Volume 7.14 | Apr 16

Mammary Cell News 7.14 April 16, 2014
Mammary Cell News
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TOP STORY
Molecular Signature for Outcomes of Triple Negative Breast Cancer
Researchers have identified a molecular mechanism that triple negative breast cancer cells use to survive and grow. The researchers found that two proteins, one called Myc, the other called thirodoxin-interacting protein (TXNIP). In triple negative breast cancer cells, the researchers discovered that Myc reduces the expression of TXNIP. [Press release from University of Utah discussing online publication in Proceedings of the National Academy of Science USA] Press Release | Abstract
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PUBLICATIONS (Ranked by impact factor of the journal)
LABORATORY RESEARCH

Inhibition of Lapatinib-Induced Kinome Reprogramming in ERBB2-Positive Breast Cancer by Targeting BET Family Bromodomains
Genetic and chemical inhibition of BET bromodomain chromatin readers suppresses transcription of many lapatinib-induced kinases involved in resistance, including ERBB3, IGF1R, DDR1, MET, and FGFRs, preventing downstream SRC/FAK signaling and AKT reactivation. [Cell Rep]
Full Article | Graphical Abstract | Press Release

Targeting Matriptase in Breast Cancer Abrogates Tumor Progression via Impairment of Stromal-Epithelial Growth Factor Signaling
Researchers demonstrated by genetic deletion and silencing that the proliferation impairment in matriptase-deficient breast cancer cells is caused by their inability to initiate activation of the c-Met signaling pathway in response to fibroblast-secreted pro-HGF. [Nat Commun] Abstract

Silencing β3 Integrin by Targeted ECO/siRNA Nanoparticles Inhibits EMT and Metastasis of Triple Negative Breast Cancer
Scientists exploited β3 integrin as a therapeutic target to treat triple-negative breast cancer (TNBC) by delivering β3 integrin siRNA via lipid ECO-based nanoparticles (ECO/siβ3). Treatment of TNBC cells with ECO/siβ3 was sufficient to effectively silence β3 integrin expression, attenuate TGF-β-mediated epithelial-mesenchymal transition and invasion, restore TGF-β-mediated cytostasis, and inhibit 3-dimensional organoid growth. [Cancer Res] Abstract | Full Article

MiRNA-621 Sensitizes Breast Cancer to Chemotherapy by Suppressing FBXO11 and Enhancing p53 Activity
Ectopic overexpression of miR-621 promoted apoptosis and increased chemosensitivity to paclitaxel and carboplatin both in cultured breast cancer cells and in xenograft tumor model. [Oncogene] Full Article

Oroxylin A Inhibits Glycolysis-Dependent Proliferation of Human Breast Cancer via Promoting SIRT3-Mediated SOD2 Transcription and HIF1α Destabilization
Investigators showed that oroxylin A inhibited glycolysis in breast cancer cells via the sirtuin 3 (SIRT3)-mediated destabilization of hypoxia-inducible factor 1α (HIF1α), which controls glycolytic gene expression. Oroxylin A promoted superoxide dismutase (SOD2) gene expression through SIRT3-regulated DNA-binding activity of FOXO3a and increased the activity of SOD2 by promoting SIRT3-mediated deacetylation. [Cell Death Dis] Full Article

HIF-Inducible miR-191 Promotes Migration in Breast Cancer through Complex Regulation of TGFβ-Signaling in Hypoxic Microenvironment
Hypoxia through hypoxia-inducible factor (HIF) brought about a time-dependent increase in the level of an oncogenic microRNA, miR-191 in various breast cancer cell lines. miR-191 enhanced breast cancer aggressiveness by promoting cell proliferation, migration and survival under hypoxia. [Sci Rep] Full Article

CRLX101, an Investigational Camptothecin-Containing Nanoparticle-Drug Conjugate, Targets Cancer Stem Cells and Impedes Resistance to Antiangiogenic Therapy in Mouse Models of Breast Cancer
Researchers tested whether inhibiting hypoxia-inducible factor 1α (HIF-1α) can reverse the stimulatory effects of antiangiogenic-induced hypoxia on breast cancer stem cells (CSCs). Breast cancer cells grown under hypoxic conditions were treated with the dual topoisomerase-1 and HIF-1α inhibitor camptothecin and assessed for their CSC content. [Breast Cancer Res Treat] Abstract | Press Release

