title: Damage control and its costs: BM failure in Fanconi anemia stems from overactive p53/p21.
abstract: Despite having well-characterized disease-associated mutations, the mechanisms underlying the progressive bone marrow failure and cancer susceptibility of Fanconi anemia have been unclear. In this issue of Cell Stem Cell, Ceccaldi et al. identify an overactive p53/p21 stress response and cell cycle arrest as an underlying cause that starts during fetal development.
authors: Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1202, USA.
authors: Bogdan
authors: B
authors: Dumitriu
authors: Neal S
authors: NS
authors: Young
mesh_terms: D000818:Animals; D001853:Bone Marrow / Q000473:pathology*; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism*; D004249:DNA Damage; D004195:Disease Models, Animal; D005199:Fanconi Anemia / Q000378:metabolism* / Q000473:pathology* / Q000628:therapy; D018380:Hematopoietic Stem Cell Transplantation; D006412:Hematopoietic Stem Cells / Q000473:pathology; D006801:Humans; D007938:Leukemia / Q000473:pathology; D051379:Mice; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D050759:Cyclin-Dependent Kinase Inhibitor p21; D016159:Tumor Suppressor Protein p53