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Deciphering the genetics and mechanisms of predisposition to multiple myeloma

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378041%3A_____%2F24%3A00597551" target="_blank" >RIV/68378041:_____/24:00597551 - isvavai.cz</a>

  • Alternative codes found

    RIV/61988987:17110/24:A25039MW RIV/00216208:11140/24:10482801 RIV/00843989:_____/24:E0111065

  • Result on the web

    <a href="https://www.nature.com/articles/s41467-024-50932-7" target="_blank" >https://www.nature.com/articles/s41467-024-50932-7</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1038/s41467-024-50932-7" target="_blank" >10.1038/s41467-024-50932-7</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Deciphering the genetics and mechanisms of predisposition to multiple myeloma

  • Original language description

    Multiple myeloma (MM) is an incurable malignancy of plasma cells. Epidemiological studies indicate a substantial heritable component, but the underlying mechanisms remain unclear. Here, in a genome-wide association study totaling 10,906 cases and 366,221 controls, we identify 35 MM risk loci, 12 of which are novel. Through functional fine-mapping and Mendelian randomization, we uncover two causal mechanisms for inherited MM risk: longer telomeres and elevated levels of B-cell maturation antigen (BCMA) and interleukin-5 receptor alpha (IL5RA) in plasma. The largest increase in BCMA and IL5RA levels is mediated by the risk variant rs34562254-A at TNFRSF13B. While individuals with loss-of-function variants in TNFRSF13B develop B-cell immunodeficiency, rs34562254-A exerts a gain-of-function effect, increasing MM risk through amplified B-cell responses. Our results represent an analysis of genetic MM predisposition, highlighting causal mechanisms contributing to MM development.

  • 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

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2024

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Nature Communications

  • ISSN

    2041-1723

  • e-ISSN

    2041-1723

  • Volume of the periodical

    15

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    15

  • Pages from-to

    6644

  • UT code for WoS article

    001284820100008

  • EID of the result in the Scopus database

    2-s2.0-85200470126