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Division of Pulmonary and Critical Care Medicine, Chang Gung Memorial Hospital, Taipei, Taiwan [C-T. Y.]; Thoracic Oncology Laboratory, UCSF Cancer Center, University of California, San Francisco, California 94115 [C-T. Y., L. Y., K. U., F. M., D. M. J.]; and Molecular Urology Laboratory, Mt. Zion Hospital, University of California, San Francisco, California 94115 [C-C. Y.]
ONYX-015 has been reported to kill selectively tumor cells lacking functional p53. Genetic alterations of INK4a/ARF locus, which is a predominant event in malignant pleural mesothelioma, may result in loss of p14ARF and subsequent disruption of p53 pathway in cancer cells. In the present study, ONYX-015 was able to kill three mesothelioma cell lines (H28, H513, and 211H) with wild-type p53 but lacking p14ARF. In contrast, MS-1 mesothelioma cells, which expressed both p53 and p14ARF, were resistant to ONYX-015. Introducing p14ARF gene into the H28 cell, a mesothelioma cell without p14ARF expression, significantly increased the resistance of this cell line to the cytolytic effect of ONYX-015. Our results suggest that human mesotheliomas with wild-type p53 yet lacking p14ARF are potential candidates for ONYX-015 therapy.
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