High-resolution loss of heterozygosity screening implicates PTPRJ as a potential tumor suppressor gene that affects susceptibility to non-hodgkin's lymphoma

Aya-Bonilla, C., Green, M.R., Camilleri, E., Benton, M., Keane, C., Marlton, P., Lea, R., Gandhi, M.K. and Griffiths, L.R. (2013) High-resolution loss of heterozygosity screening implicates PTPRJ as a potential tumor suppressor gene that affects susceptibility to non-hodgkin's lymphoma. Genes Chromosomes and Cancer, 52 5: 467-479. doi:10.1002/gcc.22044

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Author Aya-Bonilla, C.
Green, M.R.
Camilleri, E.
Benton, M.
Keane, C.
Marlton, P.
Lea, R.
Gandhi, M.K.
Griffiths, L.R.
Title High-resolution loss of heterozygosity screening implicates PTPRJ as a potential tumor suppressor gene that affects susceptibility to non-hodgkin's lymphoma
Journal name Genes Chromosomes and Cancer   Check publisher's open access policy
ISSN 1045-2257
Publication date 2013
Sub-type Article (original research)
DOI 10.1002/gcc.22044
Open Access Status
Volume 52
Issue 5
Start page 467
End page 479
Total pages 13
Place of publication Hoboken, NJ, U.S.A.
Publisher John Wiley & Sons, Inc.
Collection year 2014
Language eng
Subject 1306 Cancer Research
1311 Genetics
Abstract We employed a Hidden-Markov-Model (HMM) algorithm in loss of heterozygosity (LOH) analysis of high-density single nucleotide polymorphism (SNP) array data from Non-Hodgkin's lymphoma (NHL) entities, follicular lymphoma (FL), and diffuse large B-cell 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-cells (i.e., BCR, MAPK, and PI3K signaling), its role in B-cell development is poorly understood. LOH of PTPRJ has been described in several types of cancer but not in any hematological malignancy. Interestingly, FL cases with LOH exhibited down-regulation of PTPRJ, in contrast no significant variation of expression was shown in DLBCLs. In addition, sequence screening in Exons 5 and 13 of PTPRJ 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-representation 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-representated 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 PTPRJ gene may play a role in susceptibility to NHL, by affecting activation of PTPRJ in these B-cell lymphomas.
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Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2014 Collection
School of Medicine Publications
 
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Created: Sun, 02 Feb 2014, 11:27:38 EST by Matthew Lamb on behalf of School of Medicine