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Chemotherapy and Drug Resistance
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  • Course
  • CANCER BIOLOGY
  • Institution
  • University Of East Anglia

*Conventional Cancer Treatment * Therapeutic Window *Conventional Therapies * Gleevec *Resistance *Phenomenon *P-Glycoprotein * Drug Metabolism *Glutathione S Transferase *Dihydrofolate Reductase (DHFR)

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Document information

  • October 29, 2024
  • 6
  • 2022/2023
  • Class notes
  • Dr helen james
  • All classes

Subjects

  • therapeutic window
  • combi therapies
  • gleevec
  • drug metabolism
  • glutathione s transferase
  • conventional cancer treatment
  • conventional chemotherapies

Written for

  • University of East Anglia
  • Unknown
  • CANCER BIOLOGY
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L9: CHEMOTHERAPY AND DRUG RESISTANCE [11/10/2022]



I. CONVENTIONAL CANCER TREATMENT



 Surgery: complete removal of tumour, and cure possible if it has remained local
 Radiotherapy: multiple aspects – elimination of any residual cancer cells following surgery
(adjuvant therapy); pre-operatively (neo-adjuvant); as primary therapy; palliative
 Chemotherapy: cancers that have metastasized require systemic therapies
 Immunotherapy



II. ‘THERAPEUTIC WINDOW’



 Therapeutic window also called “therapeutic index” is the difference between the minimum
effective dose and the maximum tolerated dose (MTD)
 Ideally this should be broad



III. CONVENTIONAL CHEMOTHERAPIES – 3 TYPES



1. Alkylating agents and platinum-based drugs
(eg cyclophosphamide; cisplatin, carboplatin – all form bulky DNA adducts)
2. Antimetabolites
(eg 5-Fluorouracil (5-FU) – inhibits thymidylate synthase; methotrexate – inhibits
dihydrofolate reductase)
3. Organic drugs
(eg Dexorubicin – inhibits topoisomerase II;
Vincristine – prevents microtubule assembly;
Paclitaxel (Taxol) – blocks microtubule depolymerisation)

IV. CONVENTIONAL THERAPIES – CISPLATIN

(Cancer Therapy & DNA Damage)
 Many cancer therapies work by causing DNA damage – incl. ionising radiation and alkylating
agents (e.g. cisplatin)
 Known for many years that these therapies affect all dividing cells
 Cells cannot repair such large amounts of genomic damage, so they undergo apoptosis, or if
cancer cells lack proper cell cycle checkpoint controls, they enter “mitotic catastrophe”
(Mode of Actin)
 Cisplatin is administered intravenously
 Upon entering the cell [Cl-] is low (~4 mM), so the Cl- ligands are removed, generating a
positively charged species that reacts with nucleophilic sites on intracellular macromolecules
to form protein, RNA and DNA adducts.

, (Potential Problems)

 Deficient DNA repair systems cause some cancers => potential problems with therapies that
work by inducing DNA damage and apoptosis
- The “therapy” may not induce a response in such cancerous cells and will not lead to
apoptosis
- It would, however, lead to apoptosis of “healthy” cells
 This can enable tumours to have resistance to drugs, leading to an increase in proportion of
cancerous cells
 The treatments themselves are mutagenic, so even if they eliminate the initial cancer, they
can give rise to further tumours later



(Cisplatin Resistance)

 Postulated mechanisms of resistance to cisplatin:
- Reduced intracellular accumulation (↓ uptake or ↑ efflux) or increased inactivation by
intracellular proteins (e.g. glutathione)
- Increased repair of cisplatin adducts
- Increased ability to replicate past cisplatin adducts
- Defects in apoptotic response pathway

(Antimetabolites and Organic Drugs)




 Actions of 5-fluorouracil (5-FU) and methotrexate

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