Evidence map›Paper›PMID 28066040›Full record

ArticleTransactions of the American Clinical and Climatological Association2016

HEREDITARY, SPORADIC AND METASTATIC COLORECTAL CANCER ARE COMMONLY DRIVEN BY SPECIFIC SPECTRUMS OF DEFECTIVE DNA MISMATCH REPAIR COMPONENTS.

John M Carethers

Open access · greenAbstract read
In one paragraph

Article in Transactions of the American Clinical and Climatological Association, 2016. 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
2.0field-weighted citation impact, top 14% 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, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. THE JEREMIAH METZGER LECTURE: ENVIRONMENTAL INFLUENCES ON COLORECTAL CANCER.Transactions of the American Clinical and Climatological Association · 2024
    Article
  6. Review
  7. Development and evaluation of INTFrontiers in oncology · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  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

1 author.

John M CarethersANN ARBOR, MICHIGAN.

Funding

MICROSATELLITE INSTABILITY &DNA MISMATCH REPAIR SYSTEMR01DK067287 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARETHERS, JOHN M · 2005 to 2015
$3.2M
Inflammatory Differentiation of Colorectal Cancer Among African AmericansU01CA162147 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARETHERS, JOHN M · 2012 to 2016
$1.4M
NCI NIH HHS U01 CA162147NIDDK NIH HHS R01 DK067287
6 · The paper itself

Abstract

DNA mismatch repair (MMR) is one of several human cell mechanisms utilized to repair mutable mistakes within DNA, particularly after DNA is replicated. MMR function is dependent upon heterodimerization of specific MMR proteins that can recognize base-base mispairs as well as frameshifts at microsatellite sequences, followed by the triggering of other complementary proteins that execute excision and repair or initiate cell demise if repair is futile. MMR function is compromised in specific disease states, all of which can be biochemically recognized by faulty repair of microsatellite sequences, causing microsatellite instability. Germline mutation of an MMR gene causes Lynch syndrome, the most common inherited form of colorectal cancer (CRC), and biallelic germline mutations cause the rare constitutional mismatch repair deficiency syndrome. Somatic inactivation of MMR through epigenetic mechanisms is observed in 15% of sporadic CRC, and a smaller portion of CRCs possess biallelic somatic mutations. A novel inflammation-driven nuclear-to-cytoplasmic shift of the specific MMR protein hMSH3 is seen in up to 60% of sporadic CRCs that associates with metastasis and poor patient prognosis, unlike improved outcome when MMR is genetically inactivated. The mechanism for MMR inactication as well as the component affected dictates the clinical spectrum and clinical response for patients.

Indexed as

DNA Mismatch RepairGerm-Line MutationMicrosatellite InstabilityColorectal NeoplasmsColorectal Neoplasms, Hereditary NonpolyposisHumansMutS Homolog 3 ProteinMSH3 protein, humanMutS Homolog 3 Protein

Identifiers

PMID28066040
PMCPMC5216503
OpenAlexW2572627324

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.