Value of Magnetic Resonance Imaging Texture Analysis in the Differential Diagnosis of Benign and Malignant Breast Tumors.

Objective To investigate the difference in texture features on diffusion weighted imaging (DWI) images between breast benign and malignant tumors.Methods Patients including 56 with mass-like breast cancer, 16 with breast fibroadenoma, and 4 with intraductal papilloma of breast treated in the Hainan Hospital of Chinese PLA General Hospital were retrospectively enrolled in this study, and allocated to the benign group (20 patients) and the malignant group (56 patients) according to the post-surgically pathological results. Texture analysis was performed on axial DWI images, and five characteristic parameters including Angular Second Moment (ASM), Contrast, Correlation, Inverse Difference Moment (IDM), and Entropy were calculated. Independent sample t-test and Mann-Whitney U test were performed for intergroup comparison. Regression model was established by using Binary Logistic regression analysis, and receiver operating characteristic curve (ROC) analysis was carried out to evaluate the diagnostic efficiency.Results The texture features ASM, Contrast, Correlation and Entropy showed significant differences between the benign and malignant breast tumor groups (PASM=0.014, Pcontrast=0.019, Pcorrelation=0.010, Pentropy=0.007). The area under the ROC curve was 0.685, 0.681, 0.754, and 0.683 respectively for the positive texture variables mentioned above, and that for the combined variables (ASM, Contrast, and Entropy) was 0.802 in the model of Logistic regression. Binary Logistic regression analysis demonstrated that ASM, Contrast and Entropy were considered as the specific imaging variables for the differential diagnosis of breast benign and malignant tumors.Conclusions The texture analysis of DWI may be a simple and effective tool in the differential diagnosis between breast benign and malignant tumors.

Common polymorphism in the MMP-13 gene may contribute to the risk of human cancers: a meta-analysis.

Cancer was viewed to be driven by accumulating genetic abnormalities that generally include chromosomal abnormalities, mutations in tumor-suppressor genes, and oncogenes. The aim of this meta-analysis was to systematically summarize the possible associations between MMP-13 rs2252070 A>G variant and cancer risks. We systematically reviewed studies focusing on MMP-13 polymorphisms with human cancer susceptibility that were published before April 30, 2014. Relevant articles were identified through research of PubMed, Embase, Web of Science, Cochrane Library, CISCOM, CINAHL, Google Scholar, CBM, and CNKI databases. All analyses were calculated using the Version 12.0 STATA software. Odds ratios (OR) and 95 % confidence interval (95 % CI) were calculated. Eleven independent case-control studies were included in the meta-analysis, which involved 3,465 patients with cancers and 4,073 healthy controls. The results identified a positive association between rs2252070 A>G polymorphism and susceptibility to cancer under five genetic models (all P < 0.05). Ethnicity subgroup analysis implied that significant difference was detected for rs2252070 A>G polymorphism with increased risk of cancers among Asians and Caucasians in majority of the groups. Our findings suggest significant association for MMP-13 rs2252070 A>G to increased susceptibility to human cancer, especially in the progression of lung carcinoma.

[Effects of single versus combined use of trastuzumab and cantide on breast cancer cells SKBR3 over-expressing HER2].

OBJECTIVE: To evaluate the in vitro cytotoxic effects of cantide or herceptin on human breast cancer SKBR3 cells over-expressing HER2. METHODS: The distribution of HER2 and hTERT protein in SKBR3 cells and the effects of cantide and/or herceptin on the subcellular localization of HER2 and hTERT were observed by indirect immunofluorescent assay. The inhibition rate of herceptin and/or cantide at different concentrations on SKBR3 cells was detected by MTT assay. And the apoptotic rate of cells was evaluated by flow cytometer. RESULTS: (1) The expressions of both HER2 and hTERT proteins in SKBR3 cells were found. HER2 protein was predominant in cell membranes while hTERT protein in nuclei. After the addition of herceptin, the cytoplasmic migration of HER2 was found while there was no distinct location change of cantide. (2) In MTT assay, the single use of cantide or herceptin and the combined use of both produced inhibitory effects on SKBR3 cells while the inhibition rate was higher for combined use. The inhibitory effects became additive in the combined use of 0.4 µmol/L cantide and 0.85 µg/ml herceptin. And there were synergistic effects in the combined use of 0.4 µmol/L cantide and 1.70, 3.40, 6.88 or 13.75 µg/ml herceptin. (3) The apoptotic rate was 25.75% for cantide alone, 11.26% for herceptin alone and 41.41% for their combined use (apoptotic cells predominant in advanced stage). CONCLUSION: Due to different localizations, cantide and herceptin have different action sites in their combined use. When in single use, the inhibition rate is linearly correlated with the concentration of herceptin or cantide. And their combined use produces additive or synergistic antitumor effects on SKBR3 breast cancer cells.

MG132 selectively upregulates MICB through the DNA damage response pathway in A549 cells.

Natural killer (NK) cells recognize stress­activated NK group 2, member D (NKG2D) ligands in tumors. In the present study, the expression levels of NKG2D ligands were examined in four lung cancer cell lines (A549, PLA801D, NCI­H157 and NCI­H520). In the A549 cells, the expression of MHC class I polypeptiderelated sequence (MIC)A/B and UL16 binding protein (ULBP)1 was weak, the expression of ULBP2 was typical, and neither ULBP3 nor ULBP4 were expressed. The mechanism underlying the regulatory effect of a cancer treatment agent on the expression of NKG2D ligands was investigated using the proteasome inhibitor MG132. Following treatment for 8 h with MG132, the transcription levels of MICB and ULBP1 were upregulated 10.62­ and 11.09­fold, respectively, and the expression levels of MICB and ULBP1 were increased by 68.18 and 23.65%, respectively. Notably, MICB exhibited significant time­dependent change. MG132 increased the transcription of MICB by acting at a site in the 480­bp MICB upstream promoter. The activity of the MICB promoter was upregulated 1.77­fold following treatment with MG132. MG132 treatment improved the cytotoxicity of NK cells, which was partially blocked by an antibody targeting NKG2D, and more specifically the MICB molecule. The expression of MICB induced by MG132 was inhibited by KU­55933 [ataxia telangiectasia mutated (ATM) kinase inhibitor], wortmannin (phosphoinositide 3 kinase inhibitor) and caffeine (ATM/ATM­Rad3­related inhibitor). The phosphorylation of checkpoint kinase 2 (Chk2), an event associated with DNA damage, was observed following treatment with MG132. These results indicated that MG132 selectively upregulates the expression of MICB in A549 cells, and increases the NKG2D­mediated cytotoxicity of NK cells. The regulatory effect of MG132 may be associated with the activation of Chk2, an event associated with DNA damage. The combination of MG132 with NK cell immunotherapy may have a synergistic effect that improves the therapeutic effect of lung cancer treatment.