Cancer Stem Cell News Volume 4.46 | Dec 9 2015

Facilitated Anion Transport Induces Hyperpolarization of the Cell Membrane that Triggers Differentiation and Cell Death in Cancer Stem Cells
Scientists showed how active anionophores, capable of facilitating the transmembrane transport of chloride and bicarbonate in model phospholipid liposomes, induce acidification of the cytosol and hyperpolarization of plasma cell membranes. They demonstrated how this combined effect can be used against cancer stem cells. [J Am Chem Soc] Abstract

PTEN Deficiency Reprograms Human Neural Stem Cells towards a Glioblastoma Stem Cell-Like Phenotype
Researchers showed that targeted disruption of PTEN leads to neoplastic transformation of human neural stem cells (NSCs), but not mesenchymal stem cells. PTEN deficiency leads to the upregulation of PAX7, which in turn promotes oncogenic transformation of NSCs and instates ‘aggressiveness’ in human glioblastoma stem cells. [Nat Commun] Full Article | Press Release

HDAC Inhibition Impedes Epithelial–Mesenchymal Plasticity and Suppresses Metastatic, Castration-Resistant Prostate Cancer
To study the dynamic regulation of the epithelial–mesenchymal transition (EMT) process, researchers developed novel genetically defined cellular and in vivo model systems from which epithelial, EMT and mesenchymal-like tumor cells with Pten deletion and Kras activation can be isolated. When cultured individually, each population has the capacity to regenerate all three tumor cell populations, indicative of epithelial–mesenchymal plasticity. [Oncogene] Abstract

Identification and Analysis of CXCR4-Positive Synovial Sarcoma-Initiating Cells
Investigators analyzed whether synovial sarcoma possessed tumor-initiating cells and explored specific markers, and discovered that synovial sarcoma cell lines possessed heterogeneity by way of containing a sphere-forming subpopulation highly expressing NANOG, OCT4 and SOX2. [Oncogene] Abstract

Mesenchymal Cancer Cell-Stroma Crosstalk Promotes Niche Activation, Epithelial Reversion, and Metastatic Colonization
Scientists found that metastatic initiating cells (MICs) exhibit a high capacity for lung fibroblast activation as a result of thrombospondin 2 (THBS2) expression. Inhibiting the mesenchymal phenotype of MICs by blocking the epithelial-to-mesenchymal transition-associated kinase AXL reduces THBS2 secretion, niche-activating ability, and, consequently, metastatic competence. [Cell Rep]
Full Article | Graphical Abstract | Press Release

Genome-Wide CRISPR-Cas9 Screens Reveal Loss of Redundancy between PKMYT1 and WEE1 in Glioblastoma Stem-Like Cells
To identify therapeutic targets for glioblastoma (GBM), researchers performed genome-wide CRISPR-Cas9 knockout screens in patient-derived GBM stem-like cells and human neural stem/progenitors, non-neoplastic stem cell controls, for genes required for their in vitro growth. [Cell Rep]
Full Article | Graphical Abstract | Press Release

Niclosamide Inhibits Epithelial-Mesenchymal Transition and Tumor Growth in Lapatinib-Resistant Human Epidermal Growth Factor Receptor 2-Positive Breast Cancer
Two human epidermal growth factor receptor 2-positive breast cancer cell lines, SKBR3 and BT474, were exposed to increasing concentrations of lapatinib to establish lapatinib-resistant cultures. [Int J Biochem Cell Biol] Abstract

Glioblastoma: Defining Tumor Niches
The authors review the features and functions of the distinct glioblastoma multiforme (GBM) niches, detail the different cell constituents and the functional status of the vasculature, and discuss prospects of therapeutically targeting GBM niche constituents. [Trends Cancer] Full Article

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Stemline Therapeutics Presents Clinical Update from Ongoing SL-401 Pivotal BPDCN Trial
Stemline Therapeutics, Inc. announced the presentation of positive clinical data, including high response rates, from the lead-in and ongoing expansion stage of its SL-401 pivotal trial in blastic plasmacytoid dendritic cell neoplasm (BPDCN). [Press release from Stemline Therapeutics, Inc. discussing research presented at the 57^th American Society of Hematology (ASH) Annual Meeting, Orlando] Press Release

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Critical Outcome Technologies Pursues Orphan Drug Designation for COTI-2 Intended to Treat Li-Fraumeni Syndrome
Critical Outcome Technologies Inc. announced that it submitted an Orphan Drug Application intended for the treatment of Li-Fraumeni Syndrome to the U.S. Food and Drug Administration for its lead cancer drug candidate, COTI-2. [Critical Outcome Technologies Inc.] Press Release

Food and Drug Administration (United States)

Center for Biologics Evaluation and Research (United States)

European Medicines Agency (European Union)

Medicines and Healthcare Products Regulatory Agency (United Kingdom)

Therapeutic Goods Administration (Australia)

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Director – Cancer Center (The University of Hawai‘i Cancer Center)

Director – Cancer Institute (North Shore-LIJ Health System)

Postdoctoral Fellow – Systems Biology of Cancer Metabolism (Technion – Israel Institute of Technology)

Postdoctoral Fellow – Epigenetics and Cancer (Moffitt Cancer Center)

Assistant Member – Radioimmunotherapy (Fred Hutchinson Cancer Research Center)

Investigator – Cancer Biology (Wake Forest Baptist School of Medicine)

Postdoctoral Research Fellow – Stem Cell Research (The University of Texas Medical School At Houston)

Faculty Positions – Cancer Pharmacology (Northwestern University)

Group Leader Position – Cancer Research (Oslo University Hospital)

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