Evidence map›Paper›PMID 34771661›Full record

ReviewCancers2021

ATM Kinase Dead: From Ataxia Telangiectasia Syndrome to Cancer.

Sabrina Putti, Alessandro Giovinazzo, Matilde Merolle, Maria Laura Falchetti, Manuela Pellegrini

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Assessing Determinants of Response to PARP Inhibition in GermlineInternational journal of molecular sciences · 2025
    Article
  6. Article
  7. Article
  8. Update on Recommendations for Cancer Screening and Surveillance in Children with Genomic Instability Disorders.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. Cancers · 2023
    Article
  13. Review
  14. Article
  15. Ataxia-Telangiectasia Mutated Loss of Heterozygosity in Melanoma.International journal of molecular sciences · 2022
    Article
  16. Review
  17. Review
  18. Review
  19. 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

5 authors at 1 institution in 1 country.

Sabrina PuttiInstitute of Biochemistry and Cell Biology, IBBC-CNR, Campus Adriano Buzzati Traverso, Via Ercole Ramarini, 32, Monterotondo Scalo, 00015 Rome, Italy.ORCID 0000-0003-3335-043X
Alessandro GiovinazzoInstitute of Biochemistry and Cell Biology, IBBC-CNR, Campus Adriano Buzzati Traverso, Via Ercole Ramarini, 32, Monterotondo Scalo, 00015 Rome, Italy.ORCID 0000-0003-4420-6257
Matilde MerolleInstitute of Biochemistry and Cell Biology, IBBC-CNR, Campus Adriano Buzzati Traverso, Via Ercole Ramarini, 32, Monterotondo Scalo, 00015 Rome, Italy.
Maria Laura FalchettiInstitute of Biochemistry and Cell Biology, IBBC-CNR, Campus Adriano Buzzati Traverso, Via Ercole Ramarini, 32, Monterotondo Scalo, 00015 Rome, Italy.ORCID 0000-0002-8755-0042
Manuela PellegriniInstitute of Biochemistry and Cell Biology, IBBC-CNR, Campus Adriano Buzzati Traverso, Via Ercole Ramarini, 32, Monterotondo Scalo, 00015 Rome, Italy.ORCID 0000-0001-6387-5187
Institute of Cell Biology and Neurobiology · IT

Funding

Italian Association for Cancer Research IG 23329Regione Lazio Prot N A0375-2020-36524
6 · The paper itself

Abstract

ATM is one of the principal players of the DNA damage response. This protein exerts its role in DNA repair during cell cycle replication, oxidative stress, and DNA damage from endogenous events or exogenous agents. When is activated, ATM phosphorylates multiple substrates that participate in DNA repair, through its phosphoinositide 3-kinase like domain at the 3'end of the protein. The absence of ATM is the cause of a rare autosomal recessive disorder called Ataxia Telangiectasia characterized by cerebellar degeneration, telangiectasia, immunodeficiency, cancer susceptibility, and radiation sensitivity. There is a correlation between the severity of the phenotype and the mutations, depending on the residual activity of the protein. The analysis of patient mutations and mouse models revealed that the presence of inactive ATM, named ATM kinase-dead, is more cancer prone and lethal than its absence.

Indexed as

ATMATM-KD and cancerATM kinase activityA-T patients

Identifiers

PMID34771661
PMCPMC8583659
OpenAlexW3209155670

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.