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[Cancer Research 54, 3714-3717, July 15, 1994]
© 1994 American Association for Cancer Research

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Paradoxical Inhibition of Solid Tumor Cell Growth by bcl21

Jennifer A. Pietenpol2, Nickolas Papadopoulos, Sanford Markowitz, James K. V. Willson, Kenneth W. Kinzler and Bert Vogelstein

The Oncology Center, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231 [J. A. P., N. P., K. W. K., B. V.], and Ireland Cancer Center, University Hospitals of Cleveland, Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106 [S. M., J. K. V. W.]

The BCL2 gene product has been demonstrated to prevent apoptosis and provide a selective growth advantage to many cell types. We report an unexpected effect of bcl2 expression on the in vitro growth of several solid tumor cell lines. Expression of bcl2 in these cell lines resulted in growth inhibition similar to that seen with p53. In contrast, a COOH-terminal deletion mutant of bcl2 was unable to suppress growth. Thus, the bcl2 protein may exert distinct biological effects in different cell types.

1 This work was supported by the Preuss Foundation, the Clayton Fund, the National Foundation for Cancer Research, and NIH Grants CA35494 and CA09243. B. V. is an American Cancer Society research professor.

2 To whom requests for reprints should be addressed, at The Johns Hopkins Oncology Center, 424 North Bond St., Baltimore, MD 21231.

Received 4/21/94. Accepted 6/ 1/94.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1994 by the American Association for Cancer Research.