Lecture notes from Imperial College London, Medical Biosciences BSc, 2nd year, Pharmacology module
Pharmacology 8 on cancer drug therapies: In this session, we will refresh our memories about the hallmarks of cancer, before thinking about how some of those hallmarks might help us design and use ...
Cancer Drug Therapy
Introduction to cancer chemotherapy
- cancer = disease in which cells with 1 or more abnormalities multiply in an uncontrolled manner
(caused by genetic & environmental factors)
=> can give rise to a large mass of abnormal tissues: tumour (no physiological function)
=> can give rise to lymphomas, leukaemias...
=> disrupt metabolic, signalling, physiological functions
=> morbidity or mortality
- solid tumour: does not contain cysts/ liquid (ex: sarcomas, carcinomas, lymphomas...)
=> benign: not cancerous
=> malignant: cancerous => combination of drugs used
=> metastasis = translocation from primary site to distant locations in body (secondary tumour)
Cancer chemotherapeutic angles
= synthesis
- drug selectively target: - uncontrolled growth => greater demand for E and anabolic substrates
- less well-regulated cell cycle => replicate frequently: replicative processes
- hallmarks of cancer & their associated drugs:
*
= new
* *
increased rates of glycolysis despite availability of O2:
aerobic glycolysis (Warburg Effect) => lactate excess
*
*
- cancer chemotherapy: treatments directly exploiting anabolic, replicative and metabolic mechanisms
=> selectively kill cancer cells using cytotoxic agents (≠ cytostatic: stop growth)
=> BUT unwanted side-effects => surgical procedure remove part of tumour (debulking) before
Targeting cell cycle stages in cancer chemotherapy
- G1, S, G2 = interphase
, prepare cell for division
restriction point
- tumours grow at ≠ rate, ≠ proportion of proliferating cells at a given moment
=> growth fraction: % of cells engaged in proliferation versus resting phases at a given moment
=> chemotherapic agents targeting cell-cycle effective if high growth fraction
=> chemotherapic agents not targeting cell-cycle effective whether high/low
Alkylating agents cell-cycle specific (S): preferentially proliferating cells
- damage + chemically modify DNA => prevent cell division => cell death (lethal to tumour cells)
- covalently bind DNA at 2 separate sites (bifunctional agents)
=> cross-linkage
=> DNA strand breakage
- have a tertiary N with 2 chloroethane groups attached
=> ex: cyclophosphamide mechlorethamine
④>
!.
⑲
=> alkylation of two G (in 1 or 2 strands of DNA) by mechlorethamine
- quanim
1
1
alkyl
groups deoxyribose
↓
- BUT severe side effects because DNA damage relatively non-specific
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