PMC:5003446 / 33794-35603 JSONTXT

{"project":"2_test","denotations":[{"id":"27600067-22469134-69477885","span":{"begin":608,"end":610},"obj":"22469134"},{"id":"27600067-22086417-69477886","span":{"begin":1174,"end":1176},"obj":"22086417"},{"id":"27600067-22086417-69477887","span":{"begin":1366,"end":1368},"obj":"22086417"}],"text":"8. Classical Hodgkin Lymphoma\nClassical Hodgkin lymphoma (cHL) is characterized by presence of small numbers of neoplastic Reed-Sternberg/Hodgkin cells admixed with mixed inflammatory cells. Metaphase cytogenetic study is typically unsuccessful due to low numbers of neoplastic cells. For the same reason, SNP array is not expected to yield useful information on patient samples. Instead, SNP array 6.0 was performed on cHL cell lines and showed a UPD of chromosome 14q, which was associated with biallelic deletion of TRAF3 in one cell line, and a gain of copy number for MAP3K14 in three other cell lines [79]. With primary cHL tissues, interphase cytogenetic analyses confirmed monoallelic deletion of TRAF3 in 3/20 cases and gains of MAP3K14 in 5/16 cases. Both TRAF3 and MAP3K14 are regulators of the NF-κB pathway, which is constitutively activated in cHL. The study suggested that genetic alterations of the components of the NF-κB pathways contributed to the pathogenesis of cHL, at least in a subset of cases.\nA genome-wide association study identified five SNPs on chromosome 6p21.32 associated with nodular sclerosis cHL (NSHL), which is a common subtype of cHL [80]. Two of the SNPs, rs6903608 and rs2858870, were significantly associated with NSHL. The extended haplotype containing these five SNPs was the strongest overall predictor of risk for NSHL [80]. The haplotype with all five risk alleles for the SNPs (Hap3: AGGCT) was associated with a 70% increased risk of NSHL; while the haplotype with all five protective alleles (Hap6: GAATC) was associated with a 60% decreased risk. The DRB1*07:01 allele, which was carried by all individuals with haplotype 6 (GAATC), was associated with a 50% decreased risk of NSHL, suggesting HLA-DRB1 polymorphisms likely implicated in NSHL susceptibility."}