Evidence map›Paper›PMID 21430697›Full record

ReviewNature reviews. Cancer2011

PTEN loss in the continuum of common cancers, rare syndromes and mouse models.

M Christine Hollander, Gideon M Blumenthal, Phillip A Dennis

Erratum issuedOpen access · greenAbstract readReview
In one paragraph

Review in Nature reviews. Cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 465 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
465citing papers in PubMed, 3 pooled it
31.9field-weighted citation impact, top 1% 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

465 citing papers in PubMed, 3 syntheses or guidelines pooled it, 792 citations in OpenAlex.

  1. Pooled it
  2. The impact of PTEN deletion and ERG rearrangement on recurrence after treatment for prostate cancer: a systematic review and meta-analysis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020
    Pooled it
  3. Pooled it
  4. PIK3CB Inhibitor GSK2636771 in Cancers WithJCO precision oncology · 2025
    Trial
  5. Article
  6. Article
  7. Article
  8. Review
  9. PHLPP is neither a Phosphatase nor a Tumor Suppressor.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  10. Article
  11. Article
  12. Review
  13. The Role of CRISPR and Its Therapeutic Applications in Glioblastoma.International journal of molecular sciences · 2026
    Review
  14. Article
  15. Article
  16. The cross-talk between GSK-3β, RKIP, and PTEN as potential targets for therapeutic implications in cancer: a comprehensive insight.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2026
    Review
  17. Double jeopardy: howFrontiers in cell and developmental biology · 2026
    Review
  18. Article
  19. Article
  20. Review

405 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

M Christine HollanderMedical Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, USA.
Gideon M Blumenthal
Phillip A Dennis
National Cancer Institute · US

Funding

Development of Akt InhibitorsZIABC010450 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DENNIS, PHILLIP A. · 2009 to 2012
$4.0M
Signal Transduction Pathways that Promote Survival of Lung Cancer CellsZIASC010292 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI DENNIS, PHILLIP A. · 2009 to 2012
$4.0M
Development of Akt InhibitorsZ01BC010450 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DENNIS, PHILLIP A. · 2002 to 2008
$3.1M
Clinical Investigation of Signal Transduction InhibitorsZIABC010748 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI DENNIS, PHILLIP A. · 2009 to 2012
$2.0M
Intramural NIH HHS Z01 BC010450
6 · The paper itself

Abstract

PTEN is among the most frequently inactivated tumour suppressor genes in sporadic cancer. PTEN has dual protein and lipid phosphatase activity, and its tumour suppressor activity is dependent on its lipid phosphatase activity, which negatively regulates the PI3K-AKT-mTOR pathway. Germline mutations in PTEN have been described in a variety of rare syndromes that are collectively known as the PTEN hamartoma tumour syndromes (PHTS). Cowden syndrome is the best-described syndrome within PHTS, with approximately 80% of patients having germline PTEN mutations. Patients with Cowden syndrome have an increased incidence of cancers of the breast, thyroid and endometrium, which correspond to sporadic tumour types that commonly exhibit somatic PTEN inactivation. Pten deletion in mice leads to Cowden syndrome-like phenotypes, and tissue-specific Pten deletion has provided clues to the role of PTEN mutation and loss in specific tumour types. Studying PTEN in the continuum of rare syndromes, common cancers and mouse models provides insight into the role of PTEN in tumorigenesis and will inform targeted drug development.

Indexed as

Disease Models, AnimalAnimalsChromosomes, Human, Pair 10Genes, Tumor SuppressorGerm-Line MutationHumansMiceNeoplasmsPTEN PhosphohydrolaseSyndromePTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID21430697
PMCPMC6946181
OpenAlexW1996222881

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.