Blood pressure drug may boost effectiveness of lung cancer treatment

A blood pressure drug may make a type of lung cancer treatment more effective, suggests a new study. The early-stage research, conducted on human cells in the lab and on mice, was led by scientists from Imperial College London and Fudan University in…

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Blood pressure drug may boost effectiveness of lung cancer treatment

Join internationally-recognised experts in breast cancer at our symposium in Dublin this October #EONS2016 #EONS10 https://t.co/z4f99MWMc7

Join internationally-recognised experts in breast cancer at our symposium in Dublin this October #EONS2016 #EONS10 https://t.co/z4f99MWMc7

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Join internationally-recognised experts in breast cancer at our symposium in Dublin this October #EONS2016 #EONS10 https://t.co/z4f99MWMc7

Hypoxia-activated prodrugs in the treatment of advanced pancreatic adenocarcinoma.

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Pancreatic cancer is an aggressive malignancy with poor survival and high mortality rate with 250 000 deaths per year worldwide. The unique pancreatic cancer microenvironment serves as a major obstacle in the effective treatment of this malignancy. The microenvironment consists not only of pancreatic ductal adenocarcinoma cells but also comprises cells of pancreatic cancer stellate, vascular, and immune origin combined with a dense extracellular matrix containing collagen. The aforementioned pathology leads to an increased intratumor pressure combined with an erratic vascular proliferation within the tumor causing hypoxia and decreased drug delivery. This has led both scientists and clinicians to develop and study drugs with unique mechanisms of action to target the pancreatic cancer microenvironment. Herein, we discuss the pancreatic cancer hypoxic microenvironment, development of hypoxia-activated prodrugs, and results of trials utilizing those drugs to target pancreatic cancer. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.

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Hypoxia-activated prodrugs in the treatment of advanced pancreatic adenocarcinoma.

Glycerophosphodiesterase GDE2 Promotes Neuroblastoma Differentiation through Glypican Release and Is a Marker of Clinical Outcome

Publication date: Available online 29 September 2016
Source:Cancer Cell
Author(s): Elisa Matas-Rico, Michiel van Veen, Daniela Leyton-Puig, Jeroen van den Berg, Jan Koster, Katarzyna M. Kedziora, Bas Molenaar, Marjolein J.A. Weerts, Iris de Rink, René H. Medema, Ben N.G. Giepmans, Anastassis Perrakis, Kees Jalink, Rogier Versteeg, Wouter H. Moolenaar
Neuroblastoma is a pediatric embryonal malignancy characterized by impaired neuronal differentiation. A better understanding of neuroblastoma differentiation is essential for developing new therapeutic approaches. GDE2 (encoded by GDPD5) is a six-transmembrane-domain glycerophosphodiesterase that promotes embryonic neurogenesis. We find that high GDPD5 expression is strongly associated with favorable outcome in neuroblastoma. GDE2 induces differentiation of neuroblastoma cells, suppresses cell motility, and opposes RhoA-driven neurite retraction. GDE2 alters the Rac-RhoA activity balance and the expression of multiple differentiation-associated genes. Mechanistically, GDE2 acts by cleaving (in cis) and releasing glycosylphosphatidylinositol-anchored glypican-6, a putative co-receptor. A single point mutation in the ectodomain abolishes GDE2 function. Our results reveal GDE2 as a cell-autonomous inducer of neuroblastoma differentiation with prognostic significance and potential therapeutic value.

Graphical abstract

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Teaser

Matas-Rico et al. show that GDE2 (encoded by GDPD5) promotes differentiation and suppresses motility of neuroblastoma (NB) cells through mechanisms involving glypican-6 release, activation of differentiation genes, Rac activation, and Rho inhibition. High GDPD5 expression in NB correlates with better prognosis.

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Glycerophosphodiesterase GDE2 Promotes Neuroblastoma Differentiation through Glypican Release and Is a Marker of Clinical Outcome

Expression of Idh1R132H in the Murine Subventricular Zone Stem Cell Niche Recapitulates Features of Early Gliomagenesis

Publication date: Available online 29 September 2016
Source:Cancer Cell
Author(s): Chiara Bardella, Osama Al-Dalahmah, Daniel Krell, Pijus Brazauskas, Khalid Al-Qahtani, Marketa Tomkova, Julie Adam, Sébastien Serres, Helen Lockstone, Luke Freeman-Mills, Inga Pfeffer, Nicola Sibson, Robert Goldin, Benjamin Schuster-Böeckler, Patrick J. Pollard, Tomoyoshi Soga, James S. McCullagh, Christopher J. Schofield, Paul Mulholland, Olaf Ansorge, Skirmantas Kriaucionis, Peter J. Ratcliffe, Francis G. Szele, Ian Tomlinson
Isocitrate dehydrogenase 1 mutations drive human gliomagenesis, probably through neomorphic enzyme activity that produces D-2-hydroxyglutarate. To model this disease, we conditionally expressed Idh1R132H in the subventricular zone (SVZ) of the adult mouse brain. The mice developed hydrocephalus and grossly dilated lateral ventricles, with accumulation of 2-hydroxyglutarate and reduced α-ketoglutarate. Stem and transit amplifying/progenitor cell populations were expanded, and proliferation increased. Cells expressing SVZ markers infiltrated surrounding brain regions. SVZ cells also gave rise to proliferative subventricular nodules. DNA methylation was globally increased, while hydroxymethylation was decreased. Mutant SVZ cells overexpressed Wnt, cell-cycle and stem cell genes, and shared an expression signature with human gliomas. Idh1R132H mutation in the major adult neurogenic stem cell niche causes a phenotype resembling gliomagenesis.

Graphical abstract

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Teaser

Bardella et al. report that expression of IDH1R132H in the subventricular zone of the adult mouse brain causes features of gliomagenesis, including increased numbers of neural stem cells, cellular infiltration into surrounding brain regions, and a gene expression profile overlapping that of human gliomas.

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Expression of Idh1R132H in the Murine Subventricular Zone Stem Cell Niche Recapitulates Features of Early Gliomagenesis

Dye-conjugated Single-Walled Carbon Nanotubes Induce Photothermal Therapy under the Guidance of Near-Infrared Imaging

Recently, photothermal therapy (PTT) has become viewed as an ideal auxiliary therapeutic treatment for cancers. However, the development of safe, convenient, and highly effective photothermal agents remains a great challenge. In this study, we prepared single-walled carbon nanotubes (SWNTs) for PTT against breast tumors under the guidance of infrared fluorescent cyanines. Tumors were accurately located using near-infrared imaging (NIR) and then exposed to laser irradiation. Both the in vivo and in vitro results showed that the SWNTs have high stability and low cytotoxicity.

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Dye-conjugated Single-Walled Carbon Nanotubes Induce Photothermal Therapy under the Guidance of Near-Infrared Imaging

Hepatitis B virus mRNAs functionally sequester let-7a and enhance hepatocellular carcinoma

Hepatitis B virus (HBV) infection induces hepatocarcinogenesis and malignant progression, yet global effects of the redundant viral mRNAs produced during infection are unexplored. Here, microRNA (miRNA) target prediction and whole genome expression analysis revealed that HBV pre-C/C mRNA leads to upregulation of multiple let-7a targeted genes. A let-7a complementary region from nt 86 to 108 in the HBV genome was then identified in HBV pre-C/C, pre-S, and S mRNAs. The let-7a sequestration effect by HBV mRNAs was observed under transfection and virus infection, which is dependent on the let-7a response sequence.

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Hepatitis B virus mRNAs functionally sequester let-7a and enhance hepatocellular carcinoma