Did you know that Hodgkin's lymphoma and MS run in the same families? #ResearchSpeak #MSBlog #MSResearch
"The following genomic study suggests that there is an overlap between Hodgkin's lymphoma (HL) and MS, at least in terms of genetic susceptibility. This is interesting as these diseases share some epidemiological features, (1) they are strongly associated with EBV, (2) cluster in the same families, (3 ) occur in the same age group and (4) are linked to latitude and hence ultraviolet light or low vD levels. What the study shows is that the genetic susceptibility overlap is mainly in the HLA region. More interesting is that genetic susceptibility to developing HL is closer to other autoimmune diseases rather than to solid cancers. Could this mean that HL is an infectious disease? This is highly likely as a significant proportion of HL is due to EBV. How do I interpret these findings? I am not sure, but it may point to complex biology and suggests that people who are susceptible to developing MS or HL have problems dealing with EBV and as a result a proportion of them go onto to develop overt disease. The million dollar question is that if we can vaccinate these people with an appropriate EBV vaccine prior to them getting EBV would we prevent them developing MS and/or HL? May be we can answer this question in our lifetime."
"If we ever work out how EBV causes MS we may find clues to how it causes HL and vice versa."
Khankhanian et al. Meta-analysis of genome-wide association studies reveals genetic overlap between Hodgkin lymphoma and multiple sclerosis. Int J Epidemiol. 2016 Mar 12. pii: dyv364.
BACKGROUND: Based on epidemiological commonalities, multiple sclerosis (MS) and Hodgkin lymphoma (HL), two clinically distinct conditions, have long been suspected to be aetiologically related. MS and HL occur in roughly the same age groups, both are associated with Epstein-Barr virus infection and ultraviolet (UV) light exposure, and they cluster mutually in families (though not in individuals). We speculated if in addition to sharing environmental risk factors, MS and HL were also genetically related. Using data from genome-wide association studies (GWAS) of 1816 HL patients, 9772 MS patients and 25 255 controls, we therefore investigated the genetic overlap between the two diseases.
METHODS: From among a common denominator of 404 K single nucleotide polymorphisms (SNPs) studied, we identified SNPs and human leukocyte antigen (HLA) alleles independently associated with both diseases. Next, we assessed the cumulative genome-wide effect of MS-associated SNPs on HL and of HL-associated SNPs on MS. To provide an interpretational frame of reference, we used data from published GWAS to create a genetic network of diseases within which we analysed proximity of HL and MS to autoimmune diseases and haematological and non-haematological malignancies.
RESULTS: SNP analyses revealed genome-wide overlap between HL and MS, most prominently in the HLA region. Polygenic HL risk scores explained 4.44% of HL risk (Nagelkerke R2), but also 2.36% of MS risk. Conversely, polygenic MS risk scores explained 8.08% of MS risk and 1.94% of HL risk. In the genetic disease network, HL was closer to autoimmune diseases than to solid cancers.
CONCLUSIONS: HL displays considerable genetic overlap with MS and other autoimmune diseases.