Evidence map›Paper›PMID 24975284›Full record

ReviewCancer science2014

Safely targeting cancer stem cells via selective catenin coactivator antagonism.

Heinz-Josef Lenz, Michael Kahn

Open access · goldAbstract readReview
In one paragraph

Review in Cancer science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

108 citing papers in PubMed, 176 citations in OpenAlex.

  1. Review
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  8. Emerging roles and biomarker potential of WNT6 in human cancers.Cell communication and signaling : CCS · 2024
    Review
  9. Review
  10. Article
  11. Wnt/β-catenin signaling pathway in liver biology and tumorigenesis.In vitro cellular & developmental biology. Animal · 2024
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
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  19. Review
  20. The emerging era of personalized medicine in advanced colorectal cancer.Journal of gastroenterology and hepatology · 2022
    Review

48 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Heinz-Josef LenzUSC Norris Comprehensive Cancer Center, USC Center for Molecular Pathways and Drug Discovery, University of Southern California, Los Angeles, California, USA.
Michael Kahn
University of Southern California · USUSC Norris Comprehensive Cancer Center · US

Funding

USC/NORRIS COMPREHENSIVE CANCER CENTER (CORE) SUPPORTP30CA014089 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI Fumito Ito · 1985 to 2026
$181.4M
Efficacy of Novel Wnt Modulator in Colon CancerR01CA166161 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAHN, MICHAEL, LENZ, HEINZ JOSEF · 2013 to 2017
$2.3M
Mechanisms of beta-catenin signaling in alveolar epithelial cell differentiationR01HL112638 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BOROK, ZEA, KAHN, MICHAEL · 2013 to 2016
$2.2M
Modulation of Wnt Signaling in Models of Multiple SclerosisR21NS074392 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI GILMORE, WENDY · 2012 to 2013
$444k
Innate enteric immunity during induced Paneth cell deficiencyR21AI105057 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI OUELLETTE, ANDRE J. · 2013 to 2014
$440k
NCI NIH HHS 1R01CA166161-01A1NCI NIH HHS P30 CA014089NCI NIH HHS R01 CA166161NHLBI NIH HHS 1R01 HL112638-01NIAID NIH HHS 1R21AI105057-01NINDS NIH HHS 1R21NS074392-01
6 · The paper itself

Abstract

Throughout our life, long-lived somatic stem cells (SSC) regenerate adult tissues both during homeostatic processes and repair after injury. The role of aberrant regulation of SSC has also recently gained prominence in the field of cancer research. Following malignant transformation, so termed cancer stem cells (CSC), endowed with the same properties as SSC (i.e. the ability to both self-renew and generate differentiated progenitors), play a major part in tumor initiation, therapy resistance and ultimately relapse. The same signaling pathways involved in regulating SSC maintenance are involved in the regulation of CSC. CSC exist in a wide array of tumor types, including leukemias, and brain, breast, prostate and colon tumors. Consequently, one of the key goals in cancer research over the past decade has been to develop therapeutic strategies to safely eliminate the CSC population without damaging the endogenous SSC population. A major hurdle to this goal lies in the identification of the key mechanisms that distinguish CSC from the normal endogenous tissue stem cells. This review will discuss the discovery of the specific CBP/catenin antagonist ICG-001 and the ongoing clinical development of the second generation CBP/catenin antagonist PRI-724. Importantly, specific CBP/catenin antagonists appear to have the ability to safely eliminate CSC by taking advantage of an intrinsic differential preference in the way SSC and CSC divide.

Indexed as

AnimalsAntineoplastic AgentsBridged Bicyclo Compounds, HeterocyclicCateninsGene Expression Regulation, NeoplasticHumansNeoplasmsNeoplastic Stem CellsPeptide FragmentsPyrimidinonesSialoglycoproteinsWnt Signaling PathwayAntineoplastic Agentsbone sialoprotein (35-62), humanBridged Bicyclo Compounds, HeterocyclicCateninsICG 001Peptide FragmentsPyrimidinonesSialoglycoproteinsAsymmetricCREB-binding proteinp300symmetricWnt/catenin

Identifiers

PMID24975284
PMCPMC4175086
OpenAlexW2069561533

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.