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[Cancer Research 60, 4005-4009, August 1, 2000]
© 2000 American Association for Cancer Research

Advances in Brief

Constitutive Achaete-Scute Homologue-1 Promotes Airway Dysplasia and Lung Neuroendocrine Tumors in Transgenic Mice1

R. Ilona Linnoila, Bihong Zhao, Janet L. DeMayo, Barry D. Nelkin, Stephen B. Baylin, Franco J. DeMayo2 and Douglas W. Ball2

Cell and Cancer Biology Department, Medicine Branch, Division of Clinical Sciences, National Cancer Institute, NIH, Rockville, Maryland 20817 [R. I. L.]; Department of Molecular and Cell Biology, Baylor University School of Medicine, Houston, Texas 77030 [B. Z., J. L. D., F. J. D.]; and Oncology Center [B. D. N., S. B. B., D. W. B.] and Department of Medicine [S. B. B., D. W. B.], Johns Hopkins University School of Medicine, Baltimore, Maryland 21231

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.




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Copyright © 2000 by the American Association for Cancer Research.