HIF1A and inflammatory breast carcinoma: Because of the dramatically reduced growth of the M-SUM149, Mary-X-shEcad and 4T1-shECad clones observed in vivo in the present studies, the development of novel therapeutics against E-Cadherin and HIF-1α/glycolysis represent an attractive approach for the treatment of IBC and possibly in cancers that retain an epithelial phenotype typified by E-Cadherin expression in general.