Constitutive achaete-scute homologue-1 promotes airway dysplasia and lung neuroendocrine tumors in transgenic mice

R. I. Linnoila, B. Zhao, J. L. DeMayo, B. D. Nelkin, S. B. Baylin, F. J. DeMayo, D. W. Ball

Research output: Contribution to journalArticle

Abstract

The transcription factor achaete-scute homologue-1 (ASH1) is essential for neural differentiation during fetal development and is a cardinal feature of neuroendocrine (NE) tumors such as small cell lung cancer. To explore the potential of ASH1 to promote NE differentiation and tumorigenesis in the lung, we constitutively expressed the factor in nonendocrine airway epithelial cells using transgenic mice. Progressive airway hyperplasia and metaplasia developed beginning at 3 weeks of life. ASH1 potently enhanced the tumorigenic effect of SV40 large T antigen in airway epithelium. These doubly transgenic animals developed massive NE lung tumors, implying that ASH1 may cooperate with defects in p53, pRb, or related pathways in promoting NE lung carcinogenesis.

Original languageEnglish (US)
Pages (from-to)4005-4009
Number of pages5
JournalCancer Research
Volume60
Issue number15
StatePublished - Aug 31 2000

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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