Evidence map›Paper›PMID 23333482›Full record

ReviewMutation research

The Fanconi anemia pathway: repairing the link between DNA damage and squamous cell carcinoma.

Lindsey E Romick-Rosendale, Vivian W Y Lui, Jennifer R Grandis, Susanne I Wells

Open access · greenAbstract readReview
In one paragraph

Review in Mutation research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Skin cancer risk in hereditary mixed cancer syndromes.Hereditary cancer in clinical practice · 2025
    Review
  4. Article
  5. A RareGenes · 2022
    Article
  6. Review
  7. Post-hematopoietic stem cell transplant squamous cell carcinoma in patients with Fanconi anemia: a dreadful enemy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Lipidomic Profiling Links the Fanconi Anemia Pathway to Glycosphingolipid Metabolism in Head and Neck Cancer Cells.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  14. Article
  15. Article
  16. Review
  17. FANCD2 and DNA Damage.International journal of molecular sciences · 2017
    Review
  18. Article
  19. Review
  20. Review
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

4 authors at 3 institutions in 1 country.

Lindsey E Romick-RosendaleDivision of Oncology, Cancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.
Vivian W Y LuiDepartment of Otolaryngology, University of Pittsburgh School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Jennifer R GrandisDepartment of Otolaryngology, University of Pittsburgh School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Susanne I WellsDivision of Oncology, Cancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA. Electronic address: Susanne.Wells@cchmc.org.
University of Pittsburgh · USCincinnati Children's Hospital Medical Center · USUniversity of Cincinnati · US

Funding

WILD TYPE P53-BASED ADJUVANT IMMUNOTHERAPY FOR SCCHNP50CA097190 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Greg M. Delgoffe · 2004 to 2026
$49.6M
Papillomavirus Proteins Mediating Cancer and SenescenceR01CA102357 · NCI · CINCINNATI CHILDRENS HOSP MED CTR · PI WELLS, SUSANNE I · 2004 to 2013
$2.6M
NCI NIH HHS P50 CA097190NCI NIH HHS R01 CA102357
6 · The paper itself

Abstract

Fanconi anemia (FA) is a rare inherited recessive disease caused by mutations in one of fifteen genes known to encode FA pathway components. In response to DNA damage, nuclear FA proteins associate into high molecular weight complexes through a cascade of post-translational modifications and physical interactions, followed by the repair of damaged DNA. Hematopoietic cells are particularly sensitive to the loss of these interactions, and bone marrow failure occurs almost universally in FA patients. FA as a disease is further characterized by cancer susceptibility, which highlights the importance of the FA pathway in tumor suppression, and will be the focus of this review. Acute myeloid leukemia is the most common cancer type, often subsequent to bone marrow failure. However, FA patients are also at an extreme risk of squamous cell carcinoma (SCC) of the head and neck and gynecological tract, with an even greater incidence in those individuals who have received a bone marrow transplant and recovered from hematopoietic disease. FA tumor suppression in hematopoietic versus epithelial compartments could be mechanistically similar or distinct. Definition of compartment specific FA activities is now critical to assess the effects of today's bone marrow failure treatments on tomorrow's solid tumor development. It is our hope that current therapies can then be optimized to decrease the risk of malignant transformation in both hematopoietic and epithelial cells. Here we review our current understanding of the mechanisms of action of the Fanconi anemia pathway as it contributes to stress responses, DNA repair and squamous cell carcinoma susceptibility.

Indexed as

DNA DamageDNA RepairAnimalsCarcinoma, Squamous CellFanconi AnemiaGenetic Predisposition to DiseaseHumansProtein Processing, Post-Translational

Identifiers

PMID23333482
PMCPMC3661751
OpenAlexW2044535280

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.