Evidence map›Paper›PMID 25705018›Full record

ArticleScientific reports2015

Comparative analysis of KRAS codon 12, 13, 18, 61, and 117 mutations using human MCF10A isogenic cell lines.

Britta Stolze, Stefanie Reinhart, Lars Bulllinger, Stefan Fröhling, Claudia Scholl

Open access · goldAbstract readComparative Study
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. New developments and applications of human organoids.Nature reviews. Molecular cell biology · 2026
    Review
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  9. Observational
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  17. Structural modifications and kinetic effects ofFrontiers in molecular biosciences · 2024
    Article
  18. Article
  19. Article
  20. Review

25 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

5 authors at 3 institutions in 1 country.

Britta StolzeDepartment of Internal Medicine III, Ulm University, Ulm, Germany.
Stefanie ReinhartDepartment of Translational Oncology, National Center for Tumor Diseases (NCT), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Lars BulllingerDepartment of Internal Medicine III, Ulm University, Ulm, Germany.
Stefan Fröhling1] Department of Translational Oncology, National Center for Tumor Diseases (NCT), German Cancer Research Center (DKFZ), Heidelberg, Germany [2] Heidelberg University Hospital, Heidelberg, Germany.
Claudia Scholl1] Department of Internal Medicine III, Ulm University, Ulm, Germany [2] Department of Translational Oncology, National Center for Tumor Diseases (NCT), German Cancer Research Center (DKFZ), Heidelberg, Germany.
German Cancer Research Center · DEUniversität Ulm · DENational Center for Tumor Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KRAS mutations occur in one third of human cancers and cluster in several hotspots, with codons 12 and 13 being most commonly affected. It has been suggested that the position and type of amino acid exchange influence the transforming capacity of mutant KRAS proteins. We used MCF10A human mammary epithelial cells to establish isogenic cell lines that express different cancer-associated KRAS mutations (G12C, G12D, G12V, G13C, G13D, A18D, Q61H, K117N) at physiological or elevated levels, and investigated the biochemical and functional consequences of the different variants. The overall effects of low-expressing mutants were moderate compared to overexpressed variants, but allowed delineation of biological functions that were related to specific alleles rather than KRAS expression level. None of the mutations induced morphological changes, migratory abilities, or increased phosphorylation of ERK, PDK1, and AKT. KRAS-G12D, G12V, G13D, and K117N mediated EGF-independent proliferation, whereas anchorage-independent growth was primarily induced by K117N and Q61H. Both codon 13 mutations were associated with increased EGFR expression. Finally, global gene expression analysis of MCF10A-G13D versus MCF10A-G12D revealed distinct transcriptional changes. Together, we describe a useful resource for investigating the function of multiple KRAS mutations and provide insights into the differential effects of these variants in MCF10A cells.

Indexed as

Cell MovementCell ProliferationCell SurvivalEpidermal Growth FactorErbB ReceptorsExtracellular Signal-Regulated MAP KinasesGene Expression ProfilingHumansMutationPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPyruvate Dehydrogenase Acetyl-Transferring Kinaseras ProteinsSignal TransductionUp-RegulationEpidermal Growth FactorErbB ReceptorsExtracellular Signal-Regulated MAP KinasesPDK1 protein, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktPyruvate Dehydrogenase Acetyl-Transferring Kinaseras Proteins

Identifiers

PMID25705018
PMCPMC4336936
OpenAlexW1970383854

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.