H
Herbert B. Tanowitz
Researcher at Albert Einstein College of Medicine
Publications - 326
Citations - 14193
Herbert B. Tanowitz is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Trypanosoma cruzi & Chagas disease. The author has an hindex of 65, co-authored 326 publications receiving 13261 citations. Previous affiliations of Herbert B. Tanowitz include University of Texas Medical Branch & Jacobi Medical Center.
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Journal ArticleDOI
Antibiotics that target mitochondria effectively eradicate cancer stem cells, across multiple tumor types : treating cancer like an infectious disease
Rebecca Lamb,Béla Ózsvári,Camilla L. Lisanti,Herbert B. Tanowitz,Anthony Howell,Ubaldo E. Martinez-Outschoorn,Federica Sotgia,Michael P. Lisanti +7 more
TL;DR: It is proposed to treat cancer like an infectious disease, by repurposing FDA-approved antibiotics for anti-cancer therapy, across multiple tumor types, and these drug classes should also be considered for prevention studies, specifically focused on the prevention of tumor recurrence and distant metastasis.
Journal Article
American Trypanosomiasis (Chagas disease).
TL;DR: Gastrointestinal dysfunction is a major problem for many patients with chronic Chagas' disease, as are cardiac dysrhythmias and cardiomyopathy, and patients with advanced megacolon who have resections of the sigmoid colon and most of the rectum generally do well postoperatively.
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Caveolin-3 knock-out mice develop a progressive cardiomyopathy and show hyperactivation of the p42/44 MAPK cascade
Scott Eric Woodman,David S. Park,Alex W. Cohen,Michelle W.-C. Cheung,Madhulika Chandra,Jamshid Shirani,Baiyu Tang,Linda A. Jelicks,Richard N. Kitsis,George J. Christ,Stephen M. Factor,Herbert B. Tanowitz,Michael P. Lisanti +12 more
TL;DR: Loss of Cav-3 expression is sufficient to induce a molecular program leading to cardiac myocyte hypertrophy and cardiomyopathy, consistent with previous in vitro data demonstrating that caveolins may function as negative regulators of the p42/44 MAPK cascade.
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Caveolin-1 null mice develop cardiac hypertrophy with hyperactivation of p42/44 MAP kinase in cardiac fibroblasts
Alex W. Cohen,David S. Park,Scott Eric Woodman,Terrence M. Williams,Madhulika Chandra,Jamshid Shirani,Andrea Pereira De Souza,Richard N. Kitsis,Robert G. Russell,Louis M. Weiss,Baiyu Tang,Linda A. Jelicks,Stephen M. Factor,Vitaliy Shtutin,Herbert B. Tanowitz,Michael P. Lisanti +15 more
TL;DR: It is reported that the hearts of Cav-1 null mice are markedly abnormal, despite the fact that caveolin-1 is not expressed in cardiac myocytes, and p42/44 MAP kinase activation and cardiac hypertrophy is revealed.
Journal ArticleDOI
Stromal-epithelial metabolic coupling in cancer: integrating autophagy and metabolism in the tumor microenvironment.
Ubaldo E. Martinez-Outschoorn,Stephanos Pavlides,Anthony Howell,Richard G. Pestell,Herbert B. Tanowitz,Federica Sotgia,Michael P. Lisanti +6 more
TL;DR: It is suggested that stromal catabolism, via autophagy and mitophagy, fuels the anabolic growth of tumor cells, promoting tumor progression and metastasis, and how glutamine addiction in cancer cells fits well with this new model, by promoting oxidative mitochondrial metabolism in aggressive cancer cells.