In the past, patients with peritoneal surface malignancy were considered incurable and were only offered palliative treatments. However, in a substantial number of patients, disease progression that is isolated to peritoneum may occur. It has been realised that elimination of peritoneal surface tumours may have an impact on the survival of these cancer patients, in whom a prominent cause of death is peritoneal carcinomatosis. The focus of this PhD. thesis is on the combined treatment of cytoreductive surgery and perioperative intrapersonal chemotherapy for diffuse malignant peritoneal mesothelioma, pseudomyxoma peritonei, colorectal peritoneal carcinomatosis and resectable gastric cancer. Section one describes the major principles of management for peritoneal surface malignancy, covering the historical perspectives, the treatment rationales and the learning curve associated with the combined procedure. Section two is devoted to peritoneal mesothelioma, in trying to examine this disease from its clinical, radiologic and histopathologic aspects. A radiologic classification and a histopathologic staging system for this disease are proposed. In section three, the results of the combined treatment for pseudomyxoma peritonei are presented, including a systematic review of the literature, a case series of 50 patients from our Australian centre and a treatment failure analysis of 402 patients from the Washington Cancer Institute. These studies suggest that a disease-free state is important for long-term survival for patients with pseudomyxoma peritonei. In section four, the current evidence on the combined treatment for colorectaI peritoneal carcinomatosis is demonstrated by conducting a systematic review of the literature and survival and perioperative outcome analyses of two separate patient cohorts. These results suggest that the combined treatment is associated with an improved survival, as compared with historical controls. In the last section, a metaanalysis of the randomised controlled trials on adjuvant intraperitoneal chemotherapy for resectable gastric cancer shows that a significant improvement in survival is associated with hyperthermic intraoperative intraperitoneal chemotherapy alone or in combination with early postoperative intraperitoneal chemotherapy.

Colorectal cancer is the second leading cause of cancer-related mortality in Hong Kong and lack of selectivity has limited the success of conventional chemotherapy. Given the recent interest in the anti-cancer effects of traditional Chinese medicine (TCM), there are two approaches to studying its bioactivity: as a mixture of ingredients or as single compounds. The objective of the present study is to examine the anti-tumor effects of Angelicae Sinensis Radix (DG) and Garcinia hanburyi resin (TH) using both approaches, respectively, as they are traditionally used to treat inflammation. In the present study, their anti-cancer effects and the mechanisms of actions were examined for the development of potential novel chemotherapeutic drugs for colon cancer since inflammation is a predisposing factor for colon cancer. / DG extract and its three main bioactive phtbalides: n-butylidenephthalide, senkyunolide A and z-ligustilide (LGT), were found to be cytotoxic to HT-29 cells with IC50 values (24 h) of 20.70 +/- 0.85, 72.51 +/- 8.65, 18.74 +/- 1.14 and 41.98 +/- 3.64 mug/ml, respectively. The results evidenced that LGT induced G0/G 1 arrest and apoptosis, triggering cleavage of PARP, pro-caspases-3, -8 and -9 and nuclear fragmentation. LGT and cisplatin