Evidence map›Paper›PMID 20921626›Full record

ArticleThe Journal of clinical investigation2010

Cytokinesis failure occurs in Fanconi anemia pathway-deficient murine and human bone marrow hematopoietic cells.

Patrizia Vinciguerra, Susana A Godinho, Kalindi Parmar, David Pellman, Alan D D'Andrea

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
5.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

70 citing papers in PubMed, 114 citations in OpenAlex.

  1. Article
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  9. Article
  10. Review
  11. Article
  12. Type-I Interferon Signaling in Fanconi Anemia.Frontiers in cellular and infection microbiology · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. The Cockayne syndrome group A and B proteins are part of a ubiquitin-proteasome degradation complex regulating cell division.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  18. Review
  19. Fanconi anemia and the underlying causes of genomic instability.Environmental and molecular mutagenesis · 2020
    Review
  20. Review

10 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Patrizia VinciguerraDepartment of Radiation Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA.
Susana A Godinho
Kalindi Parmar
David Pellman
Alan D D'Andrea
Dana-Farber Cancer Institute · USHarvard University · USHoward Hughes Medical Institute · US

Funding

Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI John A. Tainer · 2001 to 2026
$89.6M
MOLECULAR PATHOGENESIS OF FANCONI ANEMIAR01HL052725 · NHLBI · DANA-FARBER CANCER INSTITUTE · PI ALAN D. D'ANDREA · 1994 to 2026
$5.9M
STRUCTURE AND FUNCTION OF THE ERYTHROPOIETIN RECEPTORR01DK043889 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI D'ANDREA, ALAN D. · 1992 to 2014
$5.3M
Molecular Pathogenesis of Fanconi AnemiaR37HL052725 · NHLBI · DANA-FARBER CANCER INSTITUTE · PI D'ANDREA, ALAN D. · 2004 to 2013
$3.9M
NCI NIH HHS P01 CA092584NCI NIH HHS P01CA092584NHLBI NIH HHS R01 HL052725NHLBI NIH HHS R01HL52725NHLBI NIH HHS R37 HL052725NIDDK NIH HHS R01 DK043889NIDDK NIH HHS R01DK43889
6 · The paper itself

Abstract

Fanconi anemia (FA) is a genomic instability disorder characterized by bone marrow failure and cancer predisposition. FA is caused by mutations in any one of several genes that encode proteins cooperating in a repair pathway and is required for cellular resistance to DNA crosslinking agents. Recent studies suggest that the FA pathway may also play a role in mitosis, since FANCD2 and FANCI, the 2 key FA proteins, are localized to the extremities of ultrafine DNA bridges (UFBs), which link sister chromatids during cell division. However, whether FA proteins regulate cell division remains unclear. Here we have shown that FA pathway-deficient cells display an increased number of UFBs compared with FA pathway-proficient cells. The UFBs were coated by BLM (the RecQ helicase mutated in Bloom syndrome) in early mitosis. In contrast, the FA protein FANCM was recruited to the UFBs at a later stage. The increased number of bridges in FA pathway-deficient cells correlated with a higher rate of cytokinesis failure resulting in binucleated cells. Binucleated cells were also detectable in primary murine FA pathway-deficient hematopoietic stem cells (HSCs) and bone marrow stromal cells from human patients with FA. Based on these observations, we suggest that cytokinesis failure followed by apoptosis may contribute to bone marrow failure in patients with FA.

Indexed as

AnimalsBone Marrow CellsCytokinesisFanconi AnemiaFanconi Anemia Complementation Group ProteinsHeLa CellsHematopoietic Stem CellsHumansMiceMice, KnockoutRecQ HelicasesRNA, Small InterferingSignal TransductionStromal CellsBloom syndrome proteinFanconi Anemia Complementation Group ProteinsRecQ HelicasesRNA, Small Interfering

Identifiers

PMID20921626
PMCPMC2964984
OpenAlexW2040083077

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.