@Article{096504017X14876245096439,
AUTHOR = {Valentina K. Todorova, Issam Makhoul, Ishwori Dhakal, Jeanne Wei, Annjanette Stone, Weleetka Carter, Aaron Owen, V. Suzanne Klimberg},
TITLE = {Polymorphic Variations Associated With Doxorubicin-Induced  Cardiotoxicity in Breast Cancer Patients},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {8},
PAGES = {1223--1229},
URL = {http://www.techscience.com/or/v25n8/56907},
ISSN = {1555-3906},
ABSTRACT = {Doxorubicin (DOX) is a commonly used antineoplastic agent for the treatment of various malignancies, and 
its use is associated with unpredictable cardiotoxicity. Susceptibility to DOX cardiotoxicity is largely patient 
dependent, suggesting genetic predisposition. We have previously found that individual sensitivity to DOX 
cardiotoxicity was associated with differential expression of genes implicated in inflammatory response and 
immune trafficking, which was consistent with the increasing number of reports highlighting the important 
role of human leukocyte antigen (HLA) complex polymorphism in hypersensitivity to drug toxicity. This pilot 
study aimed to investigate DNA from patients treated with DOX-based chemotherapy for breast cancer and to 
correlate the results with the risk for DOX-associated cardiotoxicity. We have identified 18 SNPs in nine genes 
in the HLA region (NFKBIL1, TNF-α, ATP6V1G2-DDX39B, MSH5, MICA, LTA, BAT1, and NOTCH4) and 
in the psoriasis susceptibility region of HLA-C as potential candidates for association with DOX cardiotoxicity. 
These results, albeit preliminary and involving a small number of patients, are consistent with reports showing the presence of susceptibility loci within the HLA gene region for several inflammatory and autoimmune 
diseases, and with our previous findings indicating that the increased sensitivity to DOX cardiotoxicity was 
associated with dysregulation of genes implicated both in inflammation and autoimmune disorders.},
DOI = {10.3727/096504017X14876245096439}
}