Evidence map›Paper›PMID 40066744›Full record

ArticleMolecular oncology2025

The atypical KRAS

Theresia Mair, Philip König, Milena Mijović, Jessica Kalla, Anil Baskan, Loan Tran, Kristina Draganić, Pedro Morata Saldaña, Carlos Uziel Pérez Malla, Janette Pfneissl and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

18 authors.

Theresia MairDepartment of Pathology, Medical University of Vienna, Austria.
Philip KönigDepartment of Pathology, Medical University of Vienna, Austria.
Milena MijovićDepartment of Pathology, Medical University of Vienna, Austria.
Jessica KallaDepartment of Pathology, Medical University of Vienna, Austria.
Anil BaskanDepartment of Pathology, Medical University of Vienna, Austria.
Loan TranDepartment of Pathology, Medical University of Vienna, Austria.
Kristina DraganićDepartment of Pathology, Medical University of Vienna, Austria.
Pedro Morata SaldañaDepartment of Pathology, Medical University of Vienna, Austria.
Carlos Uziel Pérez MallaDepartment of Pathology, Medical University of Vienna, Austria.
Janette PfneisslDepartment of Pathology, Medical University of Vienna, Austria.
Andreas TiefenbacherDepartment of Pathology, Medical University of Vienna, Austria.
Julijan KabiljoLudwig Boltzmann Institute Applied Diagnostics, Austria.
Velina S AtanasovaLudwig Boltzmann Institute Applied Diagnostics, Austria.
Lisa Wozelka-OltjanDepartment of Pathology, Medical University of Vienna, Austria.
Leonhard MüllauerDepartment of Pathology, Medical University of Vienna, Austria.ORCID https://orcid.org/0000-0002-3399-078X
Michael BergmannDepartment of General Surgery, Division of Visceral Surgery, Medical University of Vienna, Austria.
Raheleh Sheibani-TezerjiDepartment of Pathology, Medical University of Vienna, Austria.
Gerda EggerDepartment of Pathology, Medical University of Vienna, Austria.ORCID https://orcid.org/0000-0003-2489-155X

Funding

Austrian Science Fund 10.55776/DFH44Austrian Science Fund 10.55776/DOC59Austrian Science Fund 10.55776/F8300Austrian Science Fund 10.55776/P32771City of Vienna Fund for Innovative Interdisciplinary Cancer Research 21118City of Vienna Fund for Innovative Interdisciplinary Cancer Research 21209Österreichische Forschungsförderungsgesellschaft 879481Österreichische Forschungsförderungsgesellschaft FO999895057Österreichischen Akademie der Wissenschaften 25276
6 · The paper itself

Abstract

Transforming growth factor beta (TGF-β) exhibits complex and context-dependent cellular responses. While it mostly induces tumor-suppressive effects in early stages of tumorigenesis, tumor-promoting properties are evident in advanced disease. This TGF-β duality is still not fully understood, and whether TGF-β supports invasion and metastasis by influencing cancer cells directly, or rather through the stromal tumor compartment, remains a matter of debate. Here, we utilized a library of colorectal cancer (CRC) patient-derived tumoroids (PDTs), representing a spectrum of tumor stages, to study cancer cell-specific responses to TGF-β. Using conditions allowing for the differentiation of PDTs, we observed TGF-β-induced tumor-suppressive effects in early-stage tumoroids, whereas more advanced tumoroids were less sensitive to the treatment. Notably, one tumoroid line harboring an atypical KRAS

Indexed as

Colorectal NeoplasmsEpithelial-Mesenchymal TransitionMutationProto-Oncogene Proteins p21(ras)Transforming Growth Factor betaCell Line, TumorGene Expression Regulation, NeoplasticHumansOrganoidsKRAS protein, humanProto-Oncogene Proteins p21(ras)Transforming Growth Factor betacolorectal cancerEMTKRAS mutationsorganoidspatient‐derived tumoroidsTGF‐β

Identifiers

PMID40066744
PMCPMC12330932

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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.