Evidence map›Paper›PMID 21641392›Full record

ArticleThe American journal of pathology2011

A serrated colorectal cancer pathway predominates over the classic WNT pathway in patients with hyperplastic polyposis syndrome.

Karam S Boparai, Evelien Dekker, Mirjam M Polak, Alex R Musler, Susanne van Eeden, Carel J M van Noesel

Abstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. The role of APC in WNT pathway activation in serrated neoplasia.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018
    Article
  12. Sessile Serrated Polyps are Precursors of Colon Carcinomas With Deficient DNA Mismatch Repair.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2016
    Article
  13. Review
  14. The presence of CXCR4Oncoimmunology · 2016
    Article
  15. Serrated neoplasia-role in colorectal carcinogenesis and clinical implications.Nature reviews. Gastroenterology & hepatology · 2015
    Review
  16. Article
  17. MYH polyposis syndrome: clinical findings, genetics issues and management.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014
    Review
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Karam S BoparaiDepartment of Gastroenterology and Hepatology, Academic Medical Center, Amsterdam, The Netherlands.
Evelien Dekker
Mirjam M Polak
Alex R Musler
Susanne van Eeden
Carel J M van Noesel
Academic Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperplastic polyposis syndrome (HPS) is characterized by the presence of multiple colorectal serrated polyps and is associated with an increased colorectal cancer (CRC) risk. The mixture of distinct precursor lesion types and malignancies in HPS provides a unique model to study the canonical pathway and a proposed serrated CRC pathway in humans. To establish which CRC pathways play a role in HPS and to obtain new support for the serrated CRC pathway, we assessed the molecular characteristics of polyps (n = 84) and CRCs (n = 19) in 17 patients with HPS versus control groups of various sporadic polyps (n = 59) and sporadic microsatellite-stable CRCs (n = 16). In HPS and sporadic polyps, APC mutations were exclusively identified in adenomas, whereas BRAF mutations were confined to serrated polyps. Six of 19 HPS CRCs (32%) were identified in a serrated polyp. Mutation analysis performed in the CRC and the serrated component of these lesions showed identical BRAF mutations. One HPS CRC was located in an adenoma, both components harboring an identical APC mutation. Overall, 10 of 19 HPS CRCs (53%) carried a BRAF mutation versus none in control group CRCs (P = 0.001). Six BRAF-mutated HPS CRCs (60%) were microsatellite unstable owing to MLH1 methylation. These findings provide novel supporting evidence for the existence of a predominant serrated CRC pathway in HPS, generating microsatellite-stable and microsatellite-instable CRCs.

Indexed as

Signal TransductionAdultAgedbeta CateninCase-Control StudiesColonic PolypsColorectal NeoplasmsDNA Mutational AnalysisFemaleHumansHyperplasiaImmunohistochemistryMaleMicrosatellite InstabilityMiddle AgedProto-Oncogene Proteinsbeta CateninBRAF protein, humanCTNNB1 protein, humanKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)ras ProteinsWnt Proteins

Identifiers

PMID21641392
PMCPMC3124356
OpenAlexW2170780166

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.