synergistically reduced the viability of HT-29 cells. More interestingly, DG extract was more potent than individual phthalides, suggesting that there are other bioactive components and/or synergistic interactions. / Individual compounds purified from TH were investigated because gambogic acid isolated from this herb has been used clinically to treat cancer, 30-Epicambogin (EPC) and guttiferone K (GUTK) showed the highest cytotoxic selectivity and potency on HT-29 cells among 15 isolated compounds. IC50 values (24 h) for EPC and GUTK in HT-29 cells were 5.36+/-0.25 and 5.39+/-0.22 muM, respectively, and both induced G0/G1 arrest by down-regulation of cyclins D1, D3, CDK4 and CDK6, while up-regulation of p21Waf1/CiP1 and p27KiP1. Both compounds triggered the activation of caspases-3, -8 and -9 in apoptosis. The in vivo anti-tumor effects of GUTK were further investigated by using a subcutaneous Colon-26 mouse tumor model. GUTK (10 mg/kg i.p.) reduced tumor volume by 33.6% and potentiated the anti-tumor effects of 5-fluorouracil when administered concurrently. / Our findings revealed that DG rather than individual phthalides, is worthy for further study as a potential anti-cancer drug, due to the synergistic interactions among multi-components in the herb. On the other hand, EPC and GUTK, isolated from TH have potential to be developed as novel anti-tumor candidates for combination use with 5-fluorouracil. The results strongly support the use of different approaches to study TCM for chemotherapy, according to its traditional and empirical use. / Subsequently, the anti-proliferative effects of DG and Chuanxiong Rhizoma (CX) extracts and mixtures containing three phthalides in the proportions similar to their presence in both extracts were examined, since CX also contains the same phthalides, but in different proportions. DG extract was significantly more potent than its corresponding phthalide mixture to inhibit cancer cell proliferation and synergistic interaction was observed among the phthalides and other bioactive components, while the phthalides in CX extract interacted antagonistically with other components. / Kan, Lai Ting Winnie. / Adviser: Ge Lin. / Source: Dissertation Abstracts International, Volume: 73-02, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 267-311). / 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, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Wong, Wai Ki Vicky. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 105-131). / Abstracts in English and Chinese. / Abstract --- p.ii / 摘要 --- p.iv / Acknowledgements --- p.vi / Table of contents --- p.vii / List of tables --- p.xii / List of figures --- p.xiii / List of abbreviations --- p.xiv / Chapter Chapter 1: --- Introduction --- p.1 / Chapter Chapter 2: --- Colorectal cancer / Chapter 2.1 --- Literature Review / Chapter 2.1.1 --- Colorectal cancer --- p.8 / Chapter 2.1.2 --- Incident rate of colorectal cancer --- p.8 / Chapter 2.1.3 --- Hereditary colorectal cancer --- p.9 / Chapter 2.1.4 --- Sporadic colorectal cancer and Wnt signaling pathway --- p.10 / Chapter 2.1.5 --- Chemotherapy treatment of colorectal cancer --- p.11 / Chapter 2.1.5.1 --- 5-Fluorouracil --- p.12 / Chapter 2.1.5.2 --- Oxaliplatin --- p.14 / Chapter 2.1.5.3 --- Irinotecan --- p.14 / Chapter 2.1.6 --- Biomarkers for colorectal cancer --- p.15 / Chapter 2.1.6.1 --- Thymidylate synthase --- p.15 / Chapter 2.1.6.2 --- Dihydropyrimidine dehydrogenase --- p.16 / Chapter 2.1.6.3 --- Thymidine phosphorylase --- p.16 / Chapter 2.1.6.4 --- Microsatellite-instability status --- p.16 / Chapter 2.1.6.5 --- Clinical uses of biomarkers for colorectal cancer --- p.17 / Chapter 2.1.7 --- Choice of cell line as colorectal cancer model --- p.17 / Chapter 2.1.8 --- Aims of study --- p.17 / Chapter 2.2 --- Materials and Methods / Chapter 2.2.1 --- Verification of SW480 as a nuclear β-catenin positive cell line / Chapter 2.2.1.1 --- Maintenance of cell lines --- p.21 / Chapter 2.2.1.2 --- Antibody --- p.21 / Chapter 2.2.1.3 --- Agar block preparation for SW480 and CCD-18C0 cells --- p.22 / Chapter 2.2.1.4 --- Immunocytochemical staining --- p.22 / Chapter 2.2.2 --- Effect of anti-cancer drugs on cell viability / Chapter 2.2.2.1 --- Maintenance of cell lines --- p.22 / Chapter 2.2.2.2 --- MTT cell viability assay --- p.23 / Chapter 2.3 --- Results / Chapter 2.3.1 --- SW480 is a β-catenin positive cell line --- p.24 / Chapter 2.3.2 --- Antiproliferative effects of cytotoxic drugs in SW480 cells / Chapter 2.3.2.1 --- 5-Fluorouracil --- p.26 / Chapter 2.3.2.2 --- Oxaliplatin --- p.29 / Chapter 2.3.2.3 --- Irinotecan --- p.31 / Chapter 2.4 --- Discussion / Chapter 2.4.1 --- SW480 as a nuclear β-catenin positive cell line --- p.33 / Chapter 2.4.2 --- Antiproliferative effects of 5-fluorouracil in SW480 cells --- p.33 / Chapter 2.4.3 --- Summary --- p.34 / Chapter Chapter 3: --- Effect of 5-fluorouracil on mRNA expression in SW480 cells / Chapter 3.1 --- Literature Review / Chapter 3.1.1 --- Application of quantitative real-time polymerase chain reaction in cancer research / Chapter 3.1.1.1 --- Principles of quantitative real-time polymerase chain reaction --- p.36 / Chapter 3.1.1.2 --- Advantages of quantitative real-time polymerase chain reaction over conventional polymerase chain reaction --- p.39 / Chapter 3.1.1.3 --- Determination of colorectal cancer biomarkers by quantitative real-time polymerase chain reaction --- p.39 / Chapter 3.2 --- Materials and Methods / Chapter 3.2.1 --- Determination of the effect of 5-fluorouracil on mRNA expression in SW480 cells / Chapter 3.2.1.1 --- Treatment of cells --- p.40 / Chapter 3.2.1.2 --- Extraction of total RNA from SW480 cells --- p.40 / Chapter 3.2.1.3 --- Removal of genomic DNA --- p.41 / Chapter 3.2.1.4 --- Determination of the efficiency of genomic DNA removal --- p.42 / Chapter 3.2.1.5 --- Determination of the purity and concentration of RNA --- p.42 / Chapter 3.2.1.6 --- Determination of the integrity of RNA --- p.43 / Chapter 3.2.1.7 --- First strand cDNA synthesis --- p.44 / Chapter 3.2.1.8 --- Real-time polymerase chain reaction using human Wnt signaling pathway RT2 ProfileŕёØ PCR array --- p.44 / Chapter 3.2.1.9 --- Calculation of the fold-change in genes expression between the 5-FU treated and control SW480 cells --- p.45 / Chapter 3.3 --- Results / Chapter 3.3.1 --- The quality and quantity of RNA --- p.46 / Chapter 3.3.2 --- Effects of 5-fluorouracil on genes expression in SW480 cells --- p.48 / Chapter 3.4 --- Discussion / Chapter 3.4.1 --- Alterations in mRNA expression in 5-fluorouracil treated SW480 cells --- p.55 / Chapter 3.4.1.1 --- Extracellular signaling molecules --- p.55 / Chapter 3.4.1.2 --- Canonical Wnt signaling pathway --- p.56 / Chapter 3.4.1.3 --- Regulators of cell cycle --- p.57 / Chapter 3.4.1.4 --- Regulators of growth and proliferation --- p.58 / Chapter 3.4.1.5 --- Regulators of transcription --- p.58 / Chapter 3.4.1.6 --- Regulators of Wnt receptor signaling pathway --- p.60 / Chapter 3.4.1.7 --- Other genes involved in Wnt signaling --- p.61 / Chapter 3.4.2 --- Limitations