Cancer Amplification, also known as the over-expression of the ERBB2 gene, occurs in approximately 15-30% of breast cancers. It is strongly associated with increased disease recurrence and a poor prognosis; however, drug agents targeting<unk>  in breast cancer have significantly positively altered the otherwise poor-prognosis natural history of<unk> -positive breast cancer. Over-expression is also known to occur in ovarian, stomach, adenocarcinoma of the lung and aggressive forms of uterine cancer, such as uterine serous endometrial carcinoma, e.g.<unk>  is over-expressed in approximately 7-34% of patients with gastric cancer and in 30% of salivary duct carcinomas.<unk>  is colocalised and most of the time, coamplified with the gene GRB7, which is a proto-oncogene associated with breast, testicular germ cell, gastric, and esophageal tumours.<unk>  proteins have been shown to form clusters in cell membranes that may play a role in tumorigenesis. Evidence has also implicated<unk>  signaling in resistance to the EGFR-targeted cancer drug cetuximab. The high expression of<unk>  correlates with better survival in esophageal adenocarcinoma. The high amplification of<unk>  copy number positively contributes to the survival time of gastric cardia adenocacinoma patients. Mutations Furthermore, diverse structural alterations have been identified that cause ligand-independent firing of this receptor, doing so in the absence of receptor over-expression.<unk>  is found in a variety of tumours and some of these tumours carry point mutations in the sequence specifying the transmembrane domain of<unk> . Substitution of a valine for a glutamic acid in the transmembrane domain can result in the constitutive dimerisation of this protein in the absence of a ligand.<unk>  mutations have been found in non-small-cell lung cancers (NSCLC) and can direct treatment.
HER2/neu
HERG
BIM-1
TPA-023
STS-135 
AEMT-CC
BerEp4
OPS-301