Blood · 2003 · 780 citations · 43 references
Life SciencesGeneticsHematologyDna RepairMedical GeneticsNeoplasiaAnemiaBone Marrow Failure SyndromesDna Repair DefectsGenetic DisordersHereditary Cancer SyndromesRed Blood Cell DisordersAutosomal Recessive InheritanceCell Cycle Control ProteinsFanconi Anemia Core ComplexFanconi Anemia PathophysiologyFanconi Anemia Pathway DefectsGenetic Predisposition To CancerGermline Cancer Predisposition SyndromesInherited Bone Marrow Failure Syndromes
Fanconi anemia is an autosomal recessive disorder marked by cellular hypersensitivity to DNA cross‑linking agents, cancer predisposition, and a key role for FA proteins in DNA repair, recombination, and cell‑cycle control. The International Fanconi Anemia Registry prospectively collects data on FA patients, providing a large cohort to analyze the natural history of this rare, clinically heterogeneous disorder. Among 754 FA patients, 80 % developed bone marrow failure and 23 % had neoplasms (60 % hematologic, 40 % nonhematologic), with cumulative incidences of 90 %, 33 %, and 28 % by age 40, and multivariate analysis identified FANCC mutations and hematopoietic stem cell transplantation as poor‑risk factors, while complementation group C showed earlier BMF onset and worse survival.
Fanconi anemia (FA) is an autosomal recessive disorder characterized by cellular hypersensitivity to DNA cross-linking agents and cancer predisposition. Recent evidence for the interactions of ataxia-telangiectasia mutated protein ATM and breast cancer susceptibility proteins BRCA1 and BRCA2 (identified as FANCD1) with other known FA proteins suggests that FA proteins have a significant role in DNA repair/recombination and cell cycle control. The International Fanconi Anemia Registry (IFAR), a prospectively collected database of FA patients, allows us the unique opportunity to analyze the natural history of this rare, clinically heterogeneous disorder in a large number of patients. Of the 754 subjects in this study, 601 (80%) experienced the onset of bone marrow failure (BMF), and 173 (23%) had a total of 199 neoplasms. Of these neoplasms, 120 (60%) were hematologic and 79 (40%) were nonhematologic. The risk of developing BMF and hematologic and nonhematologic neoplasms increased with advancing age with a 90%, 33%, and 28% cumulative incidence, respectively, by 40 years of age. Univariate analysis revealed a significantly earlier onset of BMF and poorer survival for complementation group C compared with groups A and G; however, there was no significant difference in the time to hematologic or nonhematologic neoplasm development between these groups. Multivariate analysis of overall survival time shows that FANCC mutations (P =.007) and hematopoietic stem cell transplantation (P = <.0001) define a poor-risk subgroup. The results of this study of patients registered in the IFAR over a 20-year period provide information that will enable better prediction of outcome and aid clinicians with decisions regarding major therapeutic modalities.
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Cancer Risks in BRCA2 Mutation Carriers
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Interaction of the Fanconi Anemia Proteins and BRCA1 in a Common Pathway
Irene García-Higuera, Toshiyasu Taniguchi, Shridar Ganesan et al. · Molecular Cell · 2001 · 1.2K citations · Full text
Biallelic Inactivation of <i>BRCA2</i> in Fanconi Anemia
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