{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T05:49:04Z","timestamp":1775713744220,"version":"3.50.1"},"reference-count":37,"publisher":"Proceedings of the National Academy of Sciences","issue":"23","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1997,11,11]]},"abstract":"<jats:p>\n            Deletions of all or part of chromosome 10 are the most common genetic alterations in high-grade gliomas. The\n            <jats:italic>PTEN<\/jats:italic>\n            gene (also called\n            <jats:italic>MMAC1<\/jats:italic>\n            and\n            <jats:italic>TEP1<\/jats:italic>\n            ) maps to chromosome region 10q23 and has been implicated as a target of alteration in gliomas and also in other cancers such as those of the breast, prostate, and kidney. Here we sought to provide a functional test of its candidacy as a growth suppressor in glioma cells. We used a combination of Northern blot analysis, protein truncation assays, and sequence analysis to determine the types and frequency of\n            <jats:italic>PTEN<\/jats:italic>\n            mutations in glioma cell lines so that we could define appropriate recipients to assess the growth suppressive function of\n            <jats:italic>PTEN<\/jats:italic>\n            by gene transfer. Introduction of wild-type\n            <jats:italic>PTEN<\/jats:italic>\n            into glioma cells containing endogenous mutant alleles caused growth suppression, but was without effect in cells containing endogenous wild-type\n            <jats:italic>PTEN<\/jats:italic>\n            . The ectopic expression of\n            <jats:italic>PTEN<\/jats:italic>\n            alleles, which carried mutations found in primary tumors and have been shown or are expected to inactivate its phosphatase activity, caused little growth suppression. These data strongly suggest that PTEN is a protein phosphatase that exhibits functional and specific growth-suppressing activity.\n          <\/jats:p>","DOI":"10.1073\/pnas.94.23.12479","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T14:31:44Z","timestamp":1027693904000},"page":"12479-12484","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":345,"title":["Growth suppression of glioma cells by PTEN requires a functional phosphatase catalytic\u2009domain"],"prefix":"10.1073","volume":"94","author":[{"given":"Frank B.","family":"Furnari","sequence":"first","affiliation":[{"name":"Ludwig Institute for Cancer Research, Department of Medicine, Center for Molecular Genetics, and Cancer Center, University of California at San Diego, La Jolla, CA 92093-0660"}]},{"given":"Hong","family":"Lin","sequence":"additional","affiliation":[{"name":"Ludwig Institute for Cancer Research, Department of Medicine, Center for Molecular Genetics, and Cancer Center, University of California at San Diego, La Jolla, CA 92093-0660"}]},{"given":"H.-J. 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