GSTM1 polymorphisms and lung cancer risk in the Chinese population: a meta-analysis based on 47 studies.

Although a number of studies have been conducted on the association between GSTM1 polymorphisms and lung cancer in China, this association remains elusive and controversial. To clarify the effects of GSTM1 polymorphisms on the risk of lung cancer, a meta-analysis was performed in the Chinese population. Related studies were identified from PubMed, Springer Link, Ovid, Chinese Wanfang Data Knowledge Service Platform, Chinese National Knowledge Infrastructure (CNKI), and Chinese Biology Medicine (CBM) up to 5th April 2014. A total of 45 articles (47 studies) including 6,623 cases and 7,865 controls were involved in this meta-analysis. Overall, a significant association (OR = 1.45, 95%CI: 1.32-1.60) was found between the null GSTM1 and lung cancer risk when all studies in Chinese population pooled into the meta-analysis. In subgroup analyses stratified by quality score, geographic area and source of controls, the same results were observed under all the models. This meta-analysis showed that the null GSTM1 may be a potential biomarker for lung cancer risk in Chinese, but further studies with gene-gene and gene-environment interactions are required for definite conclusions.

[Correlation between high sensitive C-reactive protein, lipoprotein(a), blood uric acid and severity of coronary artery disease].

OBJECTIVE: To discuss the relationship between high sensitive C-reactive protein (hs-CRP), lipoprotein (Lp)(a), blood uric acid (BUA) and severity of coronary artery disease (CHD). METHODS: A total of 813 cases of suspected or established coronary atherosclerotic heart disease patients were recruited. The patients received selective coronary arteriography and they were divided into normal and CHD groups according to the result of selective coronary arteriography. The dividing mark was coronary artery stenosis more than 50% by selective coronary arteriography. Patients in CHD group were further divided into 1-4 vessel disease. Blood glucose, cholesterol, triglyceride, LDL-ch, hs-CRP and BUA were detected by automatic biochemical analyzer. RESULTS: Among them, 754 cases (CHD group, 92.7%) were confirmed as coronary heart disease while 59 cases (control group, 7.3%) confirmed as non-coronary heart disease. There were significantly difference between two groups (P < 0.05): hs-CRP (7.12 ± 4.48 vs 1.71 ± 1.42) mg/L, Lp(a) (0.45 ± 0.42 vs 0.18 ± 0.03) mmol/L and BUA (402 ± 103 vs 327 ± 88) µmol/L. The levels of hs-CRP, Lp(a) and BUA in different number of diseased coronary vessels significantly differed from each other (P < 0.05). A comparison of 1-vessel disease group versus 4 vessel disease group was as follows: hs-CRP (3.59 ± 2.93 vs 13.11 ± 3.00) mg/L, Lp(a) (0.37 ± 0.25 vs 0.58 ± 0.17) mmol/L and BUA (384 ± 126 vs 444 ± 91) µmol/L. Logistic regression analysis showed that hs-CRP, Lp(a) and BUA were independent risk factors of coronary artery disease. CONCLUSIONS: The elevations of hs-CRP, LP(a) and BUA promote the establishment and development of coronary artery disease. A joint detection of hs-CRP, Lp(a) and BUA shows a comparatively great value in evaluating high-risk groups and the patient's condition. And it provides references for an active intervention of clinical coronary heart disease.

Loss of Cyclin B1 followed by downregulation of Cyclin A/Cdk2, apoptosis and antiproliferation in Hela cell line.

Recent studies have shown that Cyclin B1 is overexpressed in various tumor types but present at low levels in normal tissues. To explore the possibility of employing Cyclin B1 as an anticancer target, we knocked down Cyclin B1 in an HeLa cell line using RNA interference (RNAi). Subsequently, we monitored cell cycle-related molecules by Western blot together with immunofluorescence and determined cell cycle distribution by flow cytometry. XTT and soft agar colony growth experiments were performed to detect cell viability and proliferation. Furthermore, we analyzed cell apoptosis by measuring Bcl-2 and Bax protein level and DNA-ladder assay. After performing Cyclin B1 RNAi, Cyclin B1, Cyclin A and Cdk2 protein levels were found to be markedly downregulated, whereas Cdc2 was almost unaffected; S-phase fraction increased significantly; HeLa cell viability and cell colony forming ability were markedly diminished after the RNAi; Bcl-2 was noticeably attenuated but Bax was hardly changed; and HeLa cells displayed typical DNA ladder. The loss of Cyclin B1 resulted in the downregulation of Cyclin A and Cdk2, S-phase delay and eventually led to cell apoptosis and the decrease of cell viability and proliferation. Our studies suggest that Cyclin B1 may be a promising anticancer target.

[Detecting methylation of the calcitonin gene in monitoring treatment and disease evolution for myelogenous leukemia].

BACKGROUND & OBJECTIVE: Calcitonin gene mostly appears hypomethylation in normal cells. Hypermethylation of calcitonin gene frequently implies malignancy transformation and is probably related to the progress of hematological malignancy tumors. However, studies on the significance of hypermethylation of calcitonin gene in the diagnosis and treatment of myelogenous leukemia were rarely reported. This study was designed to investigate the value of analyzing hypermethylation of the calcitonin gene for detecting minimal residual disease (MRD) and monitoring disease evolution in acute myeloid leukemia (AML) and chronic myeloid leukemia(CML). METHODS: Digestion of DNA with Hpa II in combination with polymerase chain reaction (PCR) was used to examine the methylation patterns of the calcitonin gene in 31 cases with AML, 45 cases with CML (including 33 patients in chronic phase, 2 in accelerated phase, and 10 in blast crisis), and 14 healthy adults (used as control). RESULTS: The hypermethylation of calcitonin gene was found in 25 of 31 cases with AML (80.6%), 0 of 14 healthy adults (0%) (P< 0.01). Follow-up study of 5 cases with AML showed that 4 cases who appeared hypermethylation of calcitonin gene at both diagnosis and complete remission relapsed 3, 5, 6, and 14 months respectively after complete remission; the other case without hypermethylation of calcitonin gene did not relapse 25 months after complete remission. Among 45 cases with CML, 3 of 33 in chronic phase, 2 of 2 in accelerated phase and 8 of 10 in blast crisis showed hypermethylation of calcitonin gene; there were significant differences between chronic phase group and blast crisis group (including accelerated phase) (P< 0.01); three cases with CML in chronic phase developed into blast crisis 10, 12, and 13 months after hypermethylation of calcitonin gene were detected. CONCLUSION: Analyzing hypermethylation of calcitonin gene may be useful in assessing the prognosis of AML and monitoring disease evolution in CML.