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Monogenic and polygenic inheritance become instruments for clonal selection.

Po-Ru Loh1,2, Giulio Genovese3,4,5, Steven A McCarroll6,7,8

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Age-related clonal hematopoiesis, driven by acquired mutations, increases blood cancer risk. Inherited gene variants interacting with these mutations create challenges for lifelong blood cell production.

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Area of Science:

  • Genetics
  • Hematology
  • Genomics

Background:

  • Clonal hematopoiesis, common with age, involves expanded blood cells with somatic mutations, increasing blood cancer risk.
  • Existing research shows diverse chromosomal alterations in blood clones, but drivers of clone expansion remain unclear.

Purpose of the Study:

  • To identify genes, mutations, and biological processes conferring selective advantage to mutant blood clones.
  • To analyze the relationship between acquired mutations and inherited genetic variation in a large cohort.

Main Methods:

  • Analysis of genotyping data from 482,789 UK Biobank participants.
  • Identification and analysis of 19,632 autosomal mosaic chromosomal alterations.
  • Investigation of associations between inherited variants and acquired copy-neutral loss of heterozygosity (CN-LOH) mutations.

Main Results:

  • 52 inherited rare variants in 7 genes significantly increased vulnerability to clonal hematopoiesis with specific CN-LOH mutations.
  • Acquired mutations systematically replaced or duplicated inherited risk alleles at genes including MPL, FH, NBN, MRE11, ATM, SH2B3, and TM2D3.
  • CN-LOH mutations promoted replacement of homologous chromosomal segments, increasing polygenic drive for hematopoietic cell proliferation.

Conclusions:

  • Inherited genetic variation interacts with acquired mutations to drive clonal hematopoiesis.
  • Specific genes involved in DNA damage response (MRE11, NBN, ATM) and stem cell self-renewal (MPL, SH2B3) are implicated.
  • The interplay between inherited and acquired mutations presents challenges for maintaining blood cell production throughout life.