Evidence map›Paper›PMID 14724591›Full record

ArticleOncogene2004

PTEN mutations are common in sporadic microsatellite stable colorectal cancer.

Najah T Nassif, Glenn P Lobo, Xiaojuan Wu, Christopher J A Henderson, Carl D Morrison, Charis Eng, Bin Jalaludin, Eva Segelov

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 3 pooled it
2.9field-weighted citation impact, top 9% 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

62 citing papers in PubMed, 3 syntheses or guidelines pooled it, 153 citations in OpenAlex.

  1. Molecular Biomarkers for the Evaluation of Colorectal Cancer.American journal of clinical pathology · 2017
    Guideline
  2. Guideline
  3. Pooled it
  4. Trial
  5. Trial
  6. Trial
  7. Article
  8. Obesity-Associated Colorectal Cancer.International journal of molecular sciences · 2024
    Review
  9. Cancers · 2023
    Review
  10. Review
  11. Article
  12. Review
  13. Toward Systems Pathology for PTEN Diagnostics.Cold Spring Harbor perspectives in medicine · 2020
    Review
  14. Article
  15. Precise Immunodetection of PTEN Protein in Human Neoplasia.Cold Spring Harbor perspectives in medicine · 2019
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

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

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

8 authors at 4 institutions in 3 countries.

Najah T NassifCancer Research Laboratories, South West Sydney Clinical School, University of New South Wales, Liverpool Hospital, Liverpool, NSW 2170, Australia. Najah.Nassif@uts.edu.au
Glenn P Lobo
Xiaojuan Wu
Christopher J A Henderson
Carl D Morrison
Charis Eng
Bin Jalaludin
Eva Segelov
Liverpool Hospital · AUUNSW Sydney · AUCancer Research UK Cambridge Center · GBThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The tumour suppressor gene PTEN, located at chromosome sub-band 10q23.3, encodes a dual-specificity phosphatase that negatively regulates the phosphatidylinositol 3'-kinase (PI3 K)/Akt-dependent cellular survival pathway. PTEN is frequently inactivated in many tumour types including glioblastoma, prostate and endometrial cancers. While initial studies reported that PTEN gene mutations were rare in colorectal cancer, more recent reports have shown an approximate 18% incidence of somatic PTEN mutations in colorectal tumours exhibiting microsatellite instability (MSI+). To verify the role of this gene in colorectal tumorigenesis, we analysed paired normal and tumour DNA from 41 unselected primary sporadic colorectal cancers for PTEN inactivation by mutation and/or allelic loss. We now report PTEN gene mutations in 19.5% (8/41) of tumours and allele loss, including all or part of the PTEN gene, in a further 17% (7/41) of the cases. Both PTEN alleles were affected in over half (9/15) of these cases showing PTEN genetic abnormalities. Using immunohistochemistry, we have further shown that all tumours harbouring PTEN alterations have either reduced or absent PTEN expression and this correlated strongly with later clinical stage of tumour at presentation (P=0.02). In contrast to previous reports, all but one of the tumours with PTEN gene mutations were microsatellite stable (MSI-), suggesting that PTEN is involved in a distinct pathway of colorectal tumorigenesis that is separate from the pathway of mismatch repair deficiency. This work therefore establishes the importance of PTEN in primary sporadic colorectal cancer.

Indexed as

AllelesBase SequenceColorectal NeoplasmsDNA Mutational AnalysisGenomic InstabilityHumansLoss of HeterozygosityMicrosatellite RepeatsMutationPhosphoric Monoester HydrolasesPTEN PhosphohydrolaseTumor Suppressor ProteinsPhosphoric Monoester HydrolasesPTEN PhosphohydrolasePTEN protein, humanTumor Suppressor Proteins

Identifiers

PMID14724591
OpenAlexW2040602576

What OpenQuestion holds

Textmetadata
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.