TY - JOUR
T1 - Pancreatic neoplasia induced by ras expression in acinar cells of transgenic mice
AU - Quaife, Carol J.
AU - Pinkert, Carl A.
AU - Ornitz, David M.
AU - Palmiter, Richard D.
AU - Brinster, Ralph L.
N1 - Funding Information:
We thank Mary Yagle, Glenda Froelick, and Myrna I’umbauer for technical assistance, and Dr. Peter Rabinovitch and Michael Shen for help with the flow cytometry. We also thank Drs. A. Thor and J. Schlom for providing the antibody to ras (RAP-5) and advice on how to use it. We are grateful to Dr. R. Ellis for providing the human EC and EJ ras genes. C. J. Q. was supported by a training grant (T32-ES-07032) from N.I.E.H.S. C. A. P was supported by a grant (HD-07t55) from National Institutes of Health. D. M. 0. was supported by Medical Scientist Training Program (GM-07266) at the University of Washington. The research was supported by grants (HD-09172 and CA-38635) from the NIH. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
PY - 1987/3/27
Y1 - 1987/3/27
N2 - Expression of an activated human c-H-ras oncogene under control of rat elastase I regulating elements leads to neoplasia of the fetal exocrine pancreas. In most transgenic mice bearing this gene construct, massive tumors involving all the pancreatic acinar cells develop within a few days of pancreatic differentiation. Expression of the normal c-H-ras proto-oncogene in acinar cells leads to more subtle anomalies, but no tumors develop. Thus modest amounts of the mutant ras proteins are sufficient, in an otherwise normal genetic background, to lead to neoplastic transformation of differentiating pancreatic acinar cells. In contrast, a comparable elastase-myc construct produces no pancreatic tumors in transgenic mice.
AB - Expression of an activated human c-H-ras oncogene under control of rat elastase I regulating elements leads to neoplasia of the fetal exocrine pancreas. In most transgenic mice bearing this gene construct, massive tumors involving all the pancreatic acinar cells develop within a few days of pancreatic differentiation. Expression of the normal c-H-ras proto-oncogene in acinar cells leads to more subtle anomalies, but no tumors develop. Thus modest amounts of the mutant ras proteins are sufficient, in an otherwise normal genetic background, to lead to neoplastic transformation of differentiating pancreatic acinar cells. In contrast, a comparable elastase-myc construct produces no pancreatic tumors in transgenic mice.
UR - http://www.scopus.com/inward/record.url?scp=0023666146&partnerID=8YFLogxK
U2 - 10.1016/0092-8674(87)90710-0
DO - 10.1016/0092-8674(87)90710-0
M3 - Article
C2 - 3470144
AN - SCOPUS:0023666146
SN - 0092-8674
VL - 48
SP - 1023
EP - 1034
JO - Cell
JF - Cell
IS - 6
ER -