- Anti-estrogen --- p.18 / Chapter 1.2.3.2 --- Progestins --- p.21 / Chapter 1.2.3.3 --- Aromatase inhibitor --- p.22 / Chapter 1.2.3.4 --- GnRH analogue therapy --- p.26 / Chapter 1.3 --- Estrogen pool --- p.26 / Chapter 1.4 --- Estrogen receptor --- p.30 / Chapter 1.4.1 --- General features of estrogen receptor and action mechanism --- p.30 / Chapter 1.4.2 --- Anti-estrogen binding site (AEBS) --- p.31 / Chapter 1.4.3 --- Physiological consideration --- p.32 / Chapter 1.4.3.1 --- Uterus: uterotrophic responses --- p.32 / Chapter 1.4.3.2 --- "Progesterone, the physiological estrogen antagonist" --- p.34 / Chapter 1.5 --- The role of growth factors and steroid hormones in breast cancer cell --- p.35 / Chapter 1.6 --- Alternate cytotoxic action of TAM --- p.37 / Chapter 1.7 --- In vitro models utilised in breast cancer study --- p.38 / Chapter 1.8 --- Current development of anti-estrogen --- p.39 / Chapter 1.9 --- Background about yuehchukene (YCK) --- p.41 / Chapter 2. --- Materials and methods / Chapter 2.1 --- Studies using whole animals --- p.47 / Chapter 2.1.1 --- Uterotrophic assay in rats --- p.47 / Chapter 2.1.2 --- Anti-implantation assay in rats --- p.48 / Chapter 2.1.3 --- Vaginal smear in mice --- p.49 / Chapter 2.2 --- Studies using breast cancer cells --- p.49 / Chapter 2.2.1 --- MCF-7 cell culture --- p.49 / Chapter 2.2.1.1 --- Measurement of cell number --- p.50 / Chapter 2.2.1.1.1 --- Cell count with haemocytometer --- p.50 / Chapter 2.2.1.1.2 --- Cell number estimated by DNA content in culture using Hoechst33258 --- p.51 / Chapter 2.2.1.1.3 --- Cell number estimated by [3H]-thymidine incorporation --- p.52 / Chapter 2.2.1.1.4 --- Preparation of dextran coated charcoal stripped serum --- p.52 / Chapter 2.2.2 --- MDA-MB-231 cell culture --- p.53 / Chapter 2.3 --- Studies using steroid receptors --- p.54 / Chapter 2.3.1 --- Rat uterine estrogen receptor --- p.54 / Chapter 2.3.2 --- Mice uterus and vaginal estrogen receptor --- p.55 / Chapter 2.3.3 --- MCF-7 cell estrogen receptor --- p.55 / Chapter 2.3.3.1 --- MCF-7 whole cell estrogen receptor binding --- p.55 / Chapter 2.3.3.2 --- Cytosolic estrogen receptor preparation from MCF-7 cell --- p.57 / Chapter 2.3.4 --- Progesterone receptor binding in MCF-7 cell --- p.57 / Chapter 2.3.5 --- Rat hepatic anti-estrogen binding site (AEBS) --- p.58 / Chapter 2.3.6 --- Estrogen receptor content estimation by enzyme immunoassay --- p.58 / Chapter 2.4 --- Enzyme studies related to estrogen metabolism --- p.60 / Chapter 2.4.1 --- Rat uterine ornithine decarboxylase (ODC) --- p.60 / Chapter 2.4.2 --- Rat hepatic ethoxyresorufin O-deethylase (EROD) --- p.60 / Chapter 2.4.3 --- Rat hepatic estradiol-2-hydroxylase --- p.62 / Chapter 2.4.4 --- MCF-7 cell estradiol-2-hydroxylase --- p.62 / Chapter 2.4.5 --- Human placental microsomal aromatase activity --- p.63 / Chapter 2.5 --- Enzymatic studies related to signal transduction --- p.64 / Chapter 2.5.1 --- Inhibition of Protein Kinase C activity of MCF-7 cell and protein phosphorylation --- p.64 / Chapter 2.5.2 --- Inhibition of calmodulin activation of cyclic nuleotide phosphodiesterase --- p.66 / Chapter 2.6 --- "Preparation of Pre-YCK, crude-YCK and post-YCK fractions" --- p.67 / Chapter 2.7 --- Preparation of Indole-3-carbinol acid condensation product (I3Ca) --- p.71 / Chapter 2.8 --- Studies on TCP series of YCK analogues --- p.71 / Chapter 2.9 --- List of test compounds --- p.75 / Chapter 2. 