of Q-RT-PCR --- p.61 / Chapter 3.4.3 --- Summary --- p.62 / Chapter Chapter 4: --- Effect of 5-fluorouracil on proteins expression in SW480 cells / Chapter 4.1 --- Literature Review / Chapter 4.1.1 --- From mRNA to proteins --- p.63 / Chapter 4.1.2 --- Application of proteomics in cancer research --- p.63 / Chapter 4.1.3 --- Two-dimensional gel electrophoresis --- p.64 / Chapter 4.1.4 --- Principles of MALDI TOF mass spectrometry --- p.64 / Chapter 4.1.5 --- Peptide mass fingerprinting --- p.65 / Chapter 4.1.6 --- Drug response proteins detected by proteomics in colorectal cancer cell lines --- p.65 / Chapter 4.1.7 --- Detection of biomarker in colorectal cancer formation using proteomics --- p.66 / Chapter 4.2 --- Materials and Methods / Chapter 4.2.1 --- Determination of the effect of 5-fluorouracil on proteins expression in SW480 cells / Chapter 4.2.1.1 --- Treatment of cells --- p.67 / Chapter 4.2.1.2 --- Cell lysis --- p.67 / Chapter 4.2.1.3 --- Protein quantitation of cell lysate --- p.67 / Chapter 4.2.1.4 --- Sample preparation for two-dimensional electrophoresis --- p.68 / Chapter 4.2.1.5 --- Two-dimensional electrophoresis --- p.69 / Chapter 4.2.1.6 --- Silver staining --- p.69 / Chapter 4.2.1.7 --- Image analysis --- p.70 / Chapter 4.2.1.8 --- In-gel protein digestion --- p.70 / Chapter 4.2.1.9 --- Peptide mass fingerprinting using mass spectrometry --- p.71 / Chapter 4.3 --- Results / Chapter 4.3.1 --- Protein expression patterns of 5-fluorouracil treated and untreated SW480 cells by 2-dimensional electrophoresis --- p.72 / Chapter 4.3.2 --- Identification of the differentially expressed proteins after 5-fluorouracil treatment in SW480 cells --- p.75 / Chapter 4.4 --- Discussion / Chapter 4.4.1 --- Effects of 5-fluorouracil on protein expression in SW480 cells --- p.82 / Chapter 4.4.1.1 --- Identified upregulated proteins after 5-fluorouracil treatment in SW480 cells / Chapter 4.4.1.1.1 --- Cyclophilin A --- p.83 / Chapter 4.4.1.1.2 --- Cytokeratin 19 --- p.83 / Chapter 4.4.1.1.3 --- Cytokeratin 8 --- p.84 / Chapter 4.4.1.1.4 --- RAN --- p.84 / Chapter 4.4.1.1.5 --- Heat shock protein 27 --- p.84 / Chapter 4.4.1.1.6 --- Peroxiredoxin 6 --- p.85 / Chapter 4.4.1.2 --- Identified dowiiregulated proteins after 5-fluorouracil treatment in SW480 cells / Chapter 4.4.1.2.1 --- Heat shock protein 60 --- p.86 / Chapter 4.4.1.2.2 --- Cytokeratin 18 --- p.86 / Chapter 4.4.1.2.3 --- Cytokeratin 9 --- p.86 / Chapter 4.4.1.2.4 --- Carbamoylphosphate synthetase I --- p.87 / Chapter 4.4.1.2.5 --- a-Enolase --- p.87 / Chapter 4.4.1.2.6 --- Heat shock protein 70 --- p.87 / Chapter 4.4.1.2.7 --- nm23 --- p.88 / Chapter 4.4.1.2.8 --- β-actin --- p.88 / Chapter 4.4.2 --- Limitations of proteomics profiling --- p.89 / Chapter 4.4.3 --- Summary --- p.90 / Chapter Chapter 5: --- Verification of proteinśة identities by immunocytochemical staining / Chapter 5.1 --- Materials and Methods / Chapter 5.1.1 --- Antibodies --- p.91 / Chapter 5.1.2 --- Treatment of cells --- p.91 / Chapter 5.1.3 --- Agar block preparation of SW480 cells --- p.92 / Chapter 5.1.4 --- Immunocytochemical staining and evaluation --- p.92 / Chapter 5.1.5 --- Polymer-based immunohistochemical detection system --- p.93 / Chapter 5.1.6 --- Statistical analyses --- p.93 / Chapter 5.2 --- Results / Chapter 5.2.1 --- Confirmation of proteomic findings using immunocytochemical stainings in paraffin-embedded sections of 5-fluorouracil treated and untreated SW480 cells --- p.94 / Chapter 5.3 --- Discussion / Chapter 5.3.1 --- Immunocytochemical staining to verify proteomics findings of 5-fluorouracil treated and untreated SW480 cells --- p.99 / Chapter 5.3.2 --- Limitations of ICC staining --- p.100 / Chapter 5.3.3 --- Summary --- p.100 / Chapter Chapter 6: --- Conclusions and future perspectives / Chapter 6.1 --- Significance of study --- p.101 / Chapter 6.2 --- Future perspectives --- p.102 / References --- p.105

