The loss of TP53 gene could damage its DNA-binding properties and

The loss of TP53 gene could damage its DNA-binding properties and transcription factor function, thus leading to aberrant cell proliferation. In human populations, the TP53 gene is polymorphic at amino acid 72 of the protein that it encodes. Recently, much attention has been focused

on possible associations of TP53 polymorphisms and RepSox manufacturer cancer risks. The most informative polymorphism in TP53 gene is located in exon 4 at codon 72, which encodes two distinct functional allelic forms arginine (Arg) and proline (Pro) because of a transversion G to C [15], resulting in different biochemical and biological protein features. Consequently, three distinct genotypes were created, namely, homozygous for arginine (Arg/Arg), homozygous for proline (Pro/Pro), and heterozygous (Arg/Pro). Previously, Arg variant has been KU-57788 clinical trial thought to increase susceptibility to gastric cancer[16] and Arg homozygosity might contribute to cervical Selleckchem SCH727965 cancer [17]. Nevertheless, Pro homozygosity might have an association with lung [18] and hepotocellular cancer [19] risk. The heterozygous genotype Arg/Pro has been implicated as a risk factor for bladder cancer [20]. In recent literature, inconclusive data regarding TP53 codon 72 were found in some cancers, such as gastric cancer in which controversial conclusions were obtained in Asians [21] and in individuals from Northern Brazil [22]. Similarly,

up to date, published data on the possible association of TP53 codon 72 polymorphism with breast carcinoma have also generated controversial and inconclusive results. To the best of our knowledge, whether TP53 codon 72 polymorphism could increase breast cancer risk remains largely uncertain. To clarify this

association may help us better understand the possible risk of breast cancer and therefore contribute to its prevention. As a single study may have been underpowered in clarifying Metalloexopeptidase the relationship of TP53 codon 72 polymorphisms with breast carcinoma susceptibility, in the present study we performed evidence-based quantitative meta-analyses that can increase statistical power to address the association. Materials and methods Literature search strategy for identification of the studies We carried out a search in the Medline, EMBASE, OVID, Sciencedirect, and Chinese National Knowledge Infrastructure (CNKI) without a language limitation, covering all papers published up to Jan 2009, with a combination of the following keywords: TP53, P53, codon 72, breast, carcinoma, neoplasm, tumor, cancer and polymorphism. The keywords were paired each time in order to get more relevant information. For example, the word “”breast”" was always kept and others were substituted in different moments. We evaluated potentially associated publications by checking their titles and abstracts and then procured the most relevant publications for a closer examination.

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