Evidence map›Paper›PMID 23729655›Full record

ArticleCarcinogenesis2013

Suppression of colon carcinogenesis by targeting Notch signaling.

Shingo Miyamoto, Masako Nakanishi, Daniel W Rosenberg

Open access · bronzeAbstract read
In one paragraph

Article in Carcinogenesis, 2013. 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
2.2field-weighted citation impact, top 12% 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, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Genomic Landscape of Meningiomas.Advances in experimental medicine and biology · 2023
    Article
  5. Reposition of the anti-inflammatory drug diacerein in anSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. b-Annulated 1,4-dihydropyridines as Notch inhibitors.Bioorganic & medicinal chemistry letters · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  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

3 authors at 1 institution in 1 country.

Shingo MiyamotoCenter for Molecular Medicine, University of Connecticut Health Center, 263 Farmington Avenue, Farmington, CT 06030-3103, USA.
Masako Nakanishi
Daniel W Rosenberg
UConn Health · US

Funding

Using Mouse Endoscopy for Evaluating Colon CancerR01CA125691 · NCI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI ROSENBERG, DANIEL WILLIAM · 2008 to 2012
$1.8M
NCI NIH HHS CA125691
6 · The paper itself

Abstract

Recent studies have shown that aberrant Notch signaling contributes to the pathogenesis of colorectal cancer (CRC). However, the potential therapeutic benefits of Notch pathway inhibitors, including gamma-secretase inhibitors (GSIs) on colon carcinogenesis are still unclear. In this study, the effects of the GSI, N-[N-3,5-difluorophenacetyl]-L-alanyl-S-phenylglycine methyl ester (DAPM) on colon carcinogenesis were investigated. In vitro, DAPM suppressed cell proliferation and induced the expression of Krüppel-like factor 4 (KLF4) and p21 in human colon cancer cells. Interestingly, p21-null HCT 116 cells were largely resistant to the suppressive effects of DAPM on cell proliferation compared with the parental cells. To investigate the effects of DAPM in vivo, colonoscopy was performed to establish the presence of colon tumors 9 weeks after azoxymethane treatment. After tumors were identified, mice were injected intraperitoneally every other day with either DAPM or vehicle for 4 weeks. The frequency of both large (>4mm) and small (<1mm) colon tumors was significantly reduced by DAPM treatment. Colon tumors in the DAPM-treated mice displayed increased levels of KLF4 and p21, accompanied by reduced Ki-67 staining compared with controls. Notably, in human colon tumor biopsies, KLF4 and p21 expressions were present within hyperplastic polyps, but the levels of both proteins were markedly reduced in tubular adenomas. Our results suggest that inhibition of Notch signaling by DAPM provides a potential chemopreventive strategy for patients with tubular adenomas, in part via activation of the KLF4-p21 axis.

Indexed as

Signal TransductionAmyloid Precursor Protein SecretasesAnimalsCarcinogenesisCell Line, TumorCell ProliferationColonic NeoplasmsColonic PolypsGene Expression Regulation, NeoplasticHumansKi-67 AntigenKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMiceNeoplasms, ExperimentalAmyloid Precursor Protein SecretasesDAPMKi-67 AntigenKLF4 protein, humanKlf4 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsPhenylalanineProto-Oncogene Proteins p21(ras)Receptors, Notch

Identifiers

PMID23729655
PMCPMC3786381
OpenAlexW2150059780

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.