抗肿瘤药(英文版).pptVIP

Anticancer Drugs Dr.Qamar Barakzai Department of Pharmacology Ziauddin Medical University Karachi.Pakistan * “CANCER” Refers to a Malignant neoplasm (New growth) Cancer cells can manifest: Uncontrolled Proliferation. Loss of function due to lack of ability to differentiate. Invasiveness. The ability to metastasize. Cancer arises as a result of a series of genetic changes in the cell, the main genetic lesions being: Inactivation of tumor suppressor genes. The activation of oncogenes. Antineoplastic agents Are cytotoxic not tumoricidal Only kill cells during mitosis, and Not all cancer cells are dividing at the same time. SUCCESS DEPENDS ON: Stage of cancer at time of diagnosis Type of cancer Development of drug resistance Overall health of patient. R Tumor Suppressor Genes -ve (p53) Growth Factors Oncogenes +ve S DNA Synthesis G2 Premitotic Interval M PROPHASE METAPHASE ANAPHASE TELOPHASE MITOSIS G0 G1 S PHASE SPECIFIC Cytosine Arbinoside Hydroxyurea S PHASE SPECIFIC SELF LIMITING 6-Mercaptpurine Methotrexate. M PHASE SPECIFIC vincristine vinblastine paclitaxel PHASE NONSPECIFIC alkylating agents, cis-platinum nitrosoureas, dacarbazine antibiotics procarbazine G0 Differentiation CELL GROWTH CYCLE 5 DISTINCT PHASES OF MITOSIS 1. G0 - Resting - no mitosis 2. G1 - Postmitotic - first growth 3. S - DNA synthesis phase 4. G2 - Premitotic - second growth 5. M - Mitosis phase GENERATION TIME - one complete cycle different  in all tumors, from hours to days PENTOSTATIN Inhibits adenosine Deaminase PALA Inhibits Pyrimidine Biosynthesis Purine synthesis Pyrimidine synthesis Ribonucleotides Deoxyribonucleotides DNA HYDROXYUREA Inhibit Ribonucleotide Reductase 6-MERCAPTOPURINE 6-THIOGAUNINE Inhibit Puring ring biosynthesis Inhibit Neocleotide interconversions 5-FLOUROURACIL Inhi