Acne is the most common chronic inflammatory skin diseases. Multiple factors, such as hormonal, environmental, immunological, and genetic factors, are thought to be involved in acne. However, genetic studies have yet to elucidate the full mechanism of acne. The aim of this study was to investigate the association of MMP-2 (-1306C/T) and TIMP-2 (-418G/C) polymorphisms with the risk of acne vulgaris in a Chinese Han population. We also analyzed the correlation of clinical parameters and family history in patients with acne vulgaris. This study included 251 acne patients and 121 age- and sex-matched healthy controls. Genomic DNA was extracted from peripheral blood, and genotyping was performed by PCR and DNA sequencing techniques. There is a significant correlation between the MMP-2 (-1306C/T) polymorphism and the acne vulgaris (P<0.001). Although no association was found between the TIMP-2 (-418G/C) polymorphism and the acne vulgaris, patients with the MMP-2 CT/TIMP-2 GG or GC allele are at higher risk of acne vulgaris. There is also a significant difference in the severity of the disease between acne vulgaris patients with and without family history (P<0.001). This study indicated that the MMP-2 (-1306C/T) polymorphism, in combination with the TIMP-2 (-418G/C) polymorphism, contributes to acne vulgaris susceptibility in the Chinese Han population.

446OBJECTIVE: The association between codon 72 polymorphism of the tumour protein p53 (TP53) gene -which results in a missense mutation of arginine (R) to proline (P) -and susceptibility to hepatocellular carcinoma (HCC) is controversial. A metaanalysis was performed in order to define this relationship more precisely. METHODS: Published studies of TP53 codon 72 polymorphism and the risk of HCC were identified. Data were extracted, and summary odds ratios (OR) and 95% confidence intervals (95% CI) were calculated. Pooled ORs were determined for an additive model (R/R versus P/P), a dominant model ([R/R + R/P] versus P/P) and a recessive model (R/R versus [R/P + P/P]). RESULTS: The meta-analysis included seven case-control studies (total 1511 cases and 2165 controls). The risk of cancer was significantly decreased in the overall dominant model and the dominant model in Asian populations. A significantly decreased risk was found for all models in hospital-based but not population-based studies. There was no association between polymorphism and cancer risk when data were stratified according to hepatitis B or C virus infection status. CONCLUSION: The TP53 codon 72 polymorphism may be a risk factor for HCC. KEY WORDS: HEPATOCELLULAR CARCINOMA (HCC); TUMOUR PROTEIN P53 (TP53); CODON 72; POLYMORPHISM; META-ANALYSIS IntroductionHepatocellular carcinoma (HCC) accounts for 85 -90% of primary liver cancers, which are the fifth most common cancers worldwide. 1 The distribution of HCC varies among geographic regions and ethnic groups. 2 The incidence of this disease is increasing in developed countries in spite of considerable diagnostic and therapeutic progress. Tumour protein p53 is a tumour suppressor that plays an important role in cell cycle regulation and the maintenance of genome integrity. 9 TP53 mediates the cellular response to DNA damage via effects on gene transcription, DNA synthesis and repair, genomic plasticity and apoptosis. 10 Mutation of TP53 can result in uncontrolled cell proliferation and is associated with an increased risk of several cancers, including HCC. 11Several studies have investigated the association of TP53 polymorphisms with the risk of cancer.12 -14 The most studied polymorphism in the TP53 gene is a G>C replacement in exon 4, at codon 72. 15 This results in a mis-sense mutation of arginine (R) to proline (P) 16 and the production of a protein with different biological and biochemical characteristics. There are three possible distinct TP53 genotypes: homozygous for arginine (R/R); homozygous for proline (P/P); and heterozygous (R/P). Studies regarding the possible association of this polymorphism with HCC have shown inconclusive results, and most have included only small numbers of cases and controls. This meta-analysis was conducted in order to determine the effects of this polymorphism on the risk of HCC. Materials and methods IDENTIFICATION OF STUDIESA literature search was conducted in order to identify studies that examined the association of the TP53 codon 72 polymorphism with HCC. T...