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[Resistance to anticancer drugs]

J Bénard1, O Rixe

  • 1Laboratoire de Pharmacologie clinique et moléculaire, Institut Gustave Roussy, Villejuif.

Presse Medicale (Paris, France : 1983)
|November 16, 1996
PubMed

Insights

Chemoresistance mechanisms in cancer cells, including drug efflux pumps and DNA repair, reduce chemotherapy efficacy. Understanding these processes is crucial for developing effective cancer treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Context:

  • Chemotherapy inefficacy in various cancers necessitates understanding intrinsic tumor cell chemoresistance.
  • Chemoresistance mechanisms are extensively studied in human cancer cell lines.

Purpose:

  • To describe the various chemoresistance mechanisms involved in cancer.
  • To highlight the role of detoxifying mechanisms, drug inactivation, and DNA repair in chemoresistance.
  • To emphasize the link between gene expression, proliferation, differentiation, apoptosis, and drug response.

Summary:

  • Detoxifying mechanisms like P-glycoprotein (P-gp), multidrug resistance protein (MRP), and lung resistance-related protein (LRP) efflux pumps, along with drug inactivation via glutathione and enhanced DNA repair, contribute to chemoresistance.
  • Coexistence of multiple mechanisms within tumor cells, potentially influenced by oncogenes and suppressor genes regulating cell functions, is common.
  • Identification and quantification of these biomarkers in human tumor specimens are ongoing challenges, yet crucial for therapeutic strategies.

Impact:

  • Strategies to block chemoresistance mechanisms, such as developing P-gp modulators, are being developed.
  • Ongoing research in cancer chemotherapy increasingly focuses on understanding and targeting chemoresistance mechanisms.
  • Advances in identifying and quantifying chemoresistance biomarkers will improve the efficacy of cancer chemotherapy.

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