Genetic ablation of Ptprj, a mouse cancer susceptibility gene, results in normal growth and development and does not predispose to spontaneous tumorigenesis

Francesco Trapasso, Alessandra Drusco, Stefan Costinean, Hansjuerg Alder, Rami I. Aqeilan, Rodolfo Iuliano, Eugenio Gaudio, Cinzia Raso, Nicola Zanesi, Carlo M. Croce, Alfredo Fusco*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

45 Scopus citations

Abstract

Ptprj is a ubiquitously expressed murine gene encoding a receptor-type protein tyrosine phosphatase, which has recently been proposed as a candidate gene on the locus Scc1 for colon cancer susceptibility. It has been demonstrated that PTPRJ, the human homologue of Ptprj, is involved in the control of cell growth and adhesion, being furthermore altered in several types of cancer including mammary, thyroid, lung, colon, and pancreatic cancers. To investigate the biological functions of Ptprj, we have generated mice deficient in this receptor protein tyrosine phosphatase. Ptprj-deficient mice are viable, fertile, and show no gross anatomical alterations. Furthermore, neither changes in life span nor spontaneous tumor appearance were observed in Ptprj-null mice. Our results indicate that Ptprj is dispensable for normal growth and development in mice.

Original languageAmerican English
Pages (from-to)376-382
Number of pages7
JournalDNA and Cell Biology
Volume25
Issue number6
DOIs
StatePublished - Jun 2006
Externally publishedYes

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