Cytokinesis failure and attenuation: new findings in Fanconi anemia
Philip J. Mason, Monica Bessler
Philip J. Mason, Monica Bessler
Published January 4, 2011; First published December 22, 2010
Citation Information: J Clin Invest. 2011;121(1):27-30. https://doi.org/10.1172/JCI45619.
View: Text | PDF
Category: Commentary

Cytokinesis failure and attenuation: new findings in Fanconi anemia

Abstract

The hallmarks of the rare inherited disorder Fanconi anemia (FA) are progressive bone marrow failure and susceptibility to cancer. The former is the major cause of death for patients with FA, as it usually occurs earlier in life than cancer development. Despite spectacular advances in unraveling the molecular details of FA, the origin of the bone marrow failure that is central to this condition for most patients has long been puzzling and controversial. Two studies recently published in the JCI, including one in this issue, will add to the debate. They also highlight the fact that studying rare disorders can elucidate important new clinical and biological principles.

Authors

Philip J. Mason, Monica Bessler

×

Figure 1

Cytokinesis failure in FA.

Options: View larger image (or click on image) Download as PowerPoint
Cytokinesis failure in FA. PICH-BLM UFBs are ultrafine DNA bridges that ...
PICH-BLM UFBs are ultrafine DNA bridges that have FANCD2-FANCI foci at their extremities and are most likely derived from unresolved replication intermediates. The paper by Vinciguerra et al. (7) shows that hematopoietic cells from patients with FA have an increased number of UFBs between daughter nuclei that may inhibit cytokinesis, leading to binucleated or multinucleated cells. These cells may undergo apoptosis, contributing to BMF, or may lead to genomic instability and malignancy.