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Coordination of TP53 Abnormalities in Breast Cancer: Data from Analysis of TP53 Polymorphisms, Loss of Heterozygosity, Methylation, and Mutations.

https://arctichealth.org/en/permalink/ahliterature101319
Source
Genet Test Mol Biomarkers. 2011 Aug 2;
Publication Type
Article
Date
Aug-2-2011
Author
Evgeny V Denisov
Tatiana V Sukhanovskaya
Tatiana S Dultseva
Elena A Malinovskaya
Nicolay V Litviakov
Elena M Slonimskaya
Evgeny L Choinzonov
Nadezhda V Cherdyntseva
Author Affiliation
1 Department of Experimental Oncology, Cancer Research Institute, Siberian Branch of Russian Academy of Medical Sciences , Tomsk, Russian Federation.
Source
Genet Test Mol Biomarkers. 2011 Aug 2;
Date
Aug-2-2011
Language
English
Publication Type
Article
Abstract
Aims: We have studied whether TP53 rs1042522, rs17878362, and rs1625895 alleles having a protective effect against breast cancer (BC) will be lost in tumors, whereas those allowing disease development will be retained. Methods: Analysis of TP53 polymorphisms was performed in blood leukocytes and tumors from 80 Caucasian BC patients. In addition, TP53 loss of heterozygosity (LOH), methylation, and mutations were studied in tumor DNA of BC individuals with loss of alleles of TP53 polymorphisms. Results: In breast tumors of patients heterozygous for TP53 polymorphisms, we detected loss of rs1042522 C and G and rs17878362 A2 alleles; however, the loss of the C allele was preferential. We found that loss of TP53 alleles, namely rs1042522 C, has been caused by an LOH mechanism, namely TP53 deletions, whereas TP53 point mutations frequently occurred in the retained G allele (p=0.03). In addition, we showed that BC patients with rs1042522 CC genotype were characterized by only unifocal tumors and decreased frequency of lymph node metastases (p=0.03). Conclusions: Taken together, we showed the preferential loss of the rs1042522 C allele, which is protective against BC progression, in breast tumors. Also, the loss of the C allele, which encodes p53 protein with the best DNA repair cupability according to literature data, may create prerequisites for mutations, but not for methylation in a retained G variant, as we found here. However, these results need to be confirmed because of the limited statistical power of the present study and the small sampling.
PubMed ID
21810023 View in PubMed
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Crosstalk Between the FGFR2 and TP53 Genes in Breast Cancer: Data from an Association Study and Epistatic Interaction Analysis.

https://arctichealth.org/en/permalink/ahliterature101235
Source
DNA Cell Biol. 2011 Aug 12;
Publication Type
Article
Date
Aug-12-2011
Author
Nadezhda V Cherdyntseva
Evgeny V Denisov
Nicolay V Litviakov
Vladimir N Maksimov
Elena A Malinovskaya
Natalia N Babyshkina
Elena M Slonimskaya
Mikhail I Voevoda
Evgeny L Choinzonov
Author Affiliation
1 Department of Experimental Oncology, Cancer Research Institute , Siberian Branch of Russian Academy of Medical Sciences, Tomsk, Russian Federation.
Source
DNA Cell Biol. 2011 Aug 12;
Date
Aug-12-2011
Language
English
Publication Type
Article
Abstract
To evaluate the potential for gene-gene interaction effects in sporadic breast cancer (BC) risk, we studied combinations of the fibroblast growth factor receptor 2 (FGFR2) rs1219648 and tumor protein 53 (TP53) rs1042522, rs1625895, and rs17878362 polymorphisms in BC patients (n=388) and healthy persons (n=275). In addition to a single-locus effect manifested by the association of FGFR2 rs1219648 and TP53 rs1042522 polymorphisms with high BC risk, depending on menopause status (0.001
PubMed ID
21838531 View in PubMed
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