Ng, Po Yan. / Thesis submitted in: November 2006. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 109-120). / Abstracts in English and Chinese. / Acknowledgement --- p.i / Abstract --- p.ii / 摘要 --- p.iii / Table of Contents --- p.iv / List of Figures --- p.viii / List of Tables --- p.xi / List of Abbreviation --- p.xii / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- A General Introduction to the Development and Clinical Activities of Platinum Drugs --- p.1 / Chapter 1.1.1 --- Platinum Drugs used in a Clinical Setting --- p.4 / Chapter 1.1.2 --- Platinum Drugs under Clinical Trials --- p.5 / Chapter 1.1.3 --- Platinum Compounds with Dual Mechanisms --- p.7 / Chapter 1.2 --- Platinum Drug Antitumor Mechanism --- p.9 / Chapter 1.3 --- Limitations of Platinum Drugs --- p.12 / Chapter 1.3.1 --- Toxicity --- p.12 / Chapter 1.3.2 --- Drug Resistance or Cross Resistance --- p.15 / Chapter 1.3.2.1 --- Reduced Drug Accumulation or Increased Drug Efflux --- p.16 / Chapter 1.3.2.2 --- Drug Inactivation --- p.18 / Chapter 1.3.2.3 --- Enhanced DNA Repair --- p.19 / Chapter 1.4 --- Why Combinational Therapy? --- p.21 / Chapter 1.4.1 --- Antimetabolites --- p.20 / Chapter 1.4.2 --- Topoisomerase Inhibitors --- p.22 / Chapter 1.4.3 --- Tubulin-Active Antimitotic Agents --- p.24 / Chapter 1.4.4 --- Demethylcantharidin as a potential candidate for drug combination --- p.28 / Chapter 1.5 --- Study Objectives --- p.31 / Chapter Chapter 2 --- Materials and Methods / Chapter 2.1 --- Cell Lines --- p.33 / Chapter 2.2 --- Cancer Cell Preparation / Chapter 2.2.1 --- Chemicals and Reagents --- p.33 / Chapter 2.2.2 --- Cell Culture Practice --- p.34 / Chapter 2.2.2.1 --- Subcultures --- p.35 / Chapter 2.2.2.2 --- Cryopreservation --- p.37 / Chapter 2.2.2.3 --- Thawing Cryopreservated Cells --- p.38 / Chapter 2.2.3 --- Development of Drug-Resistant Cell Lines --- p.39 / Chapter 2.3 --- Growth Inhibition Assay / Chapter 2.3.1 --- Evaluation of Cytotoxicity in vitro --- p.40 / Chapter 2.3.2 --- Drug Pretreatment --- p.43 / Chapter 2.3.3 --- Drug Pre-sensitization with Concurrent Treatment --- p.44 / Chapter 2.4 --- Calculations for Drug Combinations --- p.46 / Chapter 2.5 --- Statistical Analysis --- p.49 / Chapter Chapter 3 --- Results and Discussions / Chapter 3.1 --- In vitro Cytotoxicity and Evaluation of Drug Resistance --- p.50 / Chapter 3.2 --- Role of Leaving Ligand in a Platinum Complex --- p.58 / Chapter 3.3 --- Priority in Selecting the Most Effective Drug Combination --- p.66 / Chapter 3.4 --- Drug Combination Studies / Chapter 3.4.1 --- Drug Combination Prescreening --- p.68 / Chapter 3.4.1.1 --- Comparison of the effectiveness of the three Drug Combinations --- p.72 / Chapter 3.4.1.2 --- Rationale for Drug Combination Studies presented in Section 3.4.2 & 3.4.3 --- p.73 / Chapter 3.4.2 --- Drug Pre-sensitization Studies in Colorectal Cancer Cell Lines --- p.74 / Chapter 3.4.2.1 --- Comparison of Drug Pre-sensitization Treatment in Sensitive Colorectal Cancer Cell Lines --- p.84 / Chapter 3.4.2.2 --- Comparison of Drug Pre-sensitization Treatment in Sensitive and Oxaliplatin Resistant HCT116 Colorectal Cancer Cell Lines --- p.87 / Chapter 