Evidence map›Paper›PMID 20807115›Full record

ReviewCritical reviews in biochemistry and molecular biology2010

The Fanconi anemia pathway and ICL repair: implications for cancer therapy.

Lily C Wang, Jean Gautier

Open access · greenAbstract readReview
In one paragraph

Review in Critical reviews in biochemistry and molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

34 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025
    Review
  6. Review
  7. Review
  8. DNA Damage Responses, the Trump Card of Stem Cells in the Survival Game.Advances in experimental medicine and biology · 2024
    Review
  9. Article
  10. Article
  11. FANCL supports Parkin-mediated mitophagy in a ubiquitin ligase-independent manner.Biochimica et biophysica acta. Molecular basis of disease · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. DNA repair fidelity in stem cell maintenance, health, and disease.Biochimica et biophysica acta. Molecular basis of disease · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Lily C WangInstitute for Cancer Genetics, Columbia University, New York, NY 10032, USA.
Jean Gautier
Cancer Genetics (United States) · USColumbia University · US

Funding

Regulation of the DNA damage response by the MRN-ATM pathwayR01CA092245 · NCI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GAUTIER, JEAN · 2002 to 2015
$4.0M
Regulation of DNA Replication by MCM ProteinsR01GM077495 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GAUTIER, JEAN · 2008 to 2011
$1.4M
NCI NIH HHS CA92245NCI NIH HHS R01 CA092245NIGMS NIH HHS GM 077495NIGMS NIH HHS R01 GM077495
6 · The paper itself

Abstract

Fanconi anemia (FA) is an inherited disease caused by mutations in at least 13 genes and characterized by genomic instability. In addition to displaying strikingly heterogenous clinical phenotypes, FA patients are exquisitely sensitive to treatments with crosslinking agents that create interstrand crosslinks (ICL). In contrast to bacteria and yeast, in which ICLs are repaired through replication-dependent and -independent mechanisms, it is thought that ICLs are repaired primarily during DNA replication in vertebrates. However, recent data indicate that replication-independent ICL repair also operates in vertebrates. While the precise role of the FA pathway in ICL repair remains elusive, increasing evidence suggests that FA proteins function at different steps in the sensing, recognition and processing of ICLs, as well as in signaling from these very toxic lesions, which can be generated by a wide variety of cancer chemotherapeutic drugs. Here, we discuss some of the recent findings that have shed light on the role of the FA pathway in ICL repair, with special emphasis on the implications of these findings for cancer therapy since disruption of FA genes have been associated with cancer predisposition.

Indexed as

DNA RepairAnimalsDNA ReplicationFanconi AnemiaFanconi Anemia Complementation Group ProteinsHumansModels, BiologicalNeoplasmsSignal TransductionFanconi Anemia Complementation Group Proteins

Identifiers

PMID20807115
PMCPMC3108053
OpenAlexW1971646622

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.