Evidence map›Paper›PMID 26217075›Full record

ReviewWorld journal of gastroenterology2015

CREB-binding protein, p300, butyrate, and Wnt signaling in colorectal cancer.

Michael Bordonaro, Darina L Lazarova

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in World journal of gastroenterology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. A Model of Butyrate Activity and Resistance in CRC.Journal of cellular and molecular medicine · 2025
    Review
  5. Article
  6. Review
  7. Multi-faceted regulation of CREB family transcription factors.Frontiers in molecular neuroscience · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. The Landscape of AhR Regulators and Coregulators to Fine-Tune AhR Functions.International journal of molecular sciences · 2021
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  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

2 authors at 1 institution in 1 country.

Michael BordonaroMichael Bordonaro, Darina L Lazarova, Department of Basic Sciences, The Commonwealth Medical College, Scranton, PA 18509, United States.
Darina L LazarovaMichael Bordonaro, Darina L Lazarova, Department of Basic Sciences, The Commonwealth Medical College, Scranton, PA 18509, United States.
Geisinger Commonwealth School of Medicine · US

Funding

Determination of the role of CBP and p300 mediated Wnt signaling on colonic cellsR15CA149589 · NCI · GEISINGER COMMONWEALTH SCHOOL OF MEDICINE · PI BORDONARO, MICHAEL · 2010 to 2010
$183k
NCI NIH HHS 1R15CA149589-01NCI NIH HHS R15 CA149589
6 · The paper itself

Abstract

This paper reviews the distinctive roles played by the transcriptional coactivators CREB-binding protein (CBP) and p300 in Wnt/β-catenin signaling and cell physiology in colorectal cancer (CRC). Specifically, we focus on the effects of CBP- and p300-mediated Wnt activity on (1) neoplastic progression; (2) the activities of butyrate, a breakdown product of dietary fiber, on cell signaling and colonic cell physiology; (3) the development of resistance to histone deacetylase inhibitors (HDACis), including butyrate and synthetic HDACis, in colonic cells; and (4) the physiology and number of cancer stem cells. Mutations of the Wnt/β-catenin signaling pathway initiate the majority of CRC cases, and we have shown that hyperactivation of this pathway by butyrate and other HDACis promotes CRC cell apoptosis. This activity by butyrate may in part explain the preventive action of fiber against CRC. However, individuals with a high-fiber diet may still develop neoplasia; therefore, resistance to the chemopreventive action of butyrate likely contributes to CRC. CBP or p300 may modify the ability of butyrate to influence colonic cell physiology since the two transcriptional coactivators affect Wnt signaling, and likely, its hyperactivation by butyrate. Also, CBP and p300 likely affect colonic tumorigenesis, as well as stem cell pluripotency. Improvement of CRC prevention and therapy requires a better understanding of the alterations in Wnt signaling and gene expression that underlie neoplastic progression, stem cell fate, and the development of resistance to butyrate and clinically relevant HDACis. Detailed knowledge of how CBP- and p300 modulate colonic cell physiology may lead to new approaches for anti-CRC prevention and therapeutics, particularly with respect to combinatorial therapy of CBP/p300 inhibitors with HDACis.

Indexed as

AnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsButyratesColorectal NeoplasmsCREB-Binding ProteinDrug Resistance, NeoplasmHistone AcetyltransferasesHistone Deacetylase InhibitorsHumansMolecular Targeted Therapyp300-CBP Transcription FactorsWnt Signaling PathwayAntineoplastic AgentsButyratesCREB-Binding ProteinCREBBP protein, humanHistone AcetyltransferasesHistone Deacetylase Inhibitorsp300-CBP Transcription FactorsButyrateColorectal cancerCREB-binding proteinp300Stem cellsWnt

Identifiers

PMID26217075
PMCPMC4507093
OpenAlexW1021332480

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.