Damage control and its costs: BM failure in Fanconi anemia stems from overactive p53/p21.
editorial · Level V
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- Record sourced from PubMed, PMID 22770237.
- Also identified by DOI 10.1016/j.stem.2012.06.013 and PMC identifier 3402214.
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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.
Medical subject headings
- Bone Marrow
- Cyclin-Dependent Kinase Inhibitor p21
- DNA Damage
- Fanconi Anemia
- Tumor Suppressor Protein p53