All

What are you looking for?

All
Projects
Results
Organizations

Quick search

  • Projects supported by TA ČR
  • Excellent projects
  • Projects with the highest public support
  • Current projects

Smart search

  • That is how I find a specific +word
  • That is how I leave the -word out of the results
  • “That is how I can find the whole phrase”

Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00209805%3A_____%2F19%3A00078218" target="_blank" >RIV/00209805:_____/19:00078218 - isvavai.cz</a>

  • Result on the web

    <a href="https://www.ncbi.nlm.nih.gov/pubmed/31407831" target="_blank" >https://www.ncbi.nlm.nih.gov/pubmed/31407831</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1002/gepi.22242" target="_blank" >10.1002/gepi.22242</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Genetic overlap between autoimmune diseases and non-Hodgkin lymphoma subtypes

  • Original language description

    Epidemiologic studies show an increased risk of non-Hodgkin lymphoma (NHL) in patients with autoimmune disease (AD), due to a combination of shared environmental factors and/or genetic factors, or a causative cascade: chronic inflammation/antigen-stimulation in one disease leads to another. Here we assess shared genetic risk in genome-wide-association-studies (GWAS). Secondary analysis of GWAS of NHL subtypes (chronic lymphocytic leukemia, diffuse large B-cell lymphoma, follicular lymphoma, and marginal zone lymphoma) and ADs (rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis). Shared genetic risk was assessed by (a) description of regional genetic of overlap, (b) polygenic risk score (PRS), (c)&quot;diseasome&quot;, (d)meta-analysis. Descriptive analysis revealed few shared genetic factors between each AD and each NHL subtype. The PRS of ADs were not increased in NHL patients (nor vice versa). In the diseasome, NHLs shared more genetic etiology with ADs than solid cancers (p = .0041). A meta-analysis (combing AD with NHL) implicated genes of apoptosis and telomere length. This GWAS-based analysis four NHL subtypes and three ADs revealed few weakly-associated shared loci, explaining little total risk. This suggests common genetic variation, as assessed by GWAS in these sample sizes, may not be the primary explanation for the link between these ADs and NHLs.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30204 - Oncology

Result continuities

  • Project

    <a href="/en/project/ED2.1.00%2F03.0101" target="_blank" >ED2.1.00/03.0101: Regional Centre for Applied Molecular Oncology (RECAMO)</a><br>

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2019

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Genetic epidemiology

  • ISSN

    0741-0395

  • e-ISSN

  • Volume of the periodical

    43

  • Issue of the periodical within the volume

    7

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    20

  • Pages from-to

    844-863

  • UT code for WoS article

    000618791300009

  • EID of the result in the Scopus database

    2-s2.0-85070768686