[p16INK4a protein is a specific molecular biomarker of breast cancer].

OBJECTIVE: To investigate the expression of p16INK4a protein in breast cancer and analyze its clinical significance. METHODS: A total of 132 surgical specimens of primary breast cancer obtained between 2014 and 2015 were examined for expressions of ER, PR, CK5/6, Her-2 and p16INK4a proteins using immunohistochemistry. RESULTS: The breast cancer samples were classified into 5 molecular subtypes, namely Luminal A (58 cases), Luminal B (32 cases), Her-2-positive (21 cases), basal-like (12 cases) and normal-like (9 cases) types. p16INK4a expression was negative in 7/132 (5.30%) cases, weakly positive in 15/132 (11.36%) cases, positive in 40/132 (30.30%) cases, and strongly positive in 70/132 (53.03%) cases. When categorizing negative and weakly positive cases into negative group and the positive and strongly positive cases into positive group, the total negative and positive expression rates of p16INK4a were 16.67% (22/132) and 83.33% (110/132) in the carcinoma tissues. Statistical analysis showed the expression intensity of p16INK4a differed significantly between the age groups (P<0.05) but was not significantly correlated with ER, PR, Her-2, molecular subtypes or metastasis of the tumors. CONCLUSION: The compensatory high expression of p16INK4a is the main mechanism of cell cycle deregulation in invasive breast cancer and can be an important specific molecular marker for invasive breast cancer.

Association between MDM2 rs 2279744 polymorphism and breast cancer susceptibility: a meta-analysis based on 9,788 cases and 11,195 controls.

PURPOSE: Previous studies have suggested associations between MDM2 (mouse double minute 2 homolog) polymorphisms and cancer risk. The aim of this study was to evaluate the relationship between the MDM2 rs 2279744 polymorphism and the susceptibility of breast cancer. METHODS: We searched PubMed, Web of Knowledge, Embase, and the Chinese National Knowledge Infrastructure (CNKI) database for case-control studies published up to October 2013 that investigated MDM2 rs 2279744 polymorphism and breast cancer risk. Odds ratios (ORs) and 95% confidence intervals (CIs) were used to assess the strength of these associations. RESULTS: A total of 19 studies were identified for the meta-analysis, including 9,788 cases and 11,195 controls. The variant heterozygote (TG) was associated with breast cancer risk in the overall population (TG vs TT: OR =1.10, 95% CI =1.04-1.17, P=0.001, P=0.23 for heterogeneity test). In the subgroup analyses by ethnicity, a significantly increased risk was observed among Asians (G vs T: OR =1.12, 95% CI =1.02-1.23, P=0.02, P het=0.04; GG vs TT: OR =1.29, 95% CI =1.06-1.56, P=0.01, P het=0.04; TG vs TT: OR =1.36, 95% CI =1.15-1.60, P=0.0004, P het=0.45; dominant model TG+GG vs TT: OR =1.21, 95% CI =1.03-1.41, P=0.02, P het=0.07). However, among Caucasians, rs 2279744 was associated with breast cancer risk in only one genotype (TG vs TT: OR =1.09, 95% CI =1.00-1.18, P=0.04, P het=0.37). No publication bias was found in the present study. CONCLUSION: This meta-analysis provides evidence for the association between the MDM2 rs 2279744 polymorphism and breast cancer susceptibility. The results suggest that the MDM2 rs 2279744 polymorphism plays an important role in breast cancer, especially in Asians.

Association between APE1 Single Nucleotide Polymorphism (rs1760944) and Cancer Risk: a Meta-Analysis Based on 6,419 Cancer Cases and 6,781 Case-free Controls.

Apurinic/apyrimidinic endonuclease 1 (APE1) is an essential enzyme in the base excision repair pathway. Epidemiological studies have suggested associations between APE1 rs1760944 polymorphism and cancer risk. This study was aimed to evaluate the relationship between APE1 rs1760944 polymorphism and cancer risk. We searched Pubmed, ISI Web of Knowledge, Embase, Chinese National Knowledge Infrastructure (CNKI) databases until September 2013 to identify eligible studies. Odds ratios (ORs) and 95 % confidence intervals (CIs) were used to estimate the strength of the associations. 12 studies from 11 articles on APE1 rs1760944 genotypes and cancer risk were identified, including a total of 6,419 cancer cases and 6,781 case-free controls. Overall, APE1 rs1760944 polymorphism was significantly associated with the decreased risk of cancer in any genetic models (G vs. T: OR = 0.86, 95% CI = 0.82-0.90; homozygote comparison: OR = 0.74, 95% CI = 0.67-0.82; heterozygote comparison: OR =0.88, 95%CI = 0.81-0.95; dominant model TG+GG vs. TT: OR = 0.82, 95% CI = 0.76-0.89; recessive model GG vs. TT+TG: OR = 0.81, 95%CI = 0.75-0.88). In the stratified analysis by populations, the effect was remain in studies of Asian population (homozygote comparison: OR = 0.71, 95%CI = 0.63-0.79; heterozygote comparison: OR = 0.86, 95 %CI = 0.79- 0.94; dominant model: OR = 0.80, 95% CI = 0.74 -0.87 and recessive model: OR = 0.78, 95%CI = 0.71-0.86). Moreover, a significantly decreased risk was found in lung cancer studies (homozygote comparison: OR = 0.68, 95% CI = 0.59-0.79; heterozygote comparison: OR = 0.86, 95%CI = 0.77- 0.98; dominant model: OR = 0.80, 95%CI = 0.72-0.90 and recessive model: OR= 0.77, 95% CI= 0.68-0.87). These findings support that APE1 rs1760944 polymorphism has a possible protective effect on cancer susceptibility particularly among Asians. Further studies based on different ethnicity and various cancer types are warranted to verify our findings.

