ATBF1 and NQO1 as candidate targets for allelic loss at chromosome arm 16q in breast cancer: absence of somatic ATBF1 mutations and no role for the C609T NQO1 polymorphism.

BMC Cancer
A M Cleton-JansenC J Cornelisse

Abstract

Loss of heterozygosity (LOH) at chromosome arm 16q is frequently observed in human breast cancer, suggesting that one or more target tumor suppressor genes (TSGs) are located there. However, detailed mapping of the smallest region of LOH has not yet resulted in the identification of a TSG at 16q. Therefore, the present study attempted to identify TSGs using an approach based on mRNA expression. A cDNA microarray for the 16q region was constructed and analyzed using RNA samples from 39 breast tumors with known LOH status at 16q. Five genes were identified to show lower expression in tumors with LOH at 16q compared to tumors without LOH. The genes for NAD(P)H dehydrogenase quinone (NQO1) and AT-binding transcription factor 1 (ATBF1) were further investigated given their functions as potential TSGs. NQO1 has been implicated in carcinogenesis due to its role in quinone detoxification and in stabilization of p53. One inactive polymorphic variant of NQO1 encodes a product showing reduced enzymatic activity. However, we did not find preferential targeting of the active NQO1 allele in tumors with LOH at 16q. Immunohistochemical analysis of 354 invasive breast tumors revealed that NQO1 protein expression in a subset of breast tumors is ...Continue Reading

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Citations

Jun 28, 2011·Breast Cancer Research and Treatment·Maral JamshidiHeli Nevanlinna
Aug 4, 2012·ACS Chemical Neuroscience·Ellen GrünewaldPippa A Thomson
Jul 23, 2011·Neuroendocrinology·Sandrine M Dupré
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Jun 19, 2017·Biochemical and Biophysical Research Communications·Mei LiJiyuan Zhao
Jul 7, 2018·Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc·Mirthe de BoerPaul J van Diest

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ORIGO
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Mutation [UNK] DNA variant
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Bioconductor

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