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Institut du cancer de Montréal, Hôpital Notre-Dame, 1560 Sherbrooke East, Montréal, Canada H2L 4M1 [B. H., M. P., W. E. C. B.], and Department of Medicine, University of Montréal, Montréal, Canada [W. E. C. B.]; Centre de Recherche, Hôpital Notre-Dame, Montréal, Canada [J. W.]; and McGill University, Montréal Children's Hospital Research Institute, 2300 Tupper, Montréal, Canada [C. G.]
3 To whom requests for reprints should be addressed.
The retinoic acid receptor type β (RARβ) complementary DNA from a small cell tumor line was amplified, sequenced, and found to be homologous to the murine RARβ1. Seventeen lung tumor lines were analyzed. Five of seven small cell lung carcinoma lines expressed RARβ1, but only one other line (epidermoid) expressed the isoform, and this was at trace levels. Two other epidermoid lines, as well as three adenocarcinoma, two adenosquamous, and two large cell-derived lines did not express RARβ1. Nine adult human tissues, including lung, were analyzed, and in contrast to what has been reported for the mouse, undetectable or barely detectable levels were observed. On the other hand, a total of 13 different fetal tissues, at three different developmental stages, all expressed RARβ1. RARβ1 may be a master developmental gene in humans, and the remarkably specific association with small cell lung carcinoma suggests a molecular link between this type of cancer and development.
1 This work was supported by the Medical Research Council of Canada.
2 Present address: Whitaker College, M. I. T, Cambridge, MA.
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.
Received 10/29/93. Accepted 11/30/93.
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