Oncotarget

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Oncotarget | Interview with Dr. Anutosh Ganguly from the Department of Integrative Biology and Pharmacology, University of Texas Medical School, 6431 Fannin St., Houston, Texas 77030, USA talking about their research published in Volume 2 Issue 5 titled "Class III β-Tubulin Counteracts the Ability of Paclitaxel to Inhibit Cell Migration"

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Oncotarget | Interview with Dr. Hirbe from the Division of Medical Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA talking about their featured cover paper in Oncotarget Volume 7 Issue 7 “Spatially- and temporally-controlled postnatal p53 knockdown cooperates with embryonic Schwann cell precursor Nf1 gene loss to promote malignant peripheral nerve sheath tumor formation”

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Critically, our findings suggest for the first time that targeting BRAFWT/V600E and CDK4/6 represents a novel therapeutic strategy to treat vemurafenib-resistant or vemurafenib-naïve radioiodine-refractory BRAFWT/V600E-PTC. This combined therapy could prevent selection and expansion of aggressive PTC cell sub-clones with intrinsic resistance, targeting tumor cells either with primary or secondary resistance to BRAFV600E inhibitor.

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Audiopaper - Published in Volume 8 Issue 42 of Oncotarget - "A global comparison of the cost of patented cancer drugs in relation to global differences in wealth" by Daniel A. Goldstein from the Davidoff Cancer Center, Rabin Medical Center, Petach Tikvah, Israel and the Winship Cancer Institute, Emory University, Atlanta, GA, USA

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Sustained autophagy contributes to the metabolic adaptation of cancer cells to hypoxic and acidic microenvironments. Since cells in such environments are resistant to conventional cytotoxic drugs, inhibition of autophagy represents a promising therapeutic strategy in clinical oncology. We previously reported that the efficacy of hydroxychloroquine (HCQ), an autophagy inhibitor under clinical investigation is strongly impaired in acidic tumor environments, due to poor uptake of the drug, a phenomenon widely associated with drug resistance towards many weak bases. In this study we identified salinomycin (SAL) as a potent inhibitor of autophagy and cytotoxic agent effective on several cancer cell lines under conditions of transient and chronic acidosis. Since SAL has been reported to specifically target cancer-stem cells (CSC), we used an established model of breast CSC and CSC derived from breast cancer patients to examine whether this specificity may be associated with autophagy inhibition. We indeed found that CSC-like cells are more sensitive to autophagy inhibition compared to cells not expressing CSC markers. We also report that the ability of SAL to inhibit mammosphere formation from CSC-like cells was dramatically enhanced in acidic conditions. We propose that the development and use of clinically suitable SAL derivatives may result in improved autophagy inhibition in cancer cells and CSC in the acidic tumor microenvironment and lead to clinical benefits.

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