title: Variety in the tumor microenvironment: integrin splicing regulates stemness.
abstract: Recently in Cell Reports, Goel et al. (2014) identified mechanisms underlying cellular heterogeneity in triple negative breast cancer. They find that expression of α6 integrin and its splice variants differs between epithelial and mesenchymal tumor cell subpopulations, the latter of which relies on VEGF signaling to promote cancer stem cell function.
authors.affiliation: Department of Pathology and Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093, USA.
authors.forename: Laetitia
authors.initials: L
authors.lastname: Seguin
authors.affiliation: Department of Pathology and Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093, USA.
authors.forename: Sara M
authors.initials: SM
authors.lastname: Weis
authors.affiliation: Department of Pathology and Moores Cancer Center, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: dcheresh@ucsd.edu.
authors.forename: David A
authors.initials: DA
authors.lastname: Cheresh
mesh_terms: D005260:Female; D006801:Humans; D039503:Integrin alpha6 / Q000378:metabolism*; D014411:Neoplastic Stem Cells / Q000378:metabolism*; D012326:RNA Splicing / Q000502:physiology*
chemical_list: D039503:Integrin alpha6