Lung tumorigenesis associated with erb-B-2 and erb-B-3 overexpression in human erb-B-3 transgenic mice is enhanced by methylnitrosourea

Zhou, Hang; Liu, Huan; Lee, Keunmyoung; Qin, Xiusheng; Grasso, Adam W.; Kung, Hsing Jien; Willis, Joesph E.; Kern, Jeffrey A.; Wagner, Thomas E.; Gerson, Stanton L.

doi:10.1038/sj.onc.1205984

Cited by 17 publications

(13 citation statements)

References 27 publications

(28 reference statements)

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“…Nevertheless, the observation that both mouse and human lung adenocarcinomas have high expression of ErbB3 underscores its importance in tumorigenesis. Moreover, ErbB3 is required to drive breast epithelial cell proliferation, and overexpression of ErbB3 leads to the development of lung adenocarcinomas in mice and is associated with poor prognosis in patients with NSCLC (26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

High Expression of ErbB Family Members and Their Ligands in Lung Adenocarcinomas That Are Sensitive to Inhibition of Epidermal Growth Factor Receptor

Fujimoto¹,

Wislez

Zhang³

et al. 2005

Cancer Research

140

102

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Recent findings in tumor biopsies from lung adenocarcinoma patients suggest that somatic mutations in the genes encoding epidermal growth factor receptor (EGFR) and Kirsten ras (KRAS) confer sensitivity and resistance, respectively, to EGFR inhibition. Here, we provide evidence that these genetic mutations are not sufficient to modulate the biological response of lung adenocarcinoma cells to EGFR inhibition. We found high expression of ErbB family members, ErbB ligands, or both in three models that were sensitive to EGFR inhibition, including alveolar epithelial neoplastic lesions in mice that develop lung adenocarcinoma by oncogenic KRAS, human lung adenocarcinoma cell lines, and tumor biopsies from lung adenocarcinoma patients. Thus, lung adenocarcinoma cells that depend on EGFR for survival constitutively activate the receptor through a combination of genetic mutations and overexpression of EGFR dimeric partners and their ligands. (Cancer Res 2005; 65(24): 11478-85)

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Section: Discussionmentioning

confidence: 99%

High Expression of ErbB Family Members and Their Ligands in Lung Adenocarcinomas That Are Sensitive to Inhibition of Epidermal Growth Factor Receptor

Fujimoto¹,

Wislez

Zhang³

et al. 2005

Cancer Research

140

102

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“…Additional strong evidence for the importance of ERBB3 expression in lung tumorigenesis came from ERBB3 transgenic mice, which developed a high incidence of lung adenocarcinoma compared to nontransgenic mice, 379 in spite of lack of K-ras mutations. Mice doubly transgenic for ERBB3 and Erbb2 had an incidence of spontaneous lung tumors similar to that in ERBB3 singly transgenic mice, but developed larger tumors with a shorter latency, suggesting that Erbb2 synergized with ERBB3 in lung tumor progression.…”

Section: Erbb3 In Lung Cancermentioning

confidence: 99%

The ERBB3 receptor in cancer and cancer gene therapy

2008

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ERBB3, a member of the epidermal growth factor receptor (EGFR) family, is unique in that its tyrosine kinase domain is functionally defective. It is activated by neuregulins, by other ERBB and nonERBB receptors as well as by other kinases, and by novel mechanisms. Downstream it interacts prominently with the phosphoinositol 3-kinase/AKT survival/mitogenic pathway, but also with GRB, SHC, SRC, ABL, rasGAP, SYK and the transcription regulator EBP1. There are likely important but poorly understood roles for nuclear localization and for secreted isoforms. Studies of ERBB3 expression in primary cancers and of its mechanistic contributions in cultured cells have implicated it, with varying degrees of certainty, with causation or sustenance of cancers of the breast, ovary, prostate, certain brain cells, retina, melanocytes, colon, pancreas, stomach, oral cavity and lung. Recent results link high ERBB3 activity with escape from therapy targeting other ERBBs in lung and breast cancers. Thus a wide and centrally important role for ERBB3 in cancer is becoming increasingly apparent. Several approaches for targeting ERBB3 in cancers have been tested or proposed. Small inhibitory RNA (siRNA) to ERBB3 or AKT is showing promise as a therapeutic approach to treatment of lung adenocarcinoma.

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“…The erbB family of tyrosine kinase receptors is made of four membrane bound receptors which includes erbB-2 (HER-2 or c-Neu) [1]. Upon binding of specific ligands, these receptors 0169 induce cell differentiation, proliferation and tumorigenesis [2,3].…”

Section: Introductionmentioning

confidence: 99%

Differential expression of STAT5 and Bcl-xL, and high expression of Neu and STAT3 in non-small-cell lung carcinoma

et al. 2006

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Lung tumorigenesis associated with erb-B-2 and erb-B-3 overexpression in human erb-B-3 transgenic mice is enhanced by methylnitrosourea

Cited by 17 publications

References 27 publications

High Expression of ErbB Family Members and Their Ligands in Lung Adenocarcinomas That Are Sensitive to Inhibition of Epidermal Growth Factor Receptor

High Expression of ErbB Family Members and Their Ligands in Lung Adenocarcinomas That Are Sensitive to Inhibition of Epidermal Growth Factor Receptor

The ERBB3 receptor in cancer and cancer gene therapy

Differential expression of STAT5 and Bcl-xL, and high expression of Neu and STAT3 in non-small-cell lung carcinoma

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