Evidence map›Paper›PMID 34059798›Full record

ArticleCell death and differentiation2021

The PTEN and ATM axis controls the G1/S cell cycle checkpoint and tumorigenesis in HER2-positive breast cancer.

Christian Bassi, Jerome Fortin, Bryan E Snow, Andrew Wakeham, Jason Ho, Jillian Haight, Annick You-Ten, Emily Cianci, Luke Buckler, Chiara Gorrini and 2 more

Abstract read
In one paragraph

Article in Cell death and differentiation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. PTEN: an emerging target in rheumatoid arthritis?Cell communication and signaling : CCS · 2024
    Review
  10. Article
  11. Review
  12. Review
  13. The effects of the tumor suppressor geneTranslational cancer research · 2023
    Article
  14. Review
  15. 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

12 authors.

Christian BassiPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.
Jerome FortinPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.
Bryan E SnowPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.
Andrew WakehamPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.
Jason HoPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.
Jillian HaightPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.
Annick You-TenPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.
Emily CianciPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.ORCID http://orcid.org/0000-0003-3719-6679
Luke BucklerPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.
Chiara GorriniPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.ORCID http://orcid.org/0000-0002-5239-6671
Vuk StambolicPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada.
Tak W MakPrincess Margaret Cancer Centre, University Health Network, 610 University Ave, Toronto, ON, M5G 2C1, Canada. tak.mak@uhnresearch.ca.ORCID http://orcid.org/0000-0001-6766-861X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumor suppressor PTEN is disrupted in a large proportion of cancers, including in HER2-positive breast cancer, where its loss is associated with resistance to therapy. Upon genotoxic stress, ataxia telangiectasia mutated (ATM) is activated and phosphorylates PTEN on residue 398. To elucidate the physiological role of this molecular event, we generated and analyzed knock-in mice expressing a mutant form of PTEN that cannot be phosphorylated by ATM (PTEN-398A). This mutation accelerated tumorigenesis in a model of HER2-positive breast cancer. Mammary tumors in bi-transgenic mice carrying MMTV-neu and Pten

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsBreast NeoplasmsCarcinogenesisCell CycleCell Cycle CheckpointsFemaleHumansMammary Neoplasms, AnimalMicePTEN PhosphohydrolaseTumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsPTEN PhosphohydrolasePten protein, mouseTumor Suppressor Proteins

Identifiers

PMID34059798
PMCPMC8564521

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.