Recurrent deletions in clonal hematopoiesis are driven by microhomology-mediated end joining

Recurrent deletions in clonal hematopoiesis are driven by microhomology-mediated end joining

The mutational mechanisms that produce insertions and deletions that lead to clonal hematopoiesis are poorly understood. Here the authors show evidence that frequent deletions that are relevant to myeloid malignancies could be produced by PARP1-dependent microhomology-mediated end joining.

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Detalles Bibliográficos
Autores principales: Tzah Feldman, Akhiad Bercovich, Yoni Moskovitz, Noa Chapal-Ilani, Amanda Mitchell, Jessie J. F. Medeiros, Tamir Biezuner, Nathali Kaushansky, Mark D. Minden, Vikas Gupta, Michael Milyavsky, Zvi Livneh, Amos Tanay, Liran I. Shlush
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2021
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Science
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Acceso en línea:https://doaj.org/article/5cd49203803b4c6e921be0f40f64c457
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Descripción
Sumario:The mutational mechanisms that produce insertions and deletions that lead to clonal hematopoiesis are poorly understood. Here the authors show evidence that frequent deletions that are relevant to myeloid malignancies could be produced by PARP1-dependent microhomology-mediated end joining.

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