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 .

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.

Objective To continuously draw blood from caudal vein of SD rats which controlled by the homemade holder with an im-proved method, and the effects of this method was evaluated according to the relevant indicators. Methods The 24 SD rats should be drew the blood from the caudal vein by the improved disposable infusion needle and supplied physiological saline at the condition of ether inhala-tion anesthesia and once a day until to the thirteenth day,and then the times of draw blood and the number of survival rats only to calculate the success rate and survival rate of rats were record. Results In the 12 days,the tail vein blood of 24 SD rats were successfully collected. But a rat died of excessive ether inhalation anesthesia on the thirteenth day. The success rate was 99. 68% and the rat survival rate was 95. 83%. Conclusion The method that applying an improved disposable infusion needle and supplying physiological saline is safe and ef-fective,flexible and convenient,which is suitable for experimental study that needs to draw blood from caudal vein of the SD rat at the contin-uous time.

OBJECTIVETo investigate the association of TNF-β 252A >G variant with the risk of non-small cell lung cancer (NSCLC).

METHODSTotal 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.

RESULTSThe 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).

CONCLUSIONTNF-β genetic variant may interact with environment factor to contribute to the susceptibility to NSCLC.

Asian Continental Ancestry Group ; Carcinoma, Non-Small-Cell Lung ; Case-Control Studies ; China ; Genetic Predisposition to Disease ; Genotype ; Humans ; Lung Neoplasms ; Lymphotoxin-alpha ; Polymerase Chain Reaction ; Polymorphism, Restriction Fragment Length ; Risk ; Risk Factors ; Smoking

Objective: To investigate the clinical features and pathogenic genes of a family with osteosclerosis. Methods: Six patients and six family members from a family in Jiangsu were tested for biochemical parameters, bone metabolic markers, bone mineral density, thoracolumbar anterior lateral slices, skull positive lateral radiographs, and pelvic plain films. Meanwhile, Sanger sequencing was performed to detect gene mutations of the proband and five other family members with high bone mass. The conformation of the mutational low-density lipoprotein receptor-related protein 5 (LRP5) protein was predicted by SWISS-MODEL. Results: Four adult patients (one male and three females) were tall, with mandibular enlargement and kyphosis in the center of the lower jaw, and none of the four had fractures. Their X ray examination revealed that the skull and long bone cortex was thickened, while the sella and mandible was enlarged. In addition, the absolute values of bone mineral density at each site of all patients were significantly higher as compared with the standard age- and sex-matched adults or adolescent mean reference values, with Z scores of L2-4, femoral neck and total hip being (6.31±4.03) SD, (6.56±2.36) SD, and (7.19±2.03) SD, respectively. The results of genetic sequencing revealed that all six patients carried a heterozygous mutation (c.331G>T; D111Y) in exon 2 of LRP5 gene, while other family members showed wild type (c.331G>G; D111D). Functional prediction indicated that this mutation was located at the amino acid terminal of exon 2 of LRP5 gene, which encodes the first β-helix-generating region of LRP5 protein. Conclusion The D111Y mutation in LRP5 gene leads to a clinical phenotype characterized by benign increased bone mineral density without increasing the risk of fracture. This mutation may further affect the downstream Wnt signaling pathway by altering the spatial structure of LRP5 protein, thereby promoting maturation and differentiation of osteoblasts and resulting in osteosclerosis.