Evidence map›Paper›PMID 26744320›Full record

ArticleOncotarget2016

Oncogenic KRAS activates an embryonic stem cell-like program in human colon cancer initiation.

Anne-France Le Rolle, Thang K Chiu, Zhaoshi Zeng, Jinru Shia, Martin R Weiser, Philip B Paty, Vi K Chiu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Oncogenes, Proto-Oncogenes, and Lineage Restriction of Cancer Stem Cells.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  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

7 authors at 3 institutions in 1 country.

Anne-France Le RolleDivision of Hematology/Oncology, Department of Medicine, University of California, Irvine, CA, USA.
Thang K ChiuDepartment of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, New Orleans, LA, USA.
Zhaoshi ZengDepartment of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Jinru ShiaDepartment of Pathology, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Martin R WeiserDepartment of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Philip B PatyDepartment of Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Vi K ChiuDivision of Hematology/Oncology, Department of Medicine, University of California, Irvine, CA, USA.
Memorial Sloan Kettering Cancer Center · USUniversity of California, Irvine · USLouisiana State University Health Sciences Center New Orleans · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Christine Hui · 1994 to 2026
$57.9M
NCI NIH HHS P01CA655930-05A2NCI NIH HHS P30 CA008748NCI NIH HHS P30 CA062203NCI NIH HHS P30CA062203
6 · The paper itself

Abstract

Colorectal cancer is the third most frequently diagnosed cancer worldwide. Prevention of colorectal cancer initiation represents the most effective overall strategy to reduce its associated morbidity and mortality. Activating KRAS mutation (KRASmut) is the most prevalent oncogenic driver in colorectal cancer development, and KRASmut inhibition represents an unmet clinical need. We apply a systems-level approach to study the impact of KRASmut on stem cell signaling during human colon cancer initiation by performing gene set enrichment analysis on gene expression from human colon tissues. We find that KRASmut imposes the embryonic stem cell-like program during human colon cancer initiation from colon adenoma to stage I carcinoma. Expression of miR145, an embryonic SC program inhibitor, promotes cell lineage differentiation marker expression in KRASmut colon cancer cells and significantly suppresses their tumorigenicity. Our data support an in vivo plasticity model of human colon cancer initiation that merges the intrinsic stem cell properties of aberrant colon stem cells with the embryonic stem cell-like program induced by KRASmut to optimize malignant transformation. Inhibition of the embryonic SC-like program in KRASmut colon cancer cells reveals a novel therapeutic strategy to programmatically inhibit KRASmut tumors and prevent colon cancer.

Indexed as

3T3 CellsAdenomaAnimalsCarcinogenesisCell DifferentiationCell LineageCell Line, TumorColonColorectal NeoplasmsEmbryonic Stem CellsGene Expression Regulation, NeoplasticHumansMiceMicroRNAsNeoplastic Stem CellsProto-Oncogene Proteins p21(ras)LGR5 protein, humanMicroRNAsMIRN145 microRNA, humanProto-Oncogene Proteins p21(ras)Receptors, G-Protein-Coupledcancer plasticitycolorectal cancerembryonic stem cell-like programEMTKRAS

Identifiers

PMID26744320
PMCPMC4823026
OpenAlexW2230801460

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.