Year: 2014
Type: article
Abstract: // Berenice Ortiz 1,2 , Julie R. White 3 , Wei H. Wu 2 and Timothy A. Chan 2,4,5 1 Gerstner Sloan-Kettering Graduate School, Memorial Sloan-Kettering Cancer Center, New York, NY, USA 2 Human Oncology and Pathogenesis Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA 3 The Tri-Institutional Laboratory of Comparative Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA 4 Dept. of Radiation Oncology, Memorial Sloan-Kettering Cancer Center, New York, New York, USA 5 Brain Tumor Center, Memorial Sloan-Kettering Cancer Center, New York, New York, USA Correspondence: Timothy A. Chan, email: // Keywords : PTPRD, CDKN2A Received : May 9, 2014 Accepted : June 12, 2014 Published : June 14, 2014 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.
Source: Oncotarget
Institution: Memorial Sloan Kettering Cancer Center
Language: Yiddish
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: diamond
OpenAlex ID: W1869167622