Related Experiment Video

Updated: Dec 28, 2025

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA
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Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate DMBA-TPA

Published on: December 19, 2019

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Drug-Related Carcinogenesis: Risk Factors and Approaches for Its Prevention

G A Belitskiy1, K I Kirsanov2,3, E A Lesovaya1,4

  • 1Blokhin Russian Cancer Research Center, Ministry of Health of Russian Federation, Moscow, 115478, Russia.

Biochemistry. Biokhimiia
|February 23, 2020
PubMed

Insights

This review examines how drug metabolism and DNA repair systems influence therapy-related cancer development. Understanding genetic variations in these systems can help predict and prevent drug-induced cancer risk.

Area of Science:

  • Pharmacology
  • Genetics
  • Oncology

Background:

  • Therapy-related carcinogenesis is a significant concern.
  • Drug-induced cancers arise from complex interactions with cellular systems.
  • Polymorphisms in metabolic and repair genes can modify cancer risk.

Purpose of the Study:

  • To review the role of metabolic and repair systems in therapy-related carcinogenesis.
  • To analyze the impact of genetic polymorphism on cancer development risk.
  • To discuss prevention strategies for drug-induced cancers.

Main Methods:

  • Literature review of existing data.
  • Analysis of drug classes and their carcinogenic potential.
  • Examination of genetic polymorphisms in key enzymes and pathways.

Main Results:

  • Various drugs, including anticancer agents, analgesics, and hormones, exhibit carcinogenic activity.
  • Metabolic and repair system polymorphisms significantly affect individual susceptibility to drug-induced cancer.
  • Drug-induced carcinogenesis involves complex interactions at initiation and promotion stages.

Conclusions:

  • Metabolic and repair systems are crucial in understanding therapy-related carcinogenesis.
  • Genetic variations influence the risk of developing cancer from medical treatments.
  • Targeted prevention strategies can mitigate drug-related cancer induction.

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