The tyrosine kinase inhibitors in combination with radiotherapy enhance the inhibition of breast cancer cells and breast cancer bearing nude mice / 重庆医学

Objective In order to research the effect of tyrosine kinase inhibitor in combination with radiotherapy on the inhibi‐tion of breast cancer cells and breast cancer bearing nude mice .Methods Methyl thiazolyl tetrazolium (MTT) assay was used to e‐valuate the inhibition of different concentrations of TKI on breast cancer cells ,the breast cancer cells was divided into three groups :the TKI treatment group ,the cells in the control group (no the TKI processing) and the control group (non‐TKI and X‐ray irradia‐tion group) .The sensitivity of the cells in each group to X‐ray was compared by colony formation assay .MCF7 cells were xenograf‐ted in athymic nude mice to establish the animal model ,which was used to evaluate the effect of anti‐cancer .Results Colony form‐ing test showed that the separated use of any concentrations of the TKI inhibitor could inhibit the breast cells ,and the cell viability was significantly reduced;TKI combined with X‐ray irradiation could significantly increase the sensitivity of breast cancer cells to radiation ,and the difference was statistically significant(P<0 .05) .Compared to TKI inhibitor or X‐ray irradiation alone ,the combi‐nation of TKI inhibitor with X‐ray irradiation could inhibit the growth of tumor effectively .Conclusion The TKI inhibitor in com‐bination with radiotherapy can effectively inhibit the growth of breast cancer cells ,which provides a new theoretical basis for the im‐plementation of the clinical breast cancer radio sensitization .

TNF-β genetic variant contributes to the risk of non-small cell lung cancer / 中华预防医学杂志

<p><b>OBJECTIVE</b>To investigate the association of TNF-β 252A >G variant with the risk of non-small cell lung cancer (NSCLC).</p><p><b>METHODS</b>Total 956 patients with NSCLC were recruited between January 2000 and December 2008 at Cancer Hospital, Chinese Academy of Medical Science as the case group, and 994 frequency-matched controls were randomly selected from a pool of cancer-free subjects recruited from a nutritional group. All the participants were unrelated Han Chinese. There were no age, gender restrictions. Smoking status of the subjects was surveyed. Informed consent was obtained and 3 ml peripheral blood was collected from each subject. All samples were genotyped by polymerase chain reaction-restriction fragment length polymorphism method (PCR-RFLP). The OR and 95%CI were estimated by logistic regression to evaluate the relationship between TNF-β 252 A/G variant and the risk of lung cancer.</p><p><b>RESULTS</b>The frequencies of TNF-β 252 AA, AG and GG genotype were 30.9% (307/994) , 47.4% (471/994) and 21.7% (216/994) in lung cancer cases and 35.7% (341/956) , 48.1% (460/956) and 16.2% (155/956) in controls. Logistic regression analysis revealed that TNF-β 252 GG genotype contributed to a decreased risk of developing NSCLC (OR = 0.64, 95%CI: 0.49-0.83) compared with AA genotype. When stratified by smoking status, the individuals with 252 GG genotype had a significant increased risk of NSCLC (OR = 1.54, 95%CI:1.00-2.39) among smokers; which was less than those with AA genotype among smokers (OR = 2.88, 95%CI:1.91-2.24). When further stratified by smoking index, individuals with 252 GG genotype had a significant decreased risk of NSCLC among heavy smokers with OR (95%CI) of 2.24 (1.33-3.74), which was less than those with AA genotype (OR = 4.62, 95%CI:2.88-7.41).</p><p><b>CONCLUSION</b>TNF-β genetic variant may interact with environment factor to contribute to the susceptibility to NSCLC.</p>

Genetic variants in the promoter of cyclooxygenase 2 interacting with Hp infection and the risk of esophageal cancer / 中国综合临床

Objective To evaluate the association of COX2 genetic variants with the risk of esophageal cancer and the interaction of COX2 genetic variants with Hp infection. Methods A total of 119 patients with esophageal cancer and 238 frequency-matched controls were genotyped by polymerase chain reaction-restriction fragment length polymorphism method. Odds ratios (OR) and 95% confidence intervals ( CI) were estimated by logistic regression. Results Case-control analysis showed an increased risk of developing esophageal cancer for 1195 GA(OR =2.69,95% CI= 1. 46-5. 14) and 1195AA ( OR = 2. 30,95% CI = 1.23-4. 89) genotype carriers,respectively, compared with non 1195 GG carriers. When stratified by Hp status, the significantly increased risk of esophageal cancer was found among Hp carrier with OR (95%CI) =2.74 (1.35-5.96) ,but not among Hp non-carriers. Conclusion Genetic polymorphism in COX2 promoter region may play an important role in esophageal cancer by Hp infection.