The N-glycosylated isoform of M-NM-2-integrin as a potential biomarker and target in HER-2+ BC refractory to HER-2 targeted therapies.

ABSTRACT: Acquired resistance to trastuzumab, a rationally designed HER-2 targeting antibody, remains a major hurdle in management of HER-2 positive breast cancer (HER-2+ BC) patients. Potential resistance mechanisms are numerous, derived primarily from studies where HER-2 positive cell lines are chronically exposed to trastuzumab. Recent evidence suggests a role for epithelial-mesenchymal transition (EMT) in trastuzumab resistance, but a definitive link between the two has been difficult to establish because relevant model systems are lacking. When sub-populations of trastuzumab sensitive SKBR-3 cells were isolated using cloning rings, an (EMT) occurred spontaneously in several (3/8) clones. SKBR-3 EMT-clones featured increased spindle morphology, expressed N-glycosylated M-NM-21-integrin, and

ORGANISM(S): Homo sapiens

SUBMITTER: Kathryn Graham 

PROVIDER: E-GEOD-40152 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress