Deletion of Ptprd and Cdkn2a cooperate to accelerate tumorigenesis Journal Article


Authors: Ortiz, B.; White, J. R.; Wu, W. H.; Chan, T. A.
Article Title: Deletion of Ptprd and Cdkn2a cooperate to accelerate tumorigenesis
Abstract: PTPRD encodes the protein tyrosine phosphatase receptor type D and is frequently inactivated across many human cancers. Despite its frequent inactivation, it is unknown whether loss of PTPRD promotes tumorigenesis in vivo. PTPRD is located on chromosome 9p, as is CDKN2A, and the two loci are frequently deleted together. Here, we show that co-deletion of Ptprd and Cdkn2a cooperate to accelerate tumorigenesis. Interestingly, heterozygous loss of Ptprd was sufficient to promote tumorigenesis in our model, suggesting that Ptprd may be a haploinsufficient tumor suppressor. The loss of Ptprd resulted in changes to the tumor spectrum in mice and increased the frequency of lymphomas. In total, we reveal that Ptprd is a tumor suppressor that can promote tumorigenesis in concert with Cdkn2a loss.
Keywords: cdkn2a; ptprd
Journal Title: Oncotarget
Volume: 5
Issue: 16
ISSN: 1949-2553
Publisher: Impact Journals  
Date Published: 2014-08-01
Start Page: 6976
End Page: 6982
Language: English
PROVIDER: scopus
PUBMED: 25138050
PMCID: PMC4196177
DOI/URL:
Notes: Export Date: 1 October 2014 -- Source: Scopus
Citation Impact
MSK Authors
  1. Timothy Chan
    317 Chan
  2. Julie R White
    29 White
  3. Wei Hang Wu
    11 Wu
  4. Berenice   Ortiz
    4 Ortiz