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Physicochemical Qualities of Extracellular Polymeric Materials Produced by Three Microbial Isolates From Biofouled Ro Walls.
PURPOSE Several biomarkers have been reported to correlate with neoadjuvant chemotherapy response. Our aim was to establish the correlation between neutrophils-to-lymphocytes (NLR), lymphocytes-to-monocytes (LMR), and platelets-to-lymphocytes ratios (PLR) and the Miller Payne grade (MPG) and Residual Cancer Burden Score (RCB), as indicators to response to chemotherapy. METHODS Data were retrospectively collected from the First Surgical Clinic database between January 2016 and December 2018. RESULTS 96 patients were included in the study. The multivariate regression analysis showed a statistical correlation between oestrogen (ER) and progesterone receptor (PR) status, Ki67 over 15%, and tumour infiltrating lymphocytes (TILs) and MPG and RCB. For the three studied ratios, p value was statistical not significative. ROC curve showed a cut-off value of 2.7 NLR, for which correlation with the pathological complete response to chemotherapy (pCR) was significative (p=0.03). CONCLUSIONS Our findings suggest that NLR can be a predictive biomarker for pCR. Further studies, on larger sample size, are necessary to establish the correlation with MPG and RCB.PURPOSE The rs712 polymorphism in a let-7 microRNA-binding KRAS gene has been associated with different types of cancer, however these associations have been inconsistent. The purpose of this study was to determine the association between rs712 polymorphism in a let-7 microRNA-binding KRAS gene comparing breast cancer (BC) patients with healthy subjects from Mexican population. METHODS The genotyping of the rs712 polymorphism was performed by polymerase chain reaction (PCR) in 437 BC patients and 414 healthy women. RESULTS The observed frequencies of the rs712 polymorphism indicated an associated protective factor for BC in the dominant GT+TT model [odds ratio (OR) 0.70, 95% confidence interval (CI) 0.51-0.97, p=0.040). An association between genotype and BC patients was evident in chemotherapy response (allele GT, OR 0.032, 95% CI 0.002-0.505, p=0.014), partial chemotherapy response (genotype GT, OR 0.023, 95% CI 0.001-0.419, p=0.011), and gastric and hematological toxicity (genotype GT, OR 0.115, 95% CI 0.028-0.473, p=0.003), Luminal A BC patients with gastric and hematological toxicity (genotype TT, OR 0.236, 95% CI 0.069-0.805, p=0.021) and tobacco consumption (genotype TT, OR 0.283, 95% CI 0.001-0.802, p=0.037) and Luminal B with metastatic lymph node (genotype GT, OR 0.241, 95% CI 0.093-0.626, p=0.003). CONCLUSION Polymorphism rs712 in KRAS gene was protective factor associated with susceptibility for BC in this sample from Mexican population.PURPOSE To identify predictive factors connected with pathologic response in patients with breast cancer (BC) having received neoadjuvant chemotherapy (NACT). METHODS 49 patients with BC were investigated before and after treatment in this prospective research. Different chemotherapy regimes were administered. The Miller-Payne scoring system was used to assess the tumour response. The nuclear proliferation markers Ki67 and the expression of topoisomerase IIα (Topo IIα) were evaluated. RESULTS Six patients (12.2 %) achieved pathological complete response (pCR). Noticeable decrease of tumor cellularity was detected in all BC subtypes and pCR in the triple-negative BC (TNBC) group (p=0.007) was observed. Poorly differentiated tumors could be considered as predictive factors of pCR (p=0.07). Ki67 appeared to be a predictive marker of achieving pCR (p less then 0.001) with a threshold of 28% (AUC=0.89, 95% CI 0.75-0.96). The additional factor of reaching pCR was operable BC (p=0.04). The expression level of Topo IIα (p=0.50) and using different regimens of NACT (p=0.97) did not influence pCR achievement. CONCLUSION To sum it up, poorly differentiated carcinomas with high cellularity in the primary tumor, TNBC, Ki 67 with a threshold above 28% and operable BC can be considered as early predictors of reaching pCR.PURPOSE Twenty percent of the breast cancers are triple negative (TNBC). Despite the impressive progression in the biology of this subgroup, data is limited as compared to hormone and/or HER2 positive cases. Thus, the aim of this study was to detect the expression levels and to identify the prognostic values of MUC1, EGFR and PD-L1 in TNBC. METHODS MUC1, EGFR and PD-L1 expressions were detected by immunohistochemistry in 97 cases with TNBC. Associations between clinical and histopathological parameters with overall survival (OS) and progression-free survival (PFS) were analyzed using the Kaplan-Meier method and compared by the log-rank test. Prognostic effects were analyzed by Cox proportional hazard models. RESULTS During a median follow-up of 93 months (0.6-168.7) the mean PFS was 110.1 and OS was 121.8 months. Tumor diameter (T), involved lymph node status (N) and TNM were found to be prognostic for PFS and OS. PD-L1 in microenvironment (PD-L1 ME) and EGFR expression were found to be associated with longer PFS and OS, but MUC1 and tumor PD-L1 (PD-L1 TM) expressions were not. All combined analyses showed that in the subgroups of MUC1, PD-L1 TM or ME positive, EGFR expression was correlated with longer PFS and OS than those who were not. Older age (≥70 years), T and N status and also EGFR expression were found to be independent prognostic factors for OS in Cox regression analysis. CONCLUSION EGFR expression was found to be one of the most important prognostic factors in addition to T and N status in cases with TNBC.PURPOSE Breast cancer is one of the leading causes of mortality in women across the globe. Herein, the role and therapeutic implications of miR-322 were investigated in breast cancer. METHODS An array of breast cancer cell lines and a normal cell line were used in this study. The expression of miR-322 was determined by quantitative realtime polymerase chain reaction (qRT-PCR). Lipofectamine 2000 reagent was used to perform transfections and MTT assay was used to determine the cell viability. (L)-Dehydroascorbic DAPI and annexin V/propidium iodide (PI) assays were used to detect apoptosis. Wound healing and transwell assays were used to monitor cell migration and invasion, respectively. Protein expression was determined by western blot analysis. RESULTS The expression of miR-322 was found to be remarkably suppressed in breast cancer cells. Overexpression of miR-322 led to considerable decline in the proliferation rate and colony formation of the MCF7 breast cancer cells due to induction of apoptosis. The overexpression of miR-322 caused a significant increase in Bax and decrease in Bcl-2 expression and also enhanced the sensitivity of MCF7 cells to cisplatin and decreased their migration and invasive potential.
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