Evidence map›Paper›PMID 26697201›Full record

ReviewJournal of gastrointestinal oncology2015

Implications of mismatch repair-deficient status on management of early stage colorectal cancer.

Hisato Kawakami, Aziz Zaanan, Frank A Sinicrope

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of gastrointestinal oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 3 pooled it
6.6field-weighted citation impact, top 2% 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

46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Molecular Biomarkers for the Evaluation of Colorectal Cancer.American journal of clinical pathology · 2017
    Guideline
  4. Article
  5. Review
  6. The Relationship Between DNA Mismatch Repair Status and Clinicopathologic Characteristics in Colon Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024
    Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Molecular Oncology in Management of Colorectal Cancer.Indian journal of surgical oncology · 2021
    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.

Hisato KawakamiMayo Clinic and Mayo Cancer Center, Rochester, MN 55905, USA.
Aziz ZaananMayo Clinic and Mayo Cancer Center, Rochester, MN 55905, USA.
Frank A SinicropeMayo Clinic and Mayo Cancer Center, Rochester, MN 55905, USA.
Mayo Clinic · US

Funding

Translational Research in Colon Cancer Prevention & TreatmentK05CA142885 · NCI · MAYO CLINIC ROCHESTER · PI SINICROPE, FRANK A. · 2009 to 2013
$808k
NCI NIH HHS K05 CA142885
6 · The paper itself

Abstract

For primary colorectal cancers (CRCs), tumor stage has been the best predictor of survival after resection and the key determinant of patient management. However, considerable stage-independent variability in clinical outcome is observed that is likely due to molecular heterogeneity. This is particularly important in early stage CRCs where patients can be cured by surgery alone and only a proportion derives benefit from adjuvant chemotherapy. Thus, the identification of molecular prognostic markers to supplement conventional pathologic staging systems has the potential to guide patient management and influence outcomes. CRC is a heterogeneous disease with molecular phenotypes reflecting distinct forms of genetic instability. The chromosomal instability pathway (CIN) is the most common phenotype, accounting for 85% of all sporadic CRCs. Alternatively, the microsatellite instability (MSI) phenotype represents ~15% of all CRCs and is caused by deficient DNA mismatch repair (MMR) as a consequence of germline mutations in MMR genes or, more commonly, epigenetic silencing of the MLH1 gene with frequent mutations in the BRAF oncogene. MSI tumors have distinct phenotypic features and are consistently associated with a better stage-adjusted prognosis compared with microsatellite stable (MSS) tumors. Among non-metastatic CRCs, the difference in prognosis between MSI and MSS tumors is larger for stage II than stage III patients. On the other hand, the predictive impact of MMR status for adjuvant chemotherapy remains a contentious issue in that most studies demonstrate a lack of benefit for 5-fluorouracil (5-FU)-based adjuvant chemotherapy in stage II MSI-H CRCs, whereas it remains unclear in MSI-H stage III tumors. Here, we describe the molecular aspects of the MMR system and discuss the implications of MMR-deficient/MSI-H status in the clinical management of patients with early stage CRC.

Indexed as

adjuvant chemotherapyColorectal cancer (CRC)microsatellite instability (MSI)mismatch repair (MMR)

Identifiers

PMID26697201
PMCPMC4671842
OpenAlexW2197899459

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.