[Investigation of clinical pathology and treatments on the auricle pseudocyst].

OBJECTIVE: To study the clinical pathology and treatments on the pseudocyst of auricle. METHODS: Sixty cases of auricular pseudocyst were treated by surgery from 1993 to 2008 in our hospital. Their operation effects and the clinic pathological features were analyzed. RESULTS: The clinic pathological data showed that the source of serous effusion of auricular pseudocyst origin from cartilage membrane in the top wall. In the early stage of the cyst, the top wall of auricular pseudocyst was the cartilage membrane. With the course progresses, the cartilage membrane in the top wall of auricular pseudocyst was proliferating, thickened and generated new cartilage. The new cartilage was formed from small piece to the big one, and eventually became an entire new cartilage on the top wall of auricular pseudocyst. Serous effusion at this time was terminated, and this cyst became intra-cartilaginous effusion of auricle. Finally the fluid between cartilages was absorbed and organized. In the cyst, the new cartilage and auricle cartilage were organized and adhered together each other. The auricle became thickened and deformed. The observation of capsule wall under light microscope showed that there were a few fibrous desmoplasia, anapetia and lymphocyte infiltrating in the fibrous tissue, as well as that there were cartilage cell layers from firmness to thicker. The cartilage cells and their lacunes were small, and the cartilage capsule and the basilaris substantia was showed as eosin. This data indicated that the cartilage was neogenesis but not degenerating. Sixty patients were followed up from 3 months to 1 year. The effect of surgical treatment for the auricular pseudocyst was satisfactory. There was no auricular deformation in these patients with the operation. CONCLUSIONS: Auricular pseudocyst can be divided into the early period (acute exudative period), the medium period (cartilage formation period) and the late period (proliferative and organized period). The treatment should be based on the pathological findings of auricular pseudocyst. The operation is easy, safe and reliable. The key of the operation is the complete removal of perichondrium and cartilage at the top of auricular pseudocyst.

Increased expression of collagens, transforming growth factor-beta1, and -beta3 in gluteal muscle contracture.

BACKGROUND: Gluteal muscle contracture (GMC) is a multi-factor human chronic fibrotic disease of the gluteal muscle. Fibrotic tissue is characterized by excessive accumulation of collagen in the muscle's extracellular matrix. Transforming growth factor (TGF)-beta1 and -beta2 are thought to play an important role in fibrogenesis, while TGF-beta3 is believed to have an anti-fibrotic function. We hypothesize that the expression of collagen and TGF-betas would be up-regulated in GMC patients. METHODS: The expression of collagen type I, type III and TGF-betas were studied in 23 fibrotic samples and 23 normal/control samples in GMC patients using immunohistochemistry, reverse transcription and polymerase chain reaction (RT-PCR) and western bolt analysis. RESULTS: Compared to the unaffected adjacent muscle, increased expression of TGF-beta1 and -beta3 was associated with deposition of collagen type I and type III in the fibrotic muscle of the GMC patients at the mRNA level. Strong up-regulation of these proteins in fibrotic muscle was confirmed by immunohistochemical staining and western blot analysis. TGF-beta2 was not up-regulated in relation to GMC. CONCLUSION: This study confirmed our hypothesis that collagen types I, III, TGF-beta1 and TGF-beta3 were up-regulated in biopsy specimens obtained from patients with GMC. Complex interaction of TGF-beta1 with profibrotic function and TGF-beta3 with antifibrotic function may increase synthesis of collagens and thereby significantly contribute to the process of gluteal muscle scarring in patients with GMC.

In situ expression and significance of B7 costimulatory molecules within tissues of human gastric carcinoma.

AIM: To explore the role and significance of costimulatory molecules B7H1,B7H2 and ICOS within tissues of human gastric carcinoma and the possible mechanisms in tumor escape. METHODS: mRNA expressions of costimulatory molecules including B7H1,B7H2,ICOS and B7-1 in tissues of human gastric carcinoma were investigated by in situ hybridization using digoxigenin-labeled oligonucleotide-probes. The tissue of chronic gastric ulcer was used as a control. All data were analyzed by SPSS statistic software. RESULTS: At the site of gastric carcinoma, mRNA expression levels of B7H1, B7H2 and ICOS were much higher than that of B7-1. Their mRNA positive expression indexes were 0.512+/-0.333, 0.812+/-0.454, 0.702+/-0.359 and 0.293+/-0.253, respectively. The positively stained cells were mainly tumor infiltrating lymphocytes (TILs), and some tumor cells. The difference between them was greatly significant P<0.005. The mRNA expression levels of four molecules were not correlated to the pathological grade and matastasis of gastric carcinoma. CONCLUSION: ICOS-B7H costimulatory pathway may be predominant at the site of gastric carcinoma. B7-1mRNA might be the basis of ICOS-B7H interaction. ICOS-B7H interaction induces the production of IL-10 which inhibits the antitumor immune responses. Therefore, it is supposed that ICOS-B7H costimulatory pathway may be involved in the negative regulation of cell-mediated immune responses.