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

Repercussion of Mitochondria Deformity Induced by Anti-Hsp90 Drug 17AAG in Human Tumor Cells

Inhibiting Hsp90 chaperone roles using 17AAG induces cytostasis or apoptosis in tumor cells through destabilization of several mutated cancer promoting proteins. Although mitochondria are central in deciding the fate of cells, 17AAG induced effects on tumor cell mitochondria were largely unknown. Here, we show that Hsp90 inhibition with 17AAG first affects mitochondrial integrity in different human tumor cells, neuroblastoma, cervical cancer and glial cells. Using human neuroblastoma tumor cells, we found the early effects associated with a change in mitochondrial membrane potential, elongation and engorgement of mitochondria because of an increased matrix vacuolization. These effects are specific to Hsp90 inhibition as other chemotherapeutic drugs did not induce similar mitochondrial deformity. Further, the effects are independent of oxidative damage and cytoarchitecture destabilization since cytoskeletal disruptors and mitochondrial metabolic inhibitors also do not induce similar deformity induced by 17AAG. The 1D PAGE LC MS/MS mitochondrial proteome analysis of 17AAG treated human neuroblastoma cells showed a loss of 61% proteins from membrane, metabolic, chaperone and ribonucleoprotein families. About 31 unmapped protein IDs were identified from proteolytic processing map using Swiss-Prot accession number, and converted to the matching gene name searching the ExPASy proteomics server. Our studies display that Hsp90 inhibition effects at first embark on mitochondria of tumor cells and compromise mitochondrial integrity

Cholesterol biosynthesis and homeostasis in regulation of the cell cycle.

The cell cycle is a ubiquitous, multi-step process that is essential for growth and proliferation of cells. The role of membrane lipids in cell cycle regulation is not explored well, although a large number of cytoplasmic and nuclear regulators have been identified. We focus in this work on the role of membrane cholesterol in cell cycle regulation. In particular, we have explored the stringency of the requirement of cholesterol in the regulation of cell cycle progression. For this purpose, we utilized distal and proximal inhibitors of cholesterol biosynthesis, and monitored their effect on cell cycle progression. We show that cholesterol content increases in S phase and inhibition of cholesterol biosynthesis results in cell cycle arrest in G1 phase under certain conditions. Interestingly, G1 arrest mediated by cholesterol biosynthesis inhibitors could be reversed upon metabolic replenishment of cholesterol. Importantly, our results show that the requirement of cholesterol for G1 to S transition is absolute, and even immediate biosynthetic precursors of cholesterol, differing with cholesterol merely in a double bond, could not replace cholesterol for reversing the cell cycle arrest. These results are useful in the context of diseases, such as cancer and Alzheimer's disease, that are associated with impaired cholesterol biosynthesis and homeostasis

Cationic amphiphile with shikimic acid headgroup shows more systemic promise than its mannosyl analogue as DNA vaccine carrier in dendritic cell based genetic immunization

Mannosylated cationic vectors have been previously used for delivering DNA vaccines to antigen presenting cells (APCs) via mannose receptors expressed on the cell surface of APCs. Here we show that cationic amphiphiles containing mannose-mimicking quinic acid and shikimic acid headgroups deliver genes to APCs via mannose receptor. Cationic amphiphile with shikimic acid headgroup was more efficacious than its mannosyl counterpart in combating mouse tumor growth by dendritic cell (the most professional APC) based genetic immunization

Corrections to cationic amphiphile with shikimic acid headgroup shows more systemic promise than its mannosyl analogue as DNA vaccine carrier in dendritic cell based genetic immunization

This article does not have an abstract

Neutral lipid content increases with cell cycle progression.

<p>(A) A representative confocal image shows the presence of neutral (green) and polar (red) lipids in cells, as visualized after labeling with Nile Red. The scale bar represents 20 µm. Neutral lipids in F111 cells were quantified utilizing Nile Red labeling followed by flow cytometric analysis. Typical Nile Red labeling profile of cells is shown in panel (B). A dot plot depicting Nile Red labeling of cells in G1 (blue), S (red) and G2 (green) phases of cell cycle is shown as an inset. (C) Total cellular neutral lipid content demonstrated an increase as cells progressed from G1 to G2 <i>via</i> S phase of cell cycle. Data represent means ± SE of at least four independent experiments. See Materials and Methods for more details.</p

Representative flow cytometry histograms of F111 cells treated with lovastatin, triparanol and AY 9944.

<p>F111 cells were treated with inhibitors and fixed with cold ethanol. After fixation, cells were labeled with propidium idodide and analyzed by flow cytometry for their distribution in G1, S and G2 phases. Representative flow cytometry histograms of (A) control cells and cells treated with (B) lovastatin (2.5 µM), (C) triparanol (7.5 µM) and (D) AY 9944 (10 µM) are shown. See Materials and Methods for more details.</p

Distribution of cells in G1, S and G2 phases of cell cycle under different treatment conditions.

*<p>2.5 µM lovastatin and 7.5 µM triparanol were used for all experiments.</p

Metabolic replenishment of cholesterol restores the cell cycle distribution of lovastatin or triparanol-treated cells.

<p>In order to monitor the reversibility of lovastatin or triparanol treatment on the G1 arrest of cells, we utilized two approaches. In the first approach, cells treated with lovastatin (2.5 µM) or triparanol (7.5 µM) were further grown for 24 h in the presence of either 10 or 20% serum (shown in panels (A) and (B), respectively). In the second approach, cells treated with lovastatin (2.5 µM) or triparanol (7.5 µM) were grown for additional 24 h in 20% serum in the presence of respective inhibitors (see panels (A) and (B)). Cell numbers in G1, S and G2 phases are represented by blue, maroon and cyan bars, respectively. Values represent means ± SE of at least four independent experiments. See Materials and Methods for more details.</p