10 --- List of radio-ligands --- p.77 / Chapter 2.11 --- Miscellaneous reagents related to cell culture --- p.78 / Chapter 2.11.1 --- Culture medium --- p.78 / Chapter 2.11.2 --- Fetal calf serum --- p.78 / Chapter 2.11.3 --- Penicillin-streptomycin powder --- p.78 / Chapter 2.11.4 --- Phosphate buffer saline --- p.78 / Chapter 2.12 --- "Solvents, chemical and scintillants" --- p.78 / Chapter 3. --- Result / Chapter 3.1 --- Rat uterotrophic response with EE2 and YCK --- p.80 / Chapter 3.2 --- Mice vaginal cornification with estradiol (E2) and YCK --- p.83 / Chapter 3.3 --- Human breast cancer cell culture --- p.86 / Chapter 3.3.1 --- MCF-7 cell growth with YCK --- p.86 / Chapter 3.3.2 --- MCF-7 cell growth with YCK analogues and other related compounds --- p.91 / Chapter 3.3.3 --- MDA-MB-231 cell culture --- p.100 / Chapter 3.4 --- Receptor Binding --- p.100 / Chapter 3.4.1 --- Rat uterine estrogen receptor --- p.100 / Chapter 3.4.2 --- Mice uterine and vaginal estrogen receptor --- p.103 / Chapter 3.4.3 --- MCF-7 whole cell and cytosolic estrogen receptor --- p.103 / Chapter 3.4.4 --- MCF-7 cell progesterone receptor --- p.107 / Chapter 3.4.5 --- Rat hepatic anti-estrogen binding sites (AEBS) --- p.111 / Chapter 3.5 --- Enzyme activities related to estrogen metabolism --- p.111 / Chapter 3.5.1 --- Rat uterine ornithine decarboxylase (ODC) --- p.111 / Chapter 3.5.2 --- Rat hepatic estradiol-2-hydroxylase and ethoxyresorufin O-deethylase --- p.114 / Chapter 3.5.3 --- MCF-7 cell estradiol-2-hydroxylase --- p.121 / Chapter 3.5.4 --- Human placenta and MCF-7 cell aromatase --- p.126 / Chapter 3.6 --- Enzyme activities related to signal transduction --- p.126 / Chapter 3.6.1 --- Protein kinase C inhibition in vitro --- p.126 / Chapter 3.6.2 --- Calmodulin-dependent phosphodiesterase inhibitory actions in vitro --- p.131 / Chapter 3.7 --- Studies on TCP series of YCK analogues --- p.131 / Chapter 4. --- Discussion / Chapter 4.1 --- Estrogenicity of YCK --- p.140 / Chapter 4.2 --- Estrogenicity of YCK correlates with estrogen receptor (ER) binding --- p.141 / Chapter 4.3 --- Attenuation by YCK --- p.142 / Chapter 4.3.1 --- Attenuation by YCK on estrogen induced uterotrophic activity --- p.142 / Chapter 4.3.2 --- Attenuation by YCK on mice vaginal cornification with estradiol and YCK --- p.142 / Chapter 4.3.3 --- Attenuation by YCK on MCF-7 cell growth --- p.143 / Chapter 4.3.4 --- Attenuation of YCK on ornithine decarboxylase (ODC) induced by estrogen --- p.144 / Chapter 4.4 --- Deviation between YCK potency and RBA --- p.145 / Chapter 4.5 --- Estrogen inhibition action of YCK via non receptor binding mechanism --- p.148 / Chapter 4.6 --- Protein kinase C/ calmodulin-dependent phosphodiesterase inhibitor --- p.152 / Chapter 4.7 --- Progesterone receptor --- p.154 / Chapter 4.8 --- Aromatase inhibitor? --- p.155 / Chapter 4.9 --- Posssible mechanism for the attenuation of estrogenic action by YCK --- p.157 / Chapter 4.10 --- TCP series of YCK analogues --- p.158 / Chapter 4.11 --- Future works --- p.159 / Chapter 5. --- Reference --- p.161 / Appendix / Appendix 1 YCK analogues / Appendix 2 Structure of compounds mentioned in this thesis

