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Open AccessResearch article

MDM2 gene SNP309 T/G and p53 gene SNP72 G/C do not influence diffuse large B-cell non-Hodgkin lymphoma onset or survival in central European Caucasians

Joerg Bittenbring1 email, Frédérique Parisot2 email, Alain Wabo1 email, Monika Mueller1 email, Lynn Kerschenmeyer1 email, Markus Kreuz3 email, Lorenz Truemper4 email, Olfert Landt5 email, Alain Menzel2 email, Michael Pfreundschuh1 email and Klaus Roemer1 email

Internal Medicine I and Josè Carreras Research Center, University of Saarland Medical School, Homburg-Saar, Germany

Laboratoires Réunis, Junglister, Luxembourg

University of Leipzig, Institute for Medical Informatics, Statistics and Epidemiology, Leipzig, Germany

Hematology and Oncology, Medical School of the Georg-August-University, Göttingen, Germany

TIB MOLBIOL GmbH, Berlin, Germany

author email corresponding author email

BMC Cancer 2008, 8:116doi:10.1186/1471-2407-8-116

Published: 23 April 2008

Abstract

Background

SNP309 T/G (rs2279744) causes higher levels of MDM2, the most important negative regulator of the p53 tumor suppressor. SNP72 G/C (rs1042522) gives rise to a p53 protein with a greatly reduced capacity to induce apoptosis. Both polymorphisms have been implicated in cancer. The SNP309 G-allele has recently been reported to accelerate diffuse large B-cell lymphoma (DLBCL) formation in pre-menopausal women and suggested to constitute a genetic basis for estrogen affecting human tumorigenesis. Here we asked whether SNP309 and SNP72 are associated with DLBCL in women and are correlated with age of onset, diagnosis, or patient's survival.

Methods

SNP309 and SNP72 were PCR-genotyped in a case-control study that included 512 controls and 311 patients diagnosed with aggressive NHL. Of these, 205 were diagnosed with DLBCL.

Results

The age of onset was similar in men and women. The control and patients group showed similar SNP309 and SNP72 genotype frequencies. Importantly and in contrast to the previous findings, similar genotype frequencies were observed in female patients diagnosed by 51 years of age and those diagnosed later. Specifically, 3/20 female DLBCL patients diagnosed by 51 years of age were homozygous for SNP309 G and 2/20 DLBCL females in that age group were homozygous for SNP72 C. Neither SNP309 nor SNP72 had a significant influence on event-free and overall survival in multivariate analyses.

Conclusion

In contrast to the previous study on Ashkenazi Jewish Caucasians, DLBCL in pre-menopausal women of central European Caucasian ethnicity was not associated with SNP309 G. Neither SNP309 nor SNP72 seem to be correlated with age of onset, diagnosis, or survival of patients.


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