Germline deletion of ETV6 in familial acute lymphoblastic leukemia.
Evadnie RampersaudDavid S ZieglerIlaria IacobucciDebbie Payne-TurnerMichelle L ChurchmanKasmintan A SchraderVijai JosephKenneth OffitKatherine TuckerRosemary SuttonMeera WarbyGeorgia Chenevix-TrenchDavid G HuntsmanMaria TsoliR Scott MeadChunxu QuVasiliki LeventakiGang WuCharles G MullighanPublished in: Blood advances (2020)
Recent studies have identified germline mutations in TP53, PAX5, ETV6, and IKZF1 in kindreds with familial acute lymphoblastic leukemia (ALL), but the genetic basis of ALL in many kindreds is unknown despite mutational analysis of the exome. Here, we report a germline deletion of ETV6 identified by linkage and structural variant analysis of whole-genome sequencing data segregating in a kindred with thrombocytopenia, B-progenitor acute lymphoblastic leukemia, and diffuse large B-cell lymphoma. The 75-nt deletion removed the ETV6 exon 7 splice acceptor, resulting in exon skipping and protein truncation. The ETV6 deletion was also identified by optimal structural variant analysis of exome sequencing data. These findings identify a new mechanism of germline predisposition in ALL and implicate ETV6 germline variation in predisposition to lymphoma. Importantly, these data highlight the importance of germline structural variant analysis in the search for germline variants predisposing to familial leukemia.
Keyphrases
- acute lymphoblastic leukemia
- dna repair
- diffuse large b cell lymphoma
- allogeneic hematopoietic stem cell transplantation
- copy number
- electronic health record
- dna damage
- big data
- bone marrow
- epstein barr virus
- early onset
- acute myeloid leukemia
- oxidative stress
- genome wide
- data analysis
- single cell
- human immunodeficiency virus
- small molecule
- men who have sex with men
- hepatitis c virus
- protein protein
- hiv infected
- binding protein
- amino acid