role of overexpression in lung cancer development in conjunction with erb-B-2 overexpression

findings show that amplification of MET causes gefitinib resistance in lung cancer by driving ERBB3 (HER3)-dependent activation of PI3K, a pathway thought to be specific to EGFR/ERBB family receptors

HER3 signaling pathway plays an important role in the biological behavior of certain non-small cell lung cancers.

Increased expression of erbB3 may play an additional role in non-small-cell lung carcinomas especially in female, nonsmoker, adenocarcinoma, and with EGFR gene mutation.

Non-small cell lung carcinoma brain metastases have some significant differences in HER family receptor-related abnormalities from primary lung tumors.

Nuclear Y-box binding protein-1 is correlated with expression of HER2/ErbB2 and HER3/ErbB3 in non-small cell lung cancer.

EGFR mutation combined with HER2/3 expression is a significant predictor for gefitinib efficacy on Chinese patients with advanced non-small cell lung cancer.

The -276 C/T polymorphism was associated with the risk of lung cancer in a recessive model of never-smokers. Interestingly, the T allele conferred significantly lower promoter activity by 32% and 33% than the C allele in H2009 and H358 cell lines.

HER3 pathway activation is associated with lung cancer.

Neurotensin and its receptor NTSR1 causes EGFR, HER2 and HER3 over-expression and their autocrine/paracrine activation in lung adenocarcinomas, confirming responsiveness to erlotinib.

SNP in HER2 codon 655 and investigation of HER2 and HER3 expression could be helpful to outline the prognosis for patients with lung adenocarcinoma.

ERBB3 and ERBB4 have roles in lung adenocarcinoma

HER2/HER3 interaction and increased expression was linked to risk for poor outcome in lung cancer patients.

the identification of HER3-V855A and its functional properties for the first time clearly implicates genomic HER3 activation in the pathogenesis of lung cancer.

results suggest that the combination of a histone deacetylase inhibitor (HDACi) plus an anti-ErbB3 MoAb represents a viable strategy that warrants further evaluation for the treatment of non-small cell lung cancer (NSCLC) patients.

the present study suggests that HER2 has an important role in the regulation of the cancer stem-like cells phenotype in ALK translocated lung cancers that is mainly orchestrated by HER2/HER3 heterodimers.

Our results indicate that administration of U3-1402 alone or in combination with an EGFR-TKI may have potential as a novel therapy for EGFR-TKI-resistant EGFR-mutant non-small cell lung cancer (NSCLC)

Hydrogen bond analysis of the EGFR-ErbB3 heterodimer related to non-small cell lung cancer and drug resistance.

EGFR and HER3 expression in circulating tumor cells and tumor tissue from non-small cell lung cancer patients.

MiR-519d targets HER3 and can be used as a potential serum biomarker for non-small cell lung cancer.

Transcriptional activation of cyclin D1 via HER2/HER3 contributes to EGFR-TKI resistance in lung cancer.