Ferredoxin reductase: Pharmacogenomic assessment in colorectal cancer

Jinsheng Yu, Sharon Marsh, Ranjeet Ahluwalia, Howard L. McLeod

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22 Scopus citations

Abstract

Ferredoxin reductase (FDXR) is a putative contributor to TP53-mediated apoptosis from 5-fluorouracil chemotherapy through the generation of oxidative stress. With TaqMan real-time quantitative reverse transcription-PCR, this study established a significant difference in FDXR relative RNA expression level between tumor (median, 212.9 units) and normal tissues (median, 113.8 units) from 51 colorectal cancer patients (P < 0.001). Seven single nucleotide polymorphisms (SNPs) in the FDXR gene were discovered, with no significant difference in variant allele frequency between colon tumor and normal tissues (P > 0.05), and the common haplotypes for FDXR were not different between colon tumor and normal samples. No correlation was observed between FDXR genotype and RNA expression implying that the polymorphisms described in this study are not regulating FDXR expression in colon cancer. This genomic characterization provides the foundation for pharmacogenetic analysis of the impact of FDXR on chemotherapy for colorectal cancer.

Original languageEnglish
Pages (from-to)6170-6173
Number of pages4
JournalCancer research
Volume63
Issue number19
StatePublished - Oct 1 2003

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    Yu, J., Marsh, S., Ahluwalia, R., & McLeod, H. L. (2003). Ferredoxin reductase: Pharmacogenomic assessment in colorectal cancer. Cancer research, 63(19), 6170-6173.