{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T15:25:40Z","timestamp":1791213940257,"version":"4.1.0"},"reference-count":56,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,1,23]],"date-time":"2013-01-23T00:00:00Z","timestamp":1358899200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Chromosomes &amp;amp; Cancer"],"published-print":{"date-parts":[[2013,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We employed a Hidden\u2010Markov\u2010Model (HMM) algorithm in loss of heterozygosity (LOH) analysis of high\u2010density single nucleotide polymorphism (SNP) array data from Non\u2010Hodgkin's lymphoma (NHL) entities, follicular lymphoma (FL), and diffuse large B\u2010cell lymphoma (DLBCL). This revealed a high frequency of LOH over the chromosomal region 11p11.2, containing the gene encoding the protein tyrosine phosphatase receptor type J (PTPRJ). Although PTPRJ regulates components of key survival pathways in B\u2010cells (i.e., BCR, MAPK, and PI3K signaling), its role in B\u2010cell development is poorly understood. LOH of <jats:italic>PTPRJ<\/jats:italic> has been described in several types of cancer but not in any hematological malignancy. Interestingly, FL cases with LOH exhibited down\u2010regulation of <jats:italic>PTPRJ<\/jats:italic>, in contrast no significant variation of expression was shown in DLBCLs. In addition, sequence screening in Exons 5 and 13 of <jats:italic>PTPRJ<\/jats:italic> identified the G973A (rs2270993), T1054C (rs2270992), A1182C (rs1566734), and G2971C (rs4752904) coding SNPs (cSNPs). The A1182 allele was significantly more frequent in FLs and in NHLs with LOH. Significant over\u2010representation of the C1054 (rs2270992) and the C2971 (rs4752904) alleles were also observed in LOH cases. A haplotype analysis also revealed a significant lower frequency of haplotype GTCG in NHL cases, but it was only detected in cases with retention. Conversely, haplotype GCAC was over\u2010representated in cases with LOH. Altogether, these results indicate that the inactivation of PTPRJ may be a common lymphomagenic mechanism in these NHL subtypes and that haplotypes in <jats:italic>PTPRJ<\/jats:italic> gene may play a role in susceptibility to NHL, by affecting activation of PTPRJ in these B\u2010cell lymphomas. \u00a9 2013 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/gcc.22044","type":"journal-article","created":{"date-parts":[[2013,1,23]],"date-time":"2013-01-23T12:35:04Z","timestamp":1358944504000},"page":"467-479","source":"Crossref","is-referenced-by-count":20,"title":["High\u2010resolution loss of heterozygosity screening implicates <i>PTPRJ<\/i> as a potential tumor suppressor gene that affects susceptibility to non\u2010hodgkin's lymphoma"],"prefix":"10.1002","volume":"52","author":[{"given":"Carlos","family":"Aya\u2010Bonilla","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael 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