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Gail E. Sonenshein

Gail E. Sonenshein

D-Index & Metrics

Molecular Biology

D-Index
82
Citations
20127
World Ranking
944
National Ranking
501

Research.com Recognitions

  • 2009 - Fellow of the American Association for the Advancement of Science (AAAS)

Overview

Gail E. Sonenshein is affiliated with Tufts University in the United States. Their research spans several interconnected fields within medicine, with a particular focus on oncology and related disciplines. The main fields of study include Medicine, with subfields concentrating on Oncology, Immunology and Allergy, Cancer Research, and Radiology, Nuclear Medicine and Imaging.

The research topics primarily address molecular and cellular aspects of cancer, especially breast cancer. Major topics of work include HER2/EGFR in Cancer Research, Cell Adhesion Molecules Research, Breast Cancer Treatment Studies, and Monoclonal and Polyclonal Antibodies Research.

The scientist has coauthored papers with several collaborators. Frequent coauthors include Stefania Pianetti, Nora D. Mineva, Kathy D. Miller, Hannah H. Chen, and Sandra K. Althouse.

Publication venues for recent work include Cancer Cell International and Pharmaceutics. The following notable papers have been published:

  • ADAM8 is expressed widely in breast cancer and predicts poor outcome in hormone receptor positive, HER-2 negative patients, 2023, Cancer Cell International
  • A Novel Class of Human ADAM8 Inhibitory Antibodies for Treatment of Triple-Negative Breast Cancer, 2024, Pharmaceutics

These studies address the role of ADAM8 in breast cancer pathology and the development of inhibitory antibodies as potential treatments, reflecting a focus on translational cancer research.

Gail E. Sonenshein was awarded the title of Fellow of the American Association for the Advancement of Science (AAAS) in 2009. This designation marks recognition within the scientific community associated with their career and contributions.

Best Publications

  • Aberrant nuclear factor-kappaB/Rel expression and the pathogenesis of breast cancer.

    Mika A. Sovak;Robert E. Bellas;Dong W. Kim;Gregory J. Zanieski

  • Cell-cycle control of c-myc but not c-ras expression is lost following chemical transformation

    Judith Campisi;Harry E. Gray;Arthur B. Pardee;Michael Dean

  • Inhibition of NF-kappaB/Rel induces apoptosis of murine B cells.

    M Wu;H Lee;R E Bellas;S L Schauer

  • NF-κB and epithelial to mesenchymal transition of cancer†

    Chengyin Min;Sean F. Eddy;Sean F. Eddy;David H. Sherr;David H. Sherr;Gail E. Sonenshein;Gail E. Sonenshein

  • Protein kinase CK2 in mammary gland tumorigenesis.

    Esther Landesman-Bollag;Raphaëlle Romieu-Mourez;Diane H Song;Gail E Sonenshein

  • Differential regulation of the c-myc oncogene promoter by the NF-kappa B rel family of transcription factors.

    F A La Rosa;J W Pierce;G E Sonenshein

  • Her-2/neu overexpression induces NF-kappaB via a PI3-kinase/Akt pathway involving calpain-mediated degradation of IkappaB-alpha that can be inhibited by the tumor suppressor PTEN.

    Stefania Pianetti;Marcello Arsura;Marcello Arsura;Raphaëlle Romieu-Mourez;Robert J Coffey

  • Repression of transcription of the p27(Kip1) cyclin-dependent kinase inhibitor gene by c-Myc.

    William Yang;Jian Shen;Min Wu;Marcello Arsura

  • The RelA NF-κB subunit and the aryl hydrocarbon receptor (AhR) cooperate to transactivate the c- myc promoter in mammary cells

    Dong W. Kim;Lee Gazourian;Shafat A. Quadri;Raphaëlle Romieu-Mourez

  • TGFβ1 Inhibits NF-κB/Rel Activity Inducing Apoptosis of B Cells: Transcriptional Activation of IκBα

    Marcello Arsura;Min Wu;Gail E Sonenshein

  • Notch1 augments NF-κB activity by facilitating its nuclear retention

    Hyun Mu Shin;Lisa M Minter;Ok Hyun Cho;Sridevi Gottipati

  • Interaction of an NF-kappa B-like factor with a site upstream of the c-myc promoter.

    Mabel P. Duyao;Alan J. Buckler;Gail E. Sonenshein

  • Rel/NF-κB transcription factors and the control of apoptosis

    Gail E. Sonenshein

  • Green tea extracts decrease carcinogen‐induced mammary tumor burden in rats and rate of breast cancer cell proliferation in culture

    Kathryn T. Kavanagh;Laurie J. Hafer;Dong W. Kim;Koren K. Mann

  • Regulation of c-myc transcription and mRNA abundance by serum growth factors and cell contact

    M Dean;R A Levine;W Ran;M S Kindy

  • Elevated expression of monocyte chemoattractant protein 1 by vascular smooth muscle cells in hypercholesterolemic primates.

    Xiaohui Yu;Susan Dluz;Dana T. Graves;Lei Zhang

  • Green Tea Polyphenol Epigallocatechin-3 Gallate Inhibits Her-2/Neu Signaling, Proliferation, and Transformed Phenotype of Breast Cancer Cells

    Stefania Pianetti;Shangqin Guo;Kathryn T. Kavanagh;Gail E. Sonenshein

  • Oestrogen signalling inhibits invasive phenotype by repressing RelB and its target BCL2

    Xiaobo Wang;Karine Belguise;Nathalie Kersual;Kathrin H. Kirsch

  • Expression of a constitutive NF-kappa B-like activity is essential for proliferation of cultured bovine vascular smooth muscle cells.

    R E Bellas;J S Lee;G E Sonenshein

  • Heparin prevents vascular smooth muscle cell progression through the G1 phase of the cell cycle.

    C F Reilly;M S Kindy;K E Brown;R D Rosenberg

Frequent Co-Authors

Philip C. Trackman
Philip C. Trackman Boston University
David C. Seldin
David C. Seldin Boston University
David H. Sherr
David H. Sherr Boston University
Michael Dean
Michael Dean National Institutes of Health
Carl Franzblau
Carl Franzblau Boston University
Thomas L. Rothstein
Thomas L. Rothstein Western Michigan University
George Brawerman
George Brawerman Tufts University
Mark S. Kindy
Mark S. Kindy University of South Florida
Snorri S. Thorgeirsson
Snorri S. Thorgeirsson National Institutes of Health

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