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Mitra A.,North Bengal University | Pariyar A.,Indian Institute of Science | Bose S.,North Bengal University | Bandyopadhyay P.,North Bengal University | Sarkar A.,India Innovation Research Center
Sensors and Actuators, B: Chemical | Year: 2015

A novel phenalenone based molecular receptor, 1,1,1-tris(1-oxophenalenyl-9-N-ethyl)amine (3) bearing PLY moiety as the fluorophore has been synthesized and characterized. A thorough study on the binding behaviour of the compound with I- and other biologically relevant anions (viz. F-, Cl-, Br-, CH3COO-, N3-, HPO42-, H2PO4-, NO3-, SO42-) in solution was performed by quantitative UV-vis and fluorescence spectroscopy. The novel compound evolved as a highly selective sensor for I- ion, discriminating all other biologically important anions in solution. © 2015 Elsevier B.V. All rights reserved. Source

Majumder B.,Mitra Biotech | Baraneedharan U.,Mitra Biotech | Thiyagarajan S.,Mitra Biotech | Radhakrishnan P.,Mitra Biotech | And 24 more authors.
Nature Communications | Year: 2015

Predicting clinical response to anticancer drugs remains a major challenge in cancer treatment. Emerging reports indicate that the tumour microenvironment and heterogeneity can limit the predictive power of current biomarker-guided strategies for chemotherapy. Here we report the engineering of personalized tumour ecosystems that contextually conserve the tumour heterogeneity, and phenocopy the tumour microenvironment using tumour explants maintained in defined tumour grade-matched matrix support and autologous patient serum. The functional response of tumour ecosystems, engineered from 109 patients, to anticancer drugs, together with the corresponding clinical outcomes, is used to train a machine learning algorithm; the learned model is then applied to predict the clinical response in an independent validation group of 55 patients, where we achieve 100% sensitivity in predictions while keeping specificity in a desired high range. The tumour ecosystem and algorithm, together termed the CANScript technology, can emerge as a powerful platform for enabling personalized medicine. © 2015 Macmillan Publishers Limited. All rights reserved. Source

Connor Y.,Harvard-MIT Division of Health Sciences and Technology | Connor Y.,Massachusetts Institute of Technology | Connor Y.,Brigham and Womens Hospital | Connor Y.,Harvard University | And 27 more authors.
Nature Communications | Year: 2015

Metastasis is a major cause of mortality and remains a hurdle in the search for a cure for cancer. Not much is known about metastatic cancer cells and endothelial cross-talk, which occurs at multiple stages during metastasis. Here we report a dynamic regulation of the endothelium by cancer cells through the formation of nanoscale intercellular membrane bridges, which act as physical conduits for transfer of microRNAs. The communication between the tumour cell and the endothelium upregulates markers associated with pathological endothelium, which is reversed by pharmacological inhibition of these nanoscale conduits. These results lead us to define the notion of 'metastatic hijack': cancer cell-induced transformation of healthy endothelium into pathological endothelium via horizontal communication through the nanoscale conduits. Pharmacological perturbation of these nanoscale membrane bridges decreases metastatic foci in vivo. Targeting these nanoscale membrane bridges may potentially emerge as a new therapeutic opportunity in the management of metastatic cancer. © 2015 Macmillan Publishers Limited. All rights reserved. Source

Goldman A.,Harvard University | Goldman A.,Harvard-MIT Division of Health Sciences and Technology | Goldman A.,Brigham and Womens Hospital | Majumder B.,India Innovation Research Center | And 11 more authors.
Nature Communications | Year: 2015

Understanding the emerging models of adaptive resistance is key to overcoming cancer chemotherapy failure. Using human breast cancer explants, in vitro cell lines, mouse in vivo studies and mathematical modelling, here we show that exposure to a taxane induces phenotypic cell state transition towards a favoured transient CD44 Hi CD24 Hi chemotherapy-tolerant state. This state is associated with a clustering of CD44 and CD24 in membrane lipid rafts, leading to the activation of Src Family Kinase (SFK)/hemopoietic cell kinase (Hck) and suppression of apoptosis. The use of pharmacological inhibitors of SFK/Hck in combination with taxanes in a temporally constrained manner, where the kinase inhibitor is administered post taxane treatment, but not when co-administered, markedly sensitizes the chemotolerant cells to the chemotherapy. This approach of harnessing chemotherapy-induced phenotypic cell state transition for improving antitumour outcome could emerge as a translational strategy for the management of cancer. © 2014 Macmillan Publishers Limited. All rights reserved. Source

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