3.4.3 --- Drug Pre-sensitization Studies in Liver Cancer Cell Lines --- p.89 / Chapter 3.4.3.1 --- Comparison of Drug Pre-sensitization Treatment in Sensitive Liver Cancer Cell Lines --- p.99 / Chapter 3.4.3.2 --- Comparison of Drug Pre-sensitization Treatment in Sensitive and Cisplatin Resistant SK-Hepl Liver Cancer Cell Line --- p.101 / Chapter 3.5 --- Possible Explanation to the Observed Drug Combination Effect --- p.103 / Chapter 3.6 --- General Protocols for Drug Combinations --- p.105 / Chapter Chapter 4 --- Conclusions / Reference --- p.109 / Appendices --- p.121 / Chapter I a. --- "Raw Data of Pre-screening for HCT116 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.122 / Chapter I b. --- "Raw Data of Pre-screening for HCT116 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.123 / Chapter II a. --- "Raw Data of Pre-screening for SK-Hepl (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.124 / Chapter II b. --- "Raw Data of Pre-screening for SK-Hepl ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.125 / Chapter III a. i) --- "Isobolograms for HCT116 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.126 / Chapter III a. ii) --- "Raw Data for HCT116 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.127 / Chapter III b. i) --- "Isobolograms for HCT116 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.128 / Chapter III b. ii) --- "Raw Data for HCT116 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.129 / Chapter IV a. i) --- "Isobolograms for HCT1160xaR (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.130 / Chapter IV a. ii) --- "Raw Data for HCT1160xaR (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.131 / Chapter IV b. i) --- "Isobolograms for HCT1160xaR ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.132 / Chapter IV b. ii) --- "Raw Data for HCT1160xaR ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.133 / Chapter V a. i) --- "Isobolograms for HT29 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.134 / Chapter V a. ii) --- "Raw Data for HT29 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.135 / Chapter V b. i) --- "Isobolograms for HT29 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.136 / Chapter V b. ii) --- "Raw Data for HT29 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.137 / Chapter VI a. i) --- Isobolograms for Hep G2 (Cisplatin and [Pt(DMC)(NH3)2]) --- p.138 / Chapter VI a. ii) --- Raw Data for Hep G2 (Cisplatin and [Pt(DMC)(NH3)2]) --- p.139 / Chapter VI b. i) --- "Isobolograms for Hep G2 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.140 / Chapter VI b. ii) --- "Raw Data for Hep G2 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.141 / Chapter VII a. i) --- "isobolograms for SK Hep 1 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.142 / Chapter VII a. ii) --- "Raw Data for SK Hep 1 (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.143 / Chapter VII b.i) --- "Isobolograms for SK Hep 1 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.144 / Chapter VII b. ii) --- "Raw Data for SK Hep 1 ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.145 / Chapter VIII a. i) --- "Isobolograms for SK Hep ICisR (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.146 / Chapter VIII a. ii) --- "Raw Data for SK Hep ICisR (Cisplatin, [Pt(DMC)(NH3)2] and Pt(DMC)(NH2CH3)2])" --- p.147 / Chapter VIII b. i) --- "Isobolograms for SK Hep ICisR ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.148 / Chapter VIII b. ii) --- "Raw Data for SK Hep ICisR ([Pt(DMC)(R,R-DACH)] and Oxaliplatin)" --- p.149