Evidence map›Paper›PMID 19686080›Full record

ReviewAnnual review of genetics2009

How the fanconi anemia pathway guards the genome.

George-Lucian Moldovan, Alan D D'Andrea

Abstract readReview
In one paragraph

Review in Annual review of genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 356 papers.

0numbers the graph read from it
0cells of the map it votes in
356citing papers in PubMed
28.2field-weighted citation impact, top 1% 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

356 citing papers in PubMed, 593 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026
    Review
  7. Article
  8. Article
  9. The function of Mgs1/WRNIP1 in genome maintenance.Frontiers in molecular biosciences · 2026
    Review
  10. Article
  11. Review
  12. Mitomycin C-induced DNA double-strand breaks are enhanced by catalytical inactivation of DNA polymerase κ in mice.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025
    Article
  13. bioRxiv : the preprint server for biology · 2025
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

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

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

George-Lucian MoldovanDepartment of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA.
Alan D D'Andrea
Dana-Farber Cancer 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
SIGNAL TRANSDUCTION PATHWAYS IN STABLE PHASE CHRONIC MYELOID LEUKEMIA CELLSP01DK050654 · NIDDK · DANA-FARBER CANCER INSTITUTE · PI D'ANDREA, ALAN DAVID · 1996 to 2006
$10.3M
Genetic screens for IR resistanceU19AI067751 · NIAID · DANA-FARBER CANCER INSTITUTE · PI D'ANDREA, ALAN D. · 2005 to 2009
$9.9M
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 5P01CA092584NCI NIH HHS P01 CA092584NHLBI NIH HHS R01 HL052725NHLBI NIH HHS R01HL52725NHLBI NIH HHS R37 HL052725NIAID NIH HHS U19 AI067751NIDDK NIH HHS P01 DK050654NIDDK NIH HHS P01DK50654NIDDK NIH HHS R01 DK043889NIDDK NIH HHS R01DK43889PHS HHS U19A1067751
6 · The paper itself

Abstract

Fanconi Anemia (FA) is an inherited genomic instability disorder, caused by mutations in genes regulating replication-dependent removal of interstrand DNA crosslinks. The Fanconi Anemia pathway is thought to coordinate a complex mechanism that enlists elements of three classic DNA repair pathways, namely homologous recombination, nucleotide excision repair, and mutagenic translesion synthesis, in response to genotoxic insults. To this end, the Fanconi Anemia pathway employs a unique nuclear protein complex that ubiquitinates FANCD2 and FANCI, leading to formation of DNA repair structures. Lack of obvious enzymatic activities among most FA members has made it challenging to unravel its precise modus operandi. Here we review the current understanding of how the Fanconi Anemia pathway components participate in DNA repair and discuss the mechanisms that regulate this pathway to ensure timely, efficient, and correct restoration of chromosomal integrity.

Indexed as

DNA RepairMetabolic Networks and PathwaysAnimalsFanconi Anemia Complementation Group ProteinsGenomeHumansFanconi Anemia Complementation Group Proteins

Identifiers

PMID19686080
PMCPMC2830711
OpenAlexW2167844213

What OpenQuestion holds

Textmetadata
LicenceTDM
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.