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Significance Protein tyrosine phosphatase receptor-δ (PTPRD ) is a frequently inactivated tumor-suppressor gene. We demonstrate thatPtprd inactivation in the context ofCdkn2a/p16 Ink4a deletion is sufficient to promote tumorigenesis in vivo. Our mouse model closely recapitulates the genetic events on chromosome 9p that occur in cancer. We demonstrate that PTPRD is a haploinsufficient tumor suppressor and provide a rationale for the high frequency of heterozygous loss ofPTPRD in human glioblastoma. Finally, this study establishes loss ofPTPRD , a STAT3 phosphatase, as a cause of STAT3 hyperactivation in gliomas.

Loss of the tyrosine phosphatase PTPRD leads to aberrant STAT3 activation and promotes gliomagenesis