Journal
PHARMACOGENOMICS
Volume 14, Issue 2, Pages 205-213Publisher
FUTURE MEDICINE LTD
DOI: 10.2217/PGS.12.205
Keywords
anthracyclines; antineoplastic agents; cardiomyopathy; dilated; heart failure; pharmacogenetics
Categories
Funding
- [UL1 RR025747]
- [P01CA142538]
- [K08HL96836]
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Damage to the heart can result from both traditional chemotherapeutic agents, such as doxorubicin, and newer 'targeted' therapies, such as trastuzumab. This chemotherapeutic cardiotoxicity is potentially life-threatening and necessitates limiting or discontinuing an otherwise-effective cancer treatment. Clinical strategies focus on surveillance rather than prevention, although there are no specific therapies for this highly morbid adverse effect. Current models for prospectively predicting risk of chemotherapeutic cardiotoxicity are limited. Cardiotoxicity can occur idiosyncratically in patients without obvious demographic risk factors, suggesting a genetically determined susceptibility, and candidate-gene studies have identified a limited number of variants that increase risk. In this commentary we indicate a need for more powerful means to identify risk prospectively, and suggest that broad pharmacogenomic approaches may be fruitful.
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