Sigurgeir Ólafsson

This study shows endometriosis lesions originate from the normal endometrium through clonal expansion, with distinct clones at different body sites.

This study shows that inherited MUTYH mutations increase somatic mutation rates and specific mutational signatures in normal human cells, contributing to cancer risk without causing premature aging.

The paper shows that germline mutations in POLE or POLD1 lead to elevated mutation burdens in normal human cells and tissues, but do not cause premature aging or other phenotypic features beyond early-onset cancer.

The paper analyzes somatic mutations in colonic crypts of IBD patients and controls, finding higher mutation rates and clonal expansions in IBD-affected tissue.