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[Cancer Research 62, 3598-3602, July 1, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

Transactivation-deficient {Delta}TA-p73 Acts as an Oncogene1

Thorsten Stiewe, Sonja Zimmermann, Andreja Frilling, Helmut Esche and Brigitte M. Pützer2

Centre for Cancer Research and Cancer Therapy, Institute of Molecular Biology [T. S., S. Z., H. E., B. M. P.] and Department of General and Transplantation Surgery [A. F.], University of Essen, Medical School, D-45122 Essen, Germany

The recently discovered p53-family member p73 displays significant homology to p53, but data from primary tumors and knockout mice argue against p73 being a classical tumor suppressor. We report on the overexpression of NH2-terminally truncated, transactivation-deficient p73 proteins ({Delta}TA-p73) in human cancer cells. Moreover, we show that {Delta}TA-p73 overexpression results in malignant transformation of NIH3T3 fibroblasts and tumor growth in nude mice, thereby providing the experimental evidence for an oncogenic function of {Delta}TA-p73. Apparently, increased expression of NH2-terminally truncated p73 isoforms conveys the TP73 gene with oncogenic activity that appears to be actively selected for during tumor development.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
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Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
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Copyright © 2002 by the American Association for Cancer Research.