Experience and yield of mass breast screening among working women in major cities of India: a mixed-method study

Background: iBreastTM tool is simple, safe, a handy device which is designed for mass breast cancer screening tool in a community or hospital setting. This study determined the yield and basic characteristics of women attending the breast cancer screening programme. The study also determined the overall experience of women who underwent breast cancer screening using iBreastTM tool.Methods: This study was a multicentric, retrospective observational study conducted in Mumbai, Bangalore, Chennai and Hyderabad as a part of routine work-place breast cancer screening programme supported by Mfine. Screening was done by iBreastTM, which is a hand-held compression device. After proper clinical examination and iBreastTM scanning, results were confirmed by a consultant trained in interpretation of findings. The overall experience of the women who underwent screening was also determined using a questionnaire. Descriptive analysis was carried out by mean and standard deviation for quantitative variables, frequency and proportion for categorical variables. The qualitative assessment and thematic analysis of the qualitative data was done.Results: A total of 1080 eligible female employees were present in the approached IT companies and out of that 451 women (41.75%) had consented and participated in the screening program. The acceptance rate was highest in Bengaluru city (65%) followed by Mumbai (53%), Chennai (33%) and least in Hyderabad (18%). 31 participants documented positive findings had in the scan and were referred for further evaluation. The quantitative and qualitative data determined that iBreastTM scan was highly accepted by all participants. Customer service, screening location and overall experience was deemed good by the participants with an average score of 4.8.Conclusions: The iBreastTM has the potential to be a promising tool in providing effective diagnosis after breast examinations

Risks of gas production forecasting, using material balance equations

The risks of forecasting of the main indicators of gas field development using the system of material balance have been estimated. According to the actual data, estimates of the impact of the components of material balance equations , the algorithm as a whole and the accuracy of the input data on the reliability of the gas withdrawal forecasting have been built. It has been shown that the predominant contribution to the variation of forecast indicators is related to the precision of the determination of initial recoverable gas reserves

COST-EFFECTIVENESS ANALYSIS IN THE MANAGEMENT OF STROKE

Objective: Stroke is one of the leading causes of death and disabilities worldwide. Cost-effectiveness analysis helps identify neglected opportunities by highlighting interventions that are relatively inexpensive, yet have the potential to reduce the disease burden substantially. In India, there are wide social and economic disparities. Socioeconomic environment influences occupation, lifestyle, and nutrition of social classes which in turn would influence the prevalence and profile of stroke. By reduction of delays in access to hospital and improving provision of affordable treatments can reduce morbidity and mortality in patients with stroke in India. This study is designed to measure and compare the costs (resources consumed) and consequences (clinical, economic, and humanistic) of pharmaceutical products and services and their impact on individuals, healthcare systems and society.Methods: The purpose of this study is to analyze and conduct a cost-effectiveness analysis for the treatment of stroke in Guntur City Hospitals. The patients were treated either with aspirin or clopidogrel. The health outcomes were measured using Modified Rankin Scale, A prominent risk assessment scale for stroke. The pharmacoeconomic data were computed from the patient data collection forms.Result: The incremental cost-effectiveness ratio of aspirin and clopidogrel were calculated to be Rs. 8046.2/year.Conclusion: The study concludes that aspirin has the increased socioeconomic impact when compared to Clopidogrel and we can see that the earlier therapy has supported discharge, home-based rehabilitation along with reduced hospital stay and hence preferable

Blocks to thyroid cancer cell apoptosis can be overcome by inhibition of the MAPK and PI3K/AKT pathways

Current treatment for recurrent and aggressive/anaplastic thyroid cancers is ineffective. Novel targeted therapies aimed at the inhibition of the mutated oncoprotein BRAFV600E have shown promise in vivo and in vitro but do not result in cellular apoptosis. TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis in a tumor-selective manner by activating the extrinsic apoptotic pathway. Here, we show that a TRAIL-R2 agonist antibody, lexatumumab, induces apoptosis effectively in some thyroid cancer cell lines (HTh-7, TPC-1 and BCPAP), while more aggressive anaplastic cell lines (8505c and SW1736) show resistance. Treatment of the most resistant cell line, 8505c, using lexatumumab in combination with the BRAFV600E inhibitor, PLX4720, and the PI3K inhibitor, LY294002, (triple-drug combination) sensitizes the cells by triggering both the extrinsic and intrinsic apoptotic pathways in vitro as well as 8505c orthotopic thyroid tumors in vivo. A decrease in anti-apoptotic proteins, pAkt, Bcl-xL, Mcl-1 and c-FLIP, coupled with an increase in the activator proteins, Bax and Bim, results in an increase in the Bax to Bcl-xL ratio that appears to be critical for sensitization and subsequent apoptosis of these resistant cells. Our results suggest that targeting the death receptor pathway in thyroid cancer can be a promising strategy for inducing apoptosis in thyroid cancer cells, although combination with other kinase inhibitors may be needed in some of the more aggressive tumors initially resistant to apoptosis

MUC16-mediated activation of mTOR and c-Myc reprograms pancreatic cancer metabolism.