by Tsui Hong Teng. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 174-181). / Abstracts in English and Chinese. / A CKNO WLED GMENTS --- p.7 / ABSTRACT --- p.8-10 / Chapter Chapter 1: --- Introduction: --- p.11-44 / Chapter 1.1) --- Glucose transporters / Chapter 1.2) --- Glucose transporters and cancers / Chapter 1.3) --- Antisense strategies / Chapter 1.4) --- Cellular uptake of oligonucleotides / Chapter 1.5) --- Hyperthermia and combined treatments / Chapter Chapter 2: --- Materials and methods --- p.45-60 / Chapter 2.1) --- Materials: / Chapter 2.1a) --- Cell lines and culture media / Chapter 2.1b) --- Oligonucleotides synthesis / Chapter 2.1c) --- Chemicals / Chapter 2.2) --- Methods: / Chapter 2.2a) --- Oligonucleotide design / Chapter 2.2b) --- Oligonucleotide treatment / Chapter 2.2c) --- Flow cytometry / Chapter 2.2d) --- Confocal microscopy / Chapter 2.2e) --- MTT assay for cytotoxicity or cell proliferation / Chapter Chapter 3: --- Cellular uptake of oligonucleotide spontaneously and Lipofectin-aided: --- p.61-85 / Chapter 3.1) --- Introduction / Chapter 3.2) --- Flow cytometric studies / Chapter 3.3) --- Confocal microscopic studies / Chapter 3.4) --- Cytotoxic effect of Lipofectin alone on MCF-7 cells / Chapter 3.5) --- Discussion / Chapter Chapter 4: --- Hyperthermia can enhance oligonucleotide uptake: --- p.86-118 / Chapter 4.1) --- Introduction / Chapter 4.2) --- Flow cytometric studies / Chapter 4.3) --- Confocal microscopic studies / Chapter 4.4) --- Cytotoxic effect of hyperthermia on MCF-7 cells / Chapter 4.5) --- FITC-ODN uptake in survival cells by propidium iodide (PI) exclusion method for hyperthermia / Chapter 4.6) --- Discussion / Chapter Chapter 5: --- The antiproliferative effects of antisense molecules against Glut-1 and 5 on MCF- 7 cells transfected by Lipofectin: --- p.119-146 / Chapter 5.1) --- Introduction / Chapter 5.2) --- The growth curve of MCF-7 cells / Chapter 5.3) --- The calibration of MTT assay / Chapter 5.4) --- The effect of antisense Glut-1 concentration without Lipofectin on MCF-7 cells / Chapter 5.5) --- The effect of antisense Glut-1 concentration with Lipofectin on MCF-7 cells / Chapter 5.6) --- The effect of antisense Glut-5 concentration without Lipofectin on MCF-7 cells / Chapter 5.7) --- The effect of antisense Glut-5 concentration with Lipofectin on MCF-7cells / Chapter 5.8) --- The effect of transfection time of antisense Glut-1 on MCF-7 cells / Chapter 5.9) --- The effect of transfection time of antisense Glut-5 on MCF-7 cells / Chapter 5.10) --- The effect of transfection time of antisense Glut-5 for higher concentration on MCF-7 cells / Chapter 5.11) --- The effect of antisense Glut-1 to Lipofectin (w/w) ratio on MCF-7 cells / Chapter 5.12) --- The effect of antisense Glut-1 to Lipofection (w/w) ratio for higher transfection time on MCF-7 cells / Chapter 5.13) --- The effect of antisense Glut-5 to Lipofectin (w/w) ratio on MCF-7 cells / Chapter 5.14) --- Discussion / Chapter Chapter 6: --- Combined treatments: --- p.147-162 / Chapter 6.1) --- Introduction / Chapter 6.2) --- The effect of combined treatment of antisense Glut-1 combined with antisense Glut-5 on MCF-7 cells / Chapter 6.3) --- The chronic effect of hyperthermia for 5 hours on MCF-7 cells / Chapter 6.4) --- The effect of combined treatment between antisense Glut-1 and hyperthermia on MCF-7 cells / Chapter 6.5) --- The net effect of antisense Glut-1 in combined treatment between hyperthermia and antisense Glut-1 on MCF-7 cells / Chapter 6.6) --- The effect of combined treatment between antisense Glut-5 and hyperthermia on MCF-7 cells / Chapter 6.7) --- The net effect of antisense Glut-5 in combined treatment between hyperthermia and antisense Glut-5 on MCF-7 cells / Chapter 6.8) --- Discussion / Chapter Chapter 7: --- Discussion: --- p.163-173 / Chapter Chapter 8: --- References: --- p.174-181