Authors

Isabelle Mercier, Kimmel Cancer Center, Departments of Cancer Biology and Medical Oncology; Stem Cell Biology and Regenerative Medicine Center, Thomas Jefferson UniversityFollow
Jean-Francois Jasmin, Kimmel Cancer Center, Departments of Cancer Biology and Medical Oncology; Stem Cell Biology and Regenerative Medicine Center, Thomas Jefferson UniversityFollow
Stephanos Pavlides, Kimmel Cancer Center, Departments of Cancer Biology and Medical Oncology; Stem Cell Biology and Regenerative Medicine Center, Thomas Jefferson UniversityFollow
Carlo Minetti, Muscular and Neurodegenerative Disease Unit, University of Genoa and G. Gaslini Pediatric InstituteFollow
Neal Flomenberg, Kimmel Cancer Center, Departments of Cancer Biology and Medical Oncology; Stem Cell Biology and Regenerative Medicine Center, Thomas Jefferson UniversityFollow
Richard G Pestell, Kimmel Cancer Center, Departments of Cancer Biology and Medical Oncology; Stem Cell Biology and Regenerative Medicine Center, Thomas Jefferson UniversityFollow
Philippe G Frank, Kimmel Cancer Center, Departments of Cancer Biology and Medical Oncology; Stem Cell Biology and Regenerative Medicine Center, Thomas Jefferson UniversityFollow
Federica Sotgia, Kimmel Cancer Center, Departments of Cancer Biology and Medical Oncology; Stem Cell Biology and Regenerative Medicine Center, Thomas Jefferson University; Muscular and Neurodegenerative Disease Unit, University of Genoa and G. Gaslini Pediatric InstituteFollow
Michael P Lisanti, Kimmel Cancer Center, Departments of Cancer Biology and Medical Oncology; Stem Cell Biology and Regenerative Medicine Center, Thomas Jefferson University; Muscular and Neurodegenerative Disease Unit, University of Genoa and G. Gaslini Pediatric InstituteFollow

Document Type

Article

Publication Date

6-1-2009

Comments

This article has been peer reviewed. It was published in: Laboratory Investigation.

Volume 89, Issue 6, June 2009, Pages 614-623.

The published version is available at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796209/

DOI: 10.1038/labinvest.2009.23

Copyright © 2009 USCAP, Inc.

Abstract

Here we review the clinical and translational implications of the caveolin gene family for understanding the pathogenesis of human diseases, including breast and prostate cancers, pulmonary hypertension, cardiomyopathy, diabetes, and muscular dystrophy. Detailed phenotypic analysis of caveolin knockout mice has served to highlight the crucial role of a caveolin deficiency in the pathogenesis of many human disease processes. Mutations in the human caveolin genes are associated with a number of established genetic disorders (such as breast cancer, lipodystrophy, muscular dystrophy, and cardiomyopathy), making the caveolins important and novel targets for drug development. The implementation of new strategies for caveolin replacement therapy-including caveolin mimetic peptides-is ongoing.

PubMed ID

19333235

Included in

Oncology Commons

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