Abstract
Recently, the gene PTPRJ (protein tyrosine phosphatase receptor type J) was identified as the candidate gene for the mouse colon cancer susceptibility locus Scc1. Its human homologue PTPRJ is frequently deleted in several cancer types, including colorectal cancer. To elucidate the role of PTPRJ loss in different stages of colorectal cancer and in its pathways of progression, we expanded the previously published comparative genomic hybridization results with novel data on loss of heterozygosity (LOH) at the PTPRJ locus. We identified a strong association between the LOH of PTPRJ and the loss of chromosomal region 18q12–21 (P=0.009). This observation is specific for progressed colorectal adenomas, suggesting that an interaction between LOH of PTPRJ and loss of 18q12–21 may be involved in the development of a more progressed form of adenomas.
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Abbreviations
- CGH:
-
comparative genomic hybridization
- LOH:
-
loss of heterozygosity
- PTPRJ :
-
protein tyrosine phosphatase receptor type J
- Scc1:
-
Susceptibility to colon cancer-1
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Acknowledgements
We thank Margriet Snoek, Carlo Zanon and Tamás Csikós for comments on the manuscript. This work was supported by Dutch Cancer Society Grants NKI97-1463 (to PD) and VU97-1455 (to GM).
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Ruivenkamp, C., Hermsen, M., Postma, C. et al. LOH of PTPRJ occurs early in colorectal cancer and is associated with chromosomal loss of 18q12–21. Oncogene 22, 3472–3474 (2003). https://doi.org/10.1038/sj.onc.1206246
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DOI: https://doi.org/10.1038/sj.onc.1206246
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