Abstract
Platinum complexes are among the most commonly applied anticancer agents. The aim of current work is collection, analysing and comparative estimation of clinical trials and pharmacological indications of currently approved for application platinum detivatives: Cisplatin, Carboplatin, Oxaliplatin, Nedaplatin (Japan), Lobaplatin (China), Heptaplatin (North Korea), and Satraplatin. The other aim of the study includes the summarizing of the hystoric data for the stages of the developlement of these drugs, and the comparison of pharmacokimetic parameters, side effecs and the dose-liniting factors of the drugs. The observational study on pharmacokinetic parameters shows that protein binding decreases in order: 95% (Cisplatn); 90% (Oxaliplatin); 50% (Nedaplatin); low (Carboplatin). For every of Cisplatin, Carboplatin, Oxaliplatin have been reported more than 1000 clinical trials; for Lobaplatin, Nedaplatin, Satraplatin - about 10 trials. The differenses in dose-limiting effects are: neuro-, nephro-, ototoxicity (Cisplatin); neurotoxicity (Oxaliplatin); nephrotoxicity (Heptaplatin); myelosuppression: thrombocytopenia, neutropenia, leukopenia (Carboplatin, Nedaplatin, Satraplatin).
Highlights
Malignant tumors are the leading cause of lethality worldwide, and are a group of more than 100 different types of diseases, that are characterized by uncontrolled cell growth, local tissue invasion and distant metastases
The incidence of malignant tumors is enlarging, with the fastest increasing of lung, prostate, and colon cancers in men and breast carcinomas in women
Malignant tumors originate from different types of tissues: connective, epithelial, hematopoietic, lymphoid, nervous
Summary
Malignant tumors are the leading cause of lethality worldwide, and are a group of more than 100 different types of diseases, that are characterized by uncontrolled cell growth, local tissue invasion and distant metastases. In carcinogenesis (oncogenesis, tumorigenesis) normal cells are transformed into cancer cells This multistage process involves changes at the cellular and genetic levels, and involves initiation, promotion, malignant formation, progression, local tissue invasion and metastases. Tumors are considered a mutation in somatic cell DNA, caused by various carcinogenic factors In this process, various genetic and epigenetic tumor-specific mutations occur, which define the biological features of tumor growth: uncontrolled cell proliferation, invasion of neighboring tissues and metastasis of cells to distant tissues. Genetic abnormalities include the following genes (Saeki and SugiIchi 2001): I. cell cycle genes: p53 (brain and breast cancer); p16 (melanoma); Rb1 (retinoblastoma); VHL (renal cancer); WT1 (Wilms cancer)
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