MDM2 SNP285 does not antagonize the effect of SNP309 in lung cancer

Conflicting reports exist regarding the contribution of SNP309 in MDM2 to cancer risk. Recently, SNP285 was shown to act as an antagonist to SNP309 by overriding the effect of SNP309 on SP1‐mediated transcription. Moreover, SNP285 modified the relationship between SNP309 and risk of breast, ovarian...

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Bibliographic Details
Published in:International journal of cancer 2012-12, Vol.131 (11), p.2710-2716
Main Authors: Ryan, Bríd M., Calhoun, Kara M., Pine, Sharon R., Bowman, Elise D., Robles, Ana I., Ambs, Stefan, Harris, Curtis C.
Format: Article
Language:English
Subjects:
Aged
Alleles
Biological and medical sciences
Cancer
Case-Control Studies
Cohort Studies
Endometrial cancer
Female
Genetic Predisposition to Disease
Health risk assessment
Humans
Lung cancer
Lung Neoplasms - genetics
Male
Medical research
Medical sciences
Pneumology
Polymorphism, Single Nucleotide
Proto-Oncogene Proteins c-mdm2 - genetics
SNP285
SNP309
Tumors
Tumors of the respiratory system and mediastinum
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Summary:Conflicting reports exist regarding the contribution of SNP309 in MDM2 to cancer risk. Recently, SNP285 was shown to act as an antagonist to SNP309 by overriding the effect of SNP309 on SP1‐mediated transcription. Moreover, SNP285 modified the relationship between SNP309 and risk of breast, ovarian and endometrial cancer. We assessed whether SNP285 confounded the effect of SNP309 in lung cancer in a cohort of 720 controls and 556 cases. Our cohort included both Caucasians and African Americans. Neither SNP309 nor SNP285 was associated with lung cancer risk or survival. In addition, removal of individuals who carried the variant C allele of SNP285 did not modify the association between SNP309 with either lung cancer risk or survival. Although an effect of SNP285 has been demonstrated in breast, ovarian and endometrial cancer, our findings do not support a role for this SNP in lung cancer and raise the possibility that the effect of SNP285 is restricted to cancers in women.
ISSN:0020-7136
1097-0215
DOI:10.1002/ijc.27573