Evidence has suggested that the deficiency of PARP-1 results in DNA repair defects, genomic instability, failure of induction of cell death, and modulation of gene transcription, thereby contributing to carcinogenesis. This polymorphism is located in the sixth helix of the COOH-terminal NAD-binding region with all of the catalytic activities of the full-length enzyme. This amino acid change contributes to low polyation activities in a dosage-dependent manner, thereby impairing DNA repair and enhancing the susceptibility of variant allele carriers to damage caused by environmental carcinogens and cancer risk. Thus far, molecular epidemiological studies have indicated the genetic association of Val762Ala with the risk of many cancer types, including cancers of the breast, stomach, lung, cervix, brain, and colorectum, as well as other types of malignancies. However, these studies have not yet produced consistent results. The discrepancies of the findings are partially attributed to the limited power of individual studies with small sample sizes and differences in the baseline characteristics of included patients. Although the PARP-1 Val762Ala polymorphism and susceptibility to cancers have been discussed, all of the eligible studies have not been included, particularly case-control studies published in the past two years. Therefore, these meta-studies are disputed because of the limited number of included studies and relatively small sample size. The present meta-analysis aimed to update previous meta-analyses and derive a reliable conclusion regarding the effect of the V762A polymorphism on the function of PARP-1 in cancer. This meta-analysis also aimed to quantify the potential of heterogeneity between studies. Prolactin is a hormone secreted mainly by lactotropes in the anterior pituitary gland. This hormone is involved in several physiological functions, including mammopoiesis, lactogenesis and reproduction although it has also been implicated in the development of various peripheral tumors. In breast and prostate cancers, where local PRL production has been demonstrated, its proliferative potential via an autocrine/paracrine mechanisms has been proposed to contribute to tumor development and progression. Prolactinomas are benign tumors that constitute approximately one third of pituitary tumors. One of the main characteristics of prolactinomas is that they rarely undergo malignant transformation or local invasiveness. It has been proposed that prolactinomas have a monoclonal origin and that alterations in cell cycle regulation lead to expansion of an original mutated cell. Although several oncogenes are expressed in these adenomas, and various mutations have been associated with familial cases of anterior pituitary tumors, the mechanisms leading to sporadic adenoma formation are currently unknown.