Evidence map›Paper›PMID 23806336›Full record

ArticleMolecular cell2013

FANCD2 activates transcription of TAp63 and suppresses tumorigenesis.

Eunmi Park, Hyungjin Kim, Jung Min Kim, Benjamin Primack, Sofia Vidal-Cardenas, Ye Xu, Brendan D Price, Alea A Mills, Alan D D'Andrea

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  8. Oh, the Mutations You'll Acquire! A Systematic Overview of Cutaneous Squamous Cell Carcinoma.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2021
    Review
  9. Nutrients · 2021
    Article
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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

9 authors at 2 institutions in 1 country.

Eunmi ParkDepartment of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, 450 Brookline Avenue, Boston, MA 02215, USA.
Hyungjin Kim
Jung Min Kim
Benjamin Primack
Sofia Vidal-Cardenas
Ye Xu
Brendan D Price
Alea A Mills
Alan D D'Andrea
Harvard University · USCold Spring Harbor Laboratory · US

Funding

Transcription-Coupled & Replication-Associated Excision RepairP01CA092584 · NCI · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI John A. Tainer · 2001 to 2026
$89.6M
Xenograft CoreP01HL048546 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI FLEMING, WILLIAM H · 1994 to 2020
$36.4M
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
RADIATION MODULATION OF THE P53 GENER01CA064585 · NCI · DANA-FARBER CANCER INSTITUTE · PI PRICE, BRENDAN D · 1995 to 2016
$4.6M
Nucleosome Dynamics and the Repair of DNA DamageR01CA177884 · NCI · DANA-FARBER CANCER INST · PI PRICE, BRENDAN D · 2013 to 2017
$1.8M
NCI NIH HHS P01 CA092584NCI NIH HHS R01 CA064585NCI NIH HHS R01 CA177884NHLBI NIH HHS P01HL048546NHLBI NIH HHS R01 HL052725NHLBI NIH HHS R01HL52725NIDDK NIH HHS R01 DK043889NIDDK NIH HHS R01DK43889
6 · The paper itself

Abstract

Fanconi anemia (FA) is a rare genetic disorder characterized by an increased susceptibility to squamous cell cancers. Fifteen FA genes are known, and the encoded proteins cooperate in a common DNA repair pathway. A critical step is the monoubiquitination of the FANCD2 protein, and cells from most FA patients are deficient in this step. How monoubiquitinated FANCD2 suppresses squamous cell cancers is unknown. Here we show that Fancd2-deficient mice are prone to Ras-oncogene-driven skin carcinogenesis, while Usp1-deficient mice, expressing elevated cellular levels of Fancd2-Ub, are resistant to skin tumors. Moreover, Fancd2-Ub activates the transcription of the tumor suppressor TAp63, thereby promoting cellular senescence and blocking skin tumorigenesis. For FA patients, the reduction of FANCD2-Ub and TAp63 protein levels may account for their susceptibility to squamous cell neoplasia. Taken together, Usp1 inhibition may be a useful strategy for upregulating TAp63 and preventing or treating squamous cell cancers in the general non-FA population.

Indexed as

Genes, Tumor SuppressorTranscriptional ActivationAnimalsArabidopsis ProteinsCell ProliferationCells, CulturedCell Transformation, NeoplasticCellular SenescenceDisease ResistanceDNA DamageEndopeptidasesFanconi AnemiaFanconi Anemia Complementation Group D2 ProteinFemaleGenes, rasGenetic Predisposition to DiseaseArabidopsis ProteinsEndopeptidasesFancd2 protein, mouseFanconi Anemia Complementation Group D2 ProteinPhosphoproteinsTrans-ActivatorsTrp63 protein, mouseUbiquitin-Specific ProteasesUSP1 protein, humanUsp1 protein, mouse

Identifiers

PMID23806336
PMCPMC3897475
OpenAlexW2137101709

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.