Abstract
Fanconi anemia (FA) is a genetic disorder characterized by progressive bone marrow failure, increased susceptibility to leukemia and cancer, and genomic instabilities. Protein products encoded by 22 FA genes, identified till date, cooperate in a molecular pathway called the FA pathway to repair DNA interstrand cross-links induced by chemotherapeutic agents, such as mitomycin C and cisplatin. An accumulating number of studies have shown several new functional aspects of the FA pathway, particularly in the context of the pathogenesis of bone marrow failure. This review focuses on the following topics: (1) aldehydes as intrinsic interstrand cross-linkers; (2) cytokine-induced hematopoietic stress; (3) increased transforming growth factor-β signaling; (4) mitochondrial functions of FA proteins. These findings are expected to offer new therapeutic opportunities for bone marrow failure in FA.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
