Glutathione S-transferase M1 polymorphism and esophageal cancer risk: An updated meta-analysis based on 37 studies.

AIM: To evaluate the relationship between glutathione S-transferase M1 (GSTM1) polymorphism and susceptibility to esophageal cancer (EC). METHODS: A comprehensive search of the United States National Library of Medicine PubMed database and the Elsevier, Springer, and China National Knowledge Infrastructure databases for all relevant studies was conducted using combinations of the following terms: "glutathione S-transferase M1", "GSTM1", "polymorphism", and "EC" (until November 1, 2014). The statistical analysis was performed using the SAS software (v.9.1.3; SAS Institute, Cary, NC, United States) and the Review Manager software (v.5.0; Oxford, England); crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the association between the GSTM1 null genotype and the risk of EC. RESULTS: A total of 37 studies involving 2236 EC cases and 3243 controls were included in this meta-analysis. We observed that the GSTM1 null genotype was a significant risk factor for EC in most populations (OR = 1.33, 95%CI: 1.12-1.57, P heterogeneity < 0.000001, and I (2) = 77.0%), particularly in the Asian population (OR = 1.53, 95%CI: 1.26-1.86, P heterogeneity < 0.000001, and I (2) = 77.0%), but not in the Caucasian population (OR = 1.02, 95%CI: 0.87-1.19, P heterogeneity = 0.97, and I (2) = 0%). CONCLUSION: The GSTM1 null polymorphism may be associated with an increased risk for EC in Asian but not Caucasian populations.

[The trend of cancer mortality from 1988 to 2005 in Kaifeng county, China].

OBJECTIVE: To investigate the time trends of cancer mortality among residents in Kaifeng county, Henan province. METHODS: Data on cancer mortality from the vital registration system in Kaifeng county from 1988 to 2005 was analyzed. A total of 9543 death records (5974 males and 3567 females) due to malignant tumors were studied. A two-year-period age-specified standardized mortality rates were directly adjusted by the world standard population, and the annual percentage change (APC) of mortality were estimated by a linear logarithm regression. RESULTS: The crude cancer death rate for male was 95.09/100,000 and its age-standardized death rate was 117.41/100,000. While, the crude cancer death rate for female was 59.13/100,000 and the age-standardized death rate was 57.15/100,000. There was a significant growth tread for lung cancer (APC: 6.54%), liver cancer (5.07%) in males and breast cancer (7.04%) in females in the groups aged over 18. On the contrary, the decreasing treads for esophageal cancer in both of sexes (-7.09%, -13.53%) were also observed in this study. Meanwhile, there was no other significant changes in the trend, either in the tumor sites or mortality, was observed. CONCLUSION: In the past two decades, there has been a significant increasing trend for cancer mortality in Kaifeng county, of Henan Province. Hence, it is necessary to enhance epidemiological survey to identify risk factors at the earlier stages.

[Effects of genistein on proliferation and apoptosis in HT-29 cells].

OBJECTIVE: The study is to explore the effects of genistein on proliferation and apoptosis in human colon cancer HT-29 cells and the likely underlying molecular mechanisms. METHODS: HT-29 cultures were maintained in DMEM containing 10% fetal bovine serum. Cell proliferation was determined by MTT assay and cell cycle distribution by cytometry. Apoptosis was detected by the Cell Death Detection ELISA and cytometry. The expressions of bax, bcl-2, and PCNA were examined using reverse transcriptase-polymerase chain reaction (RT-PCR) and Western-blot both at mRNA and protein levels, respectively. RESULTS: Genistein inhibited proliferation and induced G2/M phase arrest and apoptotic death in colon cancer HT-29 cells. We investigated the effects of genistein on molecules that regulate apoptosis and cell cycle progress. Genistein increased expression of bax and significantly reduced PCNA with a slightly decrease in bcl-2 expression both at mRNA and protein level. CONCLUSION: Our results demonstrated that genistein inhibited the viability of human colon cancer HT-29 cell via induction of apoptosis mainly through regulation of PCNA and Bax/Bcl-2 expression. These data suggested a role of genistein in prevention of colon tumor and might reduce colon tumor growth.

Effects of fat-soluble extracts from vegetable powder and beta-carotene on proliferation and apoptosis of lung cancer cell YTMLC-90.

OBJECTIVE: The aim of this investigation was to study the effects of fat-soluble extracts from vegetable powder (FEFVP) and beta-carotene on the proliferation and apoptosis of cultured YTMLC-90 lung cancer cells. METHODS: The lung cancer cells were continuously exposed to a broad range of concentration of FEFVP and beta-carotene. The proliferation was evaluated in MTT test. The induction of apoptosis was evaluated by morphological change, DNA fragmentation analysis, and DNA content analysis combined with flow cytometric analysis. RESULTS: Both FEFVP and beta-carotene were found to inhibit cell proliferation and to induce morphologic changes consistent with apoptosis in YTMLC-90 cancer cells, including cellular shrinkage, chromatin condensation and nuclear fragmentation. DNA agarose gel electrophoresis showed DNA fragmentation 'ladder'. Flow cytometric analysis revealed decreased DNA content and the presence of a sub-G1 apoptotic peak. CONCLUSION: These findings are consistent with the induction of apoptosis. Moreover, the effects of FEFVP are stronger than those of beta-carotene. FEFVP inhibits the growth of YTMLC-90 probably via the induction of apoptosis cancer cells.