Thus, the predictive value of HER2 overexpression depends on the tumor type, and results of breast cancer trials cannot a priori be extrapolated to digestive cancers.
Mutations in several genes are reportedly involved in the progression of gastrointestinal cancer, including tumor protein 53 (<i>TP53</i>), APC regulator of WNT signaling pathway (<i>APC</i>), KRAS proto-oncogene GTPase (<i>KRAS</i>) and erb-b2 receptor tyrosine kinase 2 (<i>ERBB2</i>).
The purpose of this project was to compare HER2 status in GI cancer brain metastases versus matched prior sites of disease in order to determine if HER2+ disease is more common intracranially.
Preclinical studies in HER2-amplified gastrointestinal cancer models have shown that cotargeting HER2 with a monoclonal antibody and a small molecule is superior to monotherapy with either inhibitor, but the underlying cooperative mechanisms remain unexplored.
Among these, inhibitors of the epidermal growth factor receptor and HER2/neu pathways now play a major role in the management of gastrointestinal cancers in addition to other solid malignancies.
Implication of RICTOR in the mTOR inhibitor-mediated induction of insulin-like growth factor-I receptor (IGF-IR) and human epidermal growth factor receptor-2 (Her2) expression in gastrointestinal cancer cells.
EGFR and HER2 protein expression were determined in a panel of 14 human upper gastrointestinal cancer cell lines and HER2 status was assessed by fluorescent in situ hybridization.