Evidence map›Paper›PMID 19745699›Full record

ArticleThe American journal of surgical pathology2009

Beta-catenin nuclear labeling is a common feature of sessile serrated adenomas and correlates with early neoplastic progression after BRAF activation.

Shinichi Yachida, Shiyama Mudali, Sherri A Martin, Elizabeth A Montgomery, Christine A Iacobuzio-Donahue

Abstract read
In one paragraph

Article in The American journal of surgical pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.9field-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

47 citing papers in PubMed, 105 citations in OpenAlex.

  1. Article
  2. BRAFCommunications biology · 2023
    Article
  3. Article
  4. Article
  5. Article
  6. Evolving pathologic concepts of serrated lesions of the colorectum.Journal of pathology and translational medicine · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Calcium and vitamin D in the serrated neoplastic pathway: Friends or foes?World journal of gastrointestinal pathophysiology · 2018
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. 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
  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

5 authors at 2 institutions in 1 country.

Shinichi YachidaDepartment of Pathology, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA.
Shiyama Mudali
Sherri A Martin
Elizabeth A Montgomery
Christine A Iacobuzio-Donahue
Johns Hopkins University · USUniversity of Michigan–Ann Arbor · US

Funding

TARGETS OF METASTATIC PANCREATIC CANCERK08CA106610 · NCI · JOHNS HOPKINS UNIVERSITY · PI IACOBUZIO-DONAHUE, CHRISTINE A · 2004 to 2008
$701k
NCI NIH HHS CA106610NCI NIH HHS K08 CA106610
6 · The paper itself

Abstract

Recent observations indicate that some sessile serrated adenomas (SSAs) have aberrant beta-catenin nuclear labeling, implicating the Wnt pathway in the molecular progression of SSAs to colorectal carcinoma. We sought to expand upon this finding by characterizing beta-catenin expression in the full spectrum of serrated colorectal polyps, and correlating these findings with the genetic status of BRAF, KRAS and CTNNB1. Immunolabeling for beta-catenin confirmed the presence of abnormal nuclear accumulation in SSAs, with 35/54 (67%) SSAs showing nuclear labeling compared with 0/12 hyperplastic polyps. Abnormal nuclear labeling was also identified in 4/11 (36%) traditional serrated adenomas (TSAs) (P=0.00001). When SSAs were further analyzed with respect to the presence or absence of conventional epithelial dysplasia, nuclear beta-catenin labeling was seen in 8/27 (29%) SSAs without dysplasia (SSA) but in 27/27 (100%) of SSAs with dysplasia (P=0.000001). Sequencing of genomic DNA extracted from a subset of hyperplastic polyps, SSAs, SSAs with dysplasia, TSAs and tubular adenomas failed to identify any CTNNB1 mutations to account for abnormal beta-catenin nuclear labeling. However, abnormal nuclear labeling always occurred in the setting of a BRAF V600E mutation, indicating aberrant nuclear labeling occurs on a background of BRAF activation. Of interest, all 6 TSAs contained a KRAS mutation confirming that SSAs and TSAs are genetically distinct entities. These findings validate previous reports implicating activation of the Wnt signaling pathway in SSAs, and further indicate that Wnt pathway activation plays a role in the neoplastic progression of SSAs and TSAs to colonic carcinoma by mechanisms independent of CTNNB1 mutation.

Indexed as

Transcriptional ActivationAdenomaAgedBase Sequencebeta CateninCell NucleusCell Transformation, NeoplasticColonic PolypsColorectal NeoplasmsDNA Mutational AnalysisFemaleHumansHyperplasiaImmunohistochemistryMaleMiddle Agedbeta CateninBRAF protein, humanCTNNB1 protein, humanKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins B-rafProto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID19745699
PMCPMC2788075
OpenAlexW1985575478

What OpenQuestion holds

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LicenceTDM
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.