Genetic susceptibility to iatrogenic malignancy

Research output: Contribution to journalLiterature review

Published copy (DOI)


  • J M Allan
  • C S Rabkin


Publication details

DatePublished - Sep 2005
Issue number6
Number of pages14
Pages (from-to)615-628
Original languageEnglish


Iatrogenic malignancies represent a devastating and often fatal long-term effect of therapy administered for a prior condition, usually a primary cancer. Earlier diagnosis and the development of more effective cancer treatments over the last 30 years have considerably improved the long-term survival of patients. However, the burgeoning number of cancer survivors has led to a parallel increase in the number of cases of iatrogenic malignancy. Consequently, understanding host susceptibility factors, such that high-risk patients can be identified, has become a priority. However, this task is made difficult by the heterogeneity of iatrogenic malignancies. Nevertheless, the identification of polymorphic loci and pathways predicted to modify dose (e.g., glutathione S-transferases, nicotinamide adenine dinucleotide phosphate: quinone oxidoreductase, cytochrome P450, and thiopurine S-methyltransferase) or determine cellular outcome (e.g., nucleotide excision DNA repair, base excision DNA repair, DNA mismatch repair, and cell death signaling) after therapy has provided insight into how host genetics may impact on the risk of developing iatrogenic malignancy.

    Research areas

  • anthracycline, ataxia telangiectasia, chemotherapy, cytochrome P450, epipodophyllotoxin, Fanconi anemia, glutathione S-transferase, Li-Fraumeni syndrome, neurofibromatosis, Nijmegen breakage syndrome, pharmacogenetics, radiotherapy, single nucleotide polymorphism, thiopurine methyltransferase, xeroderma pigmentosum, GLUTATHIONE-S-TRANSFERASE, ACUTE MYELOID-LEUKEMIA, ACUTE LYMPHOBLASTIC-LEUKEMIA, NUCLEOTIDE EXCISION-REPAIR, NON-HODGKINS-LYMPHOMA, LI-FRAUMENI-SYNDROME, DE-NOVO AML, ATAXIA-TELANGIECTASIA, BREAST-CANCER, THIOPURINE METHYLTRANSFERASE

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