Oxidative Stress Shapes Breast Cancer Phenotype through Chronic Activation of ATM-Dependent Signaling
Researchers showed that, in MDA-MB-231 and HeLa cells, basal ATM-dependent NF-κB activation occurs through a canonical DNA damage-responsive signaling pathway as knockdown of two proteins involved in this signaling pathway, ERC1 and TAB1, results in loss of NF-κB basal activity. [Breast Cancer Res Treat] Abstract

The Active Tamoxifen Metabolite Endoxifen (4OHNDtam) Strongly Down-Regulates Cytokeratin 6 (CK6) in MCF-7 Breast Cancer Cells
The authors investigated the gene regulatory effects of the three metabolites of tamoxifen in MCF-7 breast cancer cells. Using concentrations that mimic the clinical situation, they examined effects of 4-hydroxytamoxifen, 4OHNDtam and ndesmethyltamoxifen on global gene expression in 17β-estradiol treated MCF-7 cells. [PLoS One] Abstract

CLINICAL RESEARCH

Phase II Study of Gemcitabine, Carboplatin, and Iniparib as Neoadjuvant Therapy for Triple-Negative and BRCA1/2 Mutation-Associated Breast Cancer with Assessment of a Tumor-Based Measure of Genomic Instability: PrECOG 0105
Scientists assessed efficacy, safety, and predictors of response to iniparib in combination with gemcitabine and carboplatin in early-stage triple-negative and BRCA1/2 mutation-associated breast cancer. [J Clin Oncol] Abstract

Randomized Study of Orally Administered Fluorinated Pyrimidines (Capecitabine versus S-1) in Women with Metastatic or Recurrent Breast Cancer: Japan Breast Cancer Research Network 05 Trial
Capecitabine and S-1 are orally administered fluorinated pyrimidines with high-level activity against metastatic breast cancer. This randomized, multicenter, Phase II study compared the activities and safeties of the oral fluoropyrimidines, capecitabine and S-1, in breast cancer patients. [Cancer Chemother Pharmacol] Abstract

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INDUSTRY NEWS
Pfizer Announces PALOMA-3 Trial for IBRANCE® (Palbociclib) Stopped Early Due to Efficacy Seen in Patients with HR+, HER2 Metastatic Breast Cancer Whose Disease Has Progressed following Endocrine Therapy
Pfizer Inc. announced that the Phase III PALOMA-3 trial for IBRANCE® met its primary endpoint of demonstrating an improvement in progression-free survival for the combination of IBRANCE plus fulvestrant compared with fulvestrant plus placebo in women with hormone receptor positive (HR+), human epidermal growth factor receptor 2 negative (HER2) metastatic breast cancer following disease progression during or after endocrine therapy. [Pfizer Inc.] Press Release

Medivir and Cancer Research Technology Collaborate to Develop New Class of Cancer Drugs
Medivir AB and Cancer Research Technology, Cancer Research UK’s commercialization and development arm, jointly announced a partnership to develop a new class of drugs that has shown promise for treating a range of different cancers. [Medivir AB] Press Release

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POLICY NEWS
National Institutes of Health (United States)

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)
 
EVENTS
NEW Nordic Life Sciences Days 2015
September 9-10, 2015
Stockholm, Sweden

Visit our events page to see a complete list of events in the mammary cell community.
 
JOB OPPORTUNITIES
NEW PhD Student – Epigenetic Editing to Mimic and Reverse Breast Cancer Resistance (University Medical Center Groningen)

NEW Postdoctoral Fellow – Extracellular Matrix Alterations Associated with Breast Cancer (Institute of Cancer Research)

Research Associate – Cell Separation (STEMCELL Technologies Inc.)

Senior Cancer Bioinformatics Officer – Breast Cancer (Institute of Cancer Research)

Biostatistician – Molecular and Genetic Breast Cancer Epidemiology (Netherlands Cancer Institute)

Postdoctoral Research Fellow – Prostate Cancer and Breast Cancer (Baylor College of Medicine)

Histology Research Technician (King’s College London)

Postdoctoral Position – Triple Negative Breast Cancer (King’s College London)

Postdoctoral Fellow – Breast Cancer & Stem Cell Biology (University of Cincinnati)

Postdoctoral Fellow – Gene Regulation in Breast Cancer/Stem Cell Biology (University of Cincinnati College of Medicine)


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