Evidence map›Paper›PMID 25599653›Full record

ArticleJournal of proteome research2015

Differential reprogramming of isogenic colorectal cancer cells by distinct activating KRAS mutations.

Dean E Hammond, Craig J Mageean, Emma V Rusilowicz, Julie A Wickenden, Michael J Clague, Ian A Prior

Open access · hybridAbstract read
In one paragraph

Article in Journal of proteome research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

60 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
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  15. TargetingInternational journal of molecular sciences · 2024
    Review
  16. Article
  17. YB-1 activating cascades as potential targets in KRAS-mutated tumors.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023
    Review
  18. Targeting KRAS in Colorectal Cancer: A Bench to Bedside Review.International journal of molecular sciences · 2023
    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

6 authors at 2 institutions in 1 country.

Dean E HammondDivision of Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool , Crown Street, Liverpool L69 3BX, United Kingdom.
Craig J Mageean
Emma V Rusilowicz
Julie A Wickenden
Michael J Clague
Ian A Prior
University of Liverpool · GBHorizon Discovery Group (United Kingdom) · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

Oncogenic mutations of Ras at codons 12, 13, or 61, that render the protein constitutively active, are found in ∼ 16% of all cancer cases. Among the three major Ras isoforms, KRAS is the most frequently mutated isoform in cancer. Each Ras isoform and tumor type displays a distinct pattern of codon-specific mutations. In colon cancer, KRAS is typically mutated at codon 12, but a significant fraction of patients have mutations at codon 13. Clinical data suggest different outcomes and responsiveness to treatment between these two groups. To investigate the differential effects upon cell status associated with KRAS mutations we performed a quantitative analysis of the proteome and phosphoproteome of isogenic SW48 colon cancer cell lines in which one allele of the endogenous gene has been edited to harbor specific KRAS mutations (G12V, G12D, or G13D). Each mutation generates a distinct signature, with the most variability seen between G13D and the codon 12 KRAS mutants. One notable example of specific up-regulation in KRAS codon 12 mutant SW48 cells is provided by the short form of the colon cancer stem cell marker doublecortin-like Kinase 1 (DCLK1) that can be reversed by suppression of KRAS.

Indexed as

Genes, rasMutationCell Line, TumorColorectal NeoplasmsDoublecortin-Like KinasesHumansIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesProteomicsUp-RegulationDCLK1 protein, humanDoublecortin-Like KinasesIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine Kinasescolorectal cancerisogenic cellsRassignalingSILAC phosphoproteomics

Identifiers

PMID25599653
PMCPMC4356034
OpenAlexW1996338307

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.