Evidence map›Paper›PMID 38360887›Full record

ArticleCancer gene therapy2024

Transactivation of Met signaling by oncogenic Gnaq drives the evolution of melanoma in Hgf-Cdk4 mice.

Miriam Mengoni, Andreas Dominik Braun, Sahithi Seedarala, Susanne Bonifatius, Evi Kostenis, Denny Schanze, Martin Zenker, Thomas Tüting, Evelyn Gaffal

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer gene therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 2 institutions in 1 country.

Miriam Mengoni *Laboratory for Experimental Dermatology, Department of Dermatology, University Hospital Magdeburg, 39120, Magdeburg, Germany.ORCID 0000-0002-1651-7114
Andreas Dominik Braun *Laboratory for Experimental Dermatology, Department of Dermatology, University Hospital Magdeburg, 39120, Magdeburg, Germany.ORCID 0000-0002-6954-0633
Sahithi SeedaralaLaboratory for Experimental Dermatology, Department of Dermatology, University Hospital Magdeburg, 39120, Magdeburg, Germany.
Susanne BonifatiusLaboratory for Experimental Dermatology, Department of Dermatology, University Hospital Magdeburg, 39120, Magdeburg, Germany.
Evi KostenisMolecular, Cellular and Pharmacobiology Section, Institute for Pharmaceutical Biology, University of Bonn, Nussallee 6, 53115, Bonn, Germany.
Denny SchanzeInstitute of Human Genetics, University Hospital Magdeburg, 39120, Magdeburg, Germany.ORCID 0000-0003-2748-9929
Martin ZenkerInstitute of Human Genetics, University Hospital Magdeburg, 39120, Magdeburg, Germany.ORCID 0000-0003-1618-9269
Thomas TütingLaboratory for Experimental Dermatology, Department of Dermatology, University Hospital Magdeburg, 39120, Magdeburg, Germany.ORCID 0000-0001-7146-0934
Evelyn GaffalLaboratory for Experimental Dermatology, Department of Dermatology, University Hospital Magdeburg, 39120, Magdeburg, Germany. evelyn.gaffal@med.ovgu.de.ORCID 0000-0002-4639-9841
University Hospital Magdeburg · DEUniversity of Bonn · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) FOR 2372 Project 10Deutsche Forschungsgemeinschaft (German Research Foundation) FOR 2372 Project 6Deutsche Forschungsgemeinschaft (German Research Foundation) SFB 854 Project A27, FOR 2372 Project 10Else Kröner-Fresenius-Stiftung (Else Kroner-Fresenius Foundation) 2017_Kolleg.07; TP3Else Kröner-Fresenius-Stiftung (Else Kroner-Fresenius Foundation) 2017_Kolleg.07; TP4
6 · The paper itself

Abstract

Recent pan-cancer genomic analyses have identified numerous oncogenic driver mutations that occur in a cell-type and tissue-specific distribution. For example, oncogenic mutations in Braf and Nras genes arise predominantly in melanocytic neoplasms of the epidermis, while oncogenic mutations in Gnaq/11 genes arise mostly in melanocytic lesions of the dermis or the uvea. The mechanisms promoting cell-type and tissue-specific oncogenic events currently remain poorly understood. Here, we report that Gnaq/11 hotspot mutations occur as early oncogenic drivers during the evolution of primary melanomas in Hgf-Cdk4 mice. Additional single base substitutions in the Trp53 gene and structural chromosomal aberrations favoring amplifications of the chromosomal region containing the Met receptor gene accumulate during serial tumor transplantation and in cell lines established in vitro. Mechanistically, we found that the Gnaq

Indexed as

Cyclin-Dependent Kinase 4GTP-Binding Protein alpha Subunits, Gq-G11Hepatocyte Growth FactorMelanomaProto-Oncogene Proteins c-metSignal TransductionAnimalsCell Line, TumorHumansMiceMice, TransgenicMutationTranscriptional ActivationTumor MicroenvironmentCdk4 protein, mouseCyclin-Dependent Kinase 4GNAQ protein, humanGTP-Binding Protein alpha Subunits, Gq-G11Hepatocyte Growth FactorHGF protein, mouseMET protein, humanProto-Oncogene Proteins c-met

Identifiers

PMID38360887
PMCPMC11192630
OpenAlexW4391840476

What OpenQuestion holds

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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.