MUC16, a transmembrane mucin, facilitates pancreatic adenocarcinoma progression and metastasis. In the current studies, we observed that MUC16 knockdown pancreatic cancer cells exhibit reduced glucose uptake and lactate secretion along with reduced migration and invasion potential, which can be restored by supplementing the culture media with lactate, an end product of aerobic glycolysis. MUC16 knockdown leads to inhibition of mTOR activity and reduced expression of its downstream target c-MYC, a key player in cellular growth, proliferation and metabolism. Ectopic expression of c-MYC in MUC16 knockdown pancreatic cancer cells restores the altered cellular physiology. Our LC-MS/MS based metabolomics studies indicate global metabolic alterations in MUC16 knockdown pancreatic cancer cells, as compared to the controls. Specifically, glycolytic and nucleotide metabolite pools were significantly decreased. We observed similar metabolic alterations that correlated with MUC16 expression in primary tumor tissue specimens from human pancreatic adenocarcinoma cancer patients. Overall, our results demonstrate that MUC16 plays an important role in metabolic reprogramming of pancreatic cancer cells by increasing glycolysis and enhancing motility and invasiveness

Exploring research participants’ perceptions and comprehension of the informed consent process in a pre-exposure HIV prevention study

No abstract available.http://www.retrovirology.com/content/9/S2/P238am2013ay201

A retrospective validation of CanAssist Breast in European early-stage breast cancer patient cohort

Hormone-receptor positive; Chemotherapy; Early-stage breast cancerReceptor de hormonas positivo; Quimioterapia; Cáncer de mama en fase inicialReceptor d'hormones positiu; Quimioteràpia; Càncer de mama en fase inicialCanAssist Breast (CAB), a prognostic test uses immunohistochemistry (IHC) approach coupled with artificial intelligence-based machine learning algorithm for prognosis of early-stage hormone-receptor positive, HER2/neu negative breast cancer patients. It was developed and validated in an Indian cohort. Here we report the first blinded validation of CAB in a multi-country European patient cohort. FFPE tumor samples from 864 patients were obtained from-Spain, Italy, Austria, and Germany. IHC was performed on these samples, followed by recurrence risk score prediction. The outcomes were obtained from medical records. The performance of CAB was analyzed by hazard ratios (HR) and Kaplan Meier curves. CAB stratified European cohort (n = 864) into distinct low- and high-risk groups for recurrence (P 50 years (HR: 2.93 (1.44–5.96), P = 0.0002). CAB had an HR of 2.57 (1.26–5.26), P = 0.01) in women with N1 disease. CAB stratified significantly higher proportions (77%) as low-risk over IHC4 (55%) (P < 0.0001). Additionally, 82% of IHC4 intermediate-risk patients were stratified as low-risk by CAB. Accurate risk stratification of European patients by CAB coupled with its similar performance inIndian patients shows that CAB is robust and functions independent of ethnic differences. CAB can potentially prevent overtreatment in a greater number of patients compared to IHC4 demonstrating its usefulness for adjuvant systemic therapy planning in European breast cancer patients

Silibinin-mediated metabolic reprogramming attenuates pancreatic cancer-induced cachexia and tumor growth.

Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer-related deaths in the US. Cancer-associated cachexia is present in up to 80% of PDAC patients and is associated with aggressive disease and poor prognosis. In the present studies we evaluated an anti-cancer natural product silibinin for its effectiveness in targeting pancreatic cancer aggressiveness and the cachectic properties of pancreatic cancer cells and tumors. Our results demonstrate that silibinin inhibits pancreatic cancer cell growth in a dose-dependent manner and reduces glycolytic activity of cancer cells. Our LC-MS/MS based metabolomics data demonstrates that silibinin treatment induces global metabolic reprogramming in pancreatic cancer cells. Silibinin treatment diminishes c-MYC expression, a key regulator of cancer metabolism. Furthermore, we observed reduced STAT3 signaling in silibinin-treated cancer cells. Overexpression of constitutively active STAT3 was sufficient to substantially revert the silibinin-induced downregulation of c-MYC and the metabolic phenotype. Our in vivo investigations demonstrate that silibinin reduces tumor growth and proliferation in an orthotopic mouse model of pancreatic cancer and prevents the loss of body weight and muscle. It also improves physical activity including grip strength and latency to fall in tumor-bearing mice. In conclusion, silibinin-induced metabolic reprogramming diminishes cell growth and cachectic properties of pancreatic cancer cells and animal models

Metabolic Alterations in Pancreatic Cancer Progression

Pancreatic cancer is the third leading cause of cancer-related deaths in the USA. Pancreatic tumors are characterized by enhanced glycolytic metabolism promoted by a hypoxic tumor microenvironment and a resultant acidic milieu. The metabolic reprogramming allows cancer cells to survive hostile microenvironments. Through the analysis of the principal metabolic pathways, we identified the specific metabolites that are altered during pancreatic cancer progression in the spontaneous progression (KPC) mouse model. Genetically engineered mice exhibited metabolic alterations during PanINs formation, even before the tumor development. To account for other cells in the tumor microenvironment and to focus on metabolic adaptations concerning tumorigenic cells only, we compared the metabolic profile of KPC and orthotopic tumors with those obtained from KPC-tumor derived cell lines. We observed significant upregulation of glycolysis and the pentose phosphate pathway metabolites even at the early stages of pathogenesis. Other biosynthetic pathways also demonstrated a few common perturbations. While some of the metabolic changes in tumor cells are not detectable in orthotopic and spontaneous tumors, a significant number of tumor cell-intrinsic metabolic alterations are readily detectable in the animal models. Overall, we identified that metabolic alterations in precancerous lesions are maintained during cancer development and are largely mirrored by cancer cells in culture conditions