Evidence map›Paper›PMID 24691426›Full record

ReviewBritish journal of cancer2014

Prevalence and implications of elevated microsatellite alterations at selected tetranucleotides in cancer.

M M C Watson, M Berg, K Søreide

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. The Role of Novel Bladder Cancer Diagnostic and Surveillance Biomarkers-What Should a Urologist Really Know?International journal of environmental research and public health · 2022
    Review
  4. Article
  5. Article
  6. Biomarkers and intermediate-high risk non-muscle invasive bladder cancer: a multivariate analysis of three different cellular pathways with pronostic implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Observational
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Mismatch Repair Pathway, Genome Stability and Cancer.Frontiers in molecular biosciences · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

M M C Watson1] Department of Gastrointestinal Surgery, Stavanger University Hospital, Stavanger 4068, Norway [2] Gastrointestinal Surgical Research Unit, Molecular Lab, Hillevåg, Stavanger University Hospital, Stavanger 4068, Norway.
M Berg1] Department of Gastrointestinal Surgery, Stavanger University Hospital, Stavanger 4068, Norway [2] Gastrointestinal Surgical Research Unit, Molecular Lab, Hillevåg, Stavanger University Hospital, Stavanger 4068, Norway [3] Centre of Organelle Research, University of Stavanger, Stavanger 4068, Norway.
K Søreide1] Department of Gastrointestinal Surgery, Stavanger University Hospital, Stavanger 4068, Norway [2] Gastrointestinal Surgical Research Unit, Molecular Lab, Hillevåg, Stavanger University Hospital, Stavanger 4068, Norway [3] Department of Clinical Medicine, University of Bergen, Bergen 5020, Norway.
Stavanger University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated microsatellite alterations at selected tetranucleotides (EMAST), a variation of microsatellite instability (MSI), has been reported in a variety of malignancies (e.g., neoplasias of the lung, head and neck, colorectal region, skin, urinary tract and reproductive organs). EMAST is more prominent at organ sites with potential external exposure to carcinogens (e.g., head, neck, lung, urinary bladder and colon), although the specific molecular mechanisms leading to EMAST remain elusive. Because it is often associated with advanced stages of malignancy, EMAST may be a consequence of rapid cell proliferation and increased mutagenesis. Moreover, defects in DNA mismatch repair enzyme complexes, TP53 mutation status and peritumoural inflammation involving T cells have been described in EMAST tumours. At various tumour sites, EMAST and high-frequency MSI share no clinicopathological features or molecular mechanisms, suggesting their existence as separate entities. Thus EMAST should be explored, because its presence in human cells may reflect both increased risk and the potential for early detection. In particular, the potential use of EMAST in prognosis and prediction may yield novel types of therapeutic intervention, particularly those involving the immune system. This review will summarise the current information concerning EMAST in cancer to highlight the knowledge gaps that require further research.

Indexed as

Early Detection of CancerHumansMicrosatellite InstabilityMicrosatellite RepeatsNeoplasmsPrevalencePrognosis

Identifiers

PMID24691426
PMCPMC4150258
OpenAlexW2098074852

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.