Evidence map›Paper›PMID 29376519›Full record

ReviewNature reviews. Cancer2018

Fanconi anaemia and cancer: an intricate relationship.

Grzegorz Nalepa, D Wade Clapp

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 248 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
248citing papers in PubMed, 1 pooled it
16.7field-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

248 citing papers in PubMed, 1 synthesis or guideline pooled it, 402 citations in OpenAlex.

  1. Pooled it
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  15. The Genetic and Molecular Analyses of Rare Candidate GermlineInternational journal of molecular sciences · 2026
    Article
  16. Double jeopardy: howFrontiers in cell and developmental biology · 2026
    Review
  17. Article
  18. Review
  19. The function of Mgs1/WRNIP1 in genome maintenance.Frontiers in molecular biosciences · 2026
    Review
  20. Review

188 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 2 institutions in 1 country.

Grzegorz NalepaDepartment of Pediatrics, Section of Pediatric Hematology-Oncology, Wells Center for Pediatric Research, Indiana University School of Medicine, 1044 W Walnut Street, R4-421, Indianapolis, Indiana 46202, USA.
D Wade ClappRiley Hospital for Children at Indiana University Health, 705 Riley Hospital Drive, Room 5900, Indianapolis, Indiana 46202, USA.
Indiana University Health · USIndiana University School of Medicine

Funding

Mitotic failure in Fanconi anemia: mechanisms and role in carcinogenesisR01HL132921 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI CLAPP, DAVID W · 2017 to 2020
$1.8M
NHLBI NIH HHS R01 HL132921
6 · The paper itself

Abstract

Fanconi anaemia (FA) is a genetic disorder that is characterized by bone marrow failure (BMF), developmental abnormalities and predisposition to cancer. Together with other proteins involved in DNA repair processes and cell division, the FA proteins maintain genome homeostasis, and germline mutation of any one of the genes that encode FA proteins causes FA. Monoallelic inactivation of some FA genes, such as FA complementation group D1 (FANCD1; also known as the breast and ovarian cancer susceptibility gene BRCA2), leads to adult-onset cancer predisposition but does not cause FA, and somatic mutations in FA genes occur in cancers in the general population. Carcinogenesis resulting from a dysregulated FA pathway is multifaceted, as FA proteins monitor multiple complementary genome-surveillance checkpoints throughout interphase, where monoubiquitylation of the FANCD2-FANCI heterodimer by the FA core complex promotes recruitment of DNA repair effectors to chromatin lesions to resolve DNA damage and mitosis. In this Review, we discuss how the FA pathway safeguards genome integrity throughout the cell cycle and show how studies of FA have revealed opportunities to develop rational therapeutics for this genetic disease and for malignancies that acquire somatic mutations within the FA pathway.

Indexed as

MutationBRCA1 ProteinBRCA2 ProteinCarcinoma, Squamous CellDNA RepairFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinGenetic Predisposition to DiseaseGenomic InstabilityHumansLeukemia, Myeloid, AcuteNeoplasmsBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanFANCD2 protein, humanFanconi Anemia Complementation Group D2 Protein

Identifiers

PMID29376519
OpenAlexW2784483500

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.