Fanconi anemia and the cell cycle: New perspectives on aneuploidy

Grzegorz Nalepa, D. Wade Clapp

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

Fanconi anemia (FA) is a complex heterogenic disorder of genomic instability, bone marrow failure, cancer predisposition, and congenital malformations. The FA signaling network orchestrates the DNA damage recognition and repair in interphase as well as proper execution of mitosis. Loss of FA signaling causes chromosome instability by weakening the spindle assembly checkpoint, disrupting centrosome maintenance, disturbing resolution of ultrafine anaphase bridges, and dysregulating cytokinesis. Thus, the FA genes function as guardians of genome stability throughout the cell cycle. This review discusses recent advances in diagnosis and clinical management of Fanconi anemia and presents the new insights into the origins of genomic instability in FA. These new discoveries may facilitate the development of rational therapeutic strategies for FA and for FA-deficient malignancies in the general population.

Original languageEnglish (US)
JournalF1000Prime Reports
Volume6
DOIs
StatePublished - Apr 1 2014

ASJC Scopus subject areas

  • Medicine(all)

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