Evidence map›Paper›PMID 32866776›Full record

ReviewDNA repair2020

Roles for MDC1 in cancer development and treatment.

Sophie E Ruff, Susan K Logan, Michael J Garabedian, Tony T Huang

Open access · greenAbstract readReview
In one paragraph

Review in DNA repair, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Rare, Yet Targetable: New Perspectives on Ampullary Carcinomas.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. A perspective on tumor radiation resistance following high-LET radiation treatment.Journal of cancer research and clinical oncology · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

4 authors at 1 institution in 1 country.

Sophie E RuffDepartment of Microbiology, New York University School of Medicine, New York, NY, 10016, USA; Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY, 10016, USA.
Susan K LoganDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY, 10016, USA; Department of Urology, New York University School of Medicine, New York, NY, 10016, USA.
Michael J GarabedianDepartment of Microbiology, New York University School of Medicine, New York, NY, 10016, USA; Department of Urology, New York University School of Medicine, New York, NY, 10016, USA. Electronic address: michael.garabedian@nyulangone.org.
Tony T HuangDepartment of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, NY, 10016, USA. Electronic address: Tony.Huang@nyulangone.org.
New York University · US

Funding

TRAINING PROGRAM IN MOLECULAR ONCOLOGY &IMMUNOLOGYT32CA009161 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI CARROLL, WILLIAM L., LEVY, DAVID E · 1985 to 2020
$13.3M
Medical Scientist Research Service AwardT32GM136573 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI SULMAN, ERIK · 2020 to 2024
$6.8M
Role of Deubiquitination in Fanconi Anemia Cancer Susceptibility PathwayR01GM084244 · NIGMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, TONY TUNG · 2009 to 2013
$2.3M
Mechanisms of reversible DUB oxidation in genome stability pathways - RevisionR01ES025166 · NIEHS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HUANG, TONY TUNG · 2015 to 2020
$2.3M
NCI NIH HHS T32 CA009161NIEHS NIH HHS R01 ES025166NIGMS NIH HHS R01 GM084244NIGMS NIH HHS T32 GM136573
6 · The paper itself

Abstract

The DNA damage response (DDR) is necessary to maintain genome integrity and prevent the accumulation of oncogenic mutations. Consequently, proteins involved in the DDR often serve as tumor suppressors, carrying out the crucial task of keeping DNA fidelity intact. Mediator of DNA damage checkpoint 1 (MDC1) is a scaffold protein involved in the early steps of the DDR. MDC1 interacts directly with γ-H2AX, the phosphorylated form of H2AX, a commonly used marker for DNA damage. It then propagates the phosphorylation of H2AX by recruiting ATM kinase. While the function of MDC1 in the DDR has been reviewed previously, its role in cancer has not been reviewed, and numerous studies have recently identified a link between MDC1 and carcinogenesis. This includes MDC1 functioning as a tumor suppressor, with its loss serving as a biomarker for cancer and contributor to drug sensitivity. Studies also indicate that MDC1 operates outside of its traditional role in DDR, and functions as a co-regulator of nuclear receptor transcriptional activity, and that mutations in MDC1 are present in tumors and can also cause germline predisposition to cancer. This review will discuss reports that link MDC1 to cancer and identify MDC1 as an important player in tumor formation, progression, and treatment. We also discuss mechanisms by which MDC1 levels are regulated and how this contributes to tumor formation.

Indexed as

CarcinogenesisAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsHumansMutationNeoplasmsTranscription, GeneticAdaptor Proteins, Signal TransducingCell Cycle ProteinsMDC1 protein, humanCancerDNA damage responseDNA damaging agentsMDC1Transcriptional co-regulatorγ-H2AX

Identifiers

PMID32866776
PMCPMC7669677
OpenAlexW3048843697

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.