Evidence map›Paper›PMID 40316714›Full record

ArticleNPJ precision oncology2025

Kinome profiling reveals pathogenic variant specific protein signalling networks in MEN2 children with Medullary Thyroid Cancer.

B Rix, R Chauhan, Z Masoumi, E Grönroos, C E Brain, O K Ogunbiyi, K Swarbrick, C Swanton, D Bonnet, T R Kurzawinski and 3 more

Abstract read
In one paragraph

Article in NPJ precision oncology, 2025. 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
–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

0 citing papers in PubMed.

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

13 authors.

B RixProteoStem Lab, Centre for Blood Research, York Biomedical Research Institute, Department of Biology, University of York, York, UK.
R ChauhanSignalling and Structural Biology Laboratory, Francis Crick Institute, London, UK.
Z MasoumiProteoStem Lab, Centre for Blood Research, York Biomedical Research Institute, Department of Biology, University of York, York, UK.
E GrönroosCancer evolution and genome instability laboratory, Francis Crick Institute, London, UK.
C E BrainDepartment of Endocrinology, Great Ormond Street Hospital, London, UK.
O K OgunbiyiNIHR Great Ormond Street Hospital Biomedical Research Centre (BRC), London, UK.
K SwarbrickNIHR Great Ormond Street Hospital Biomedical Research Centre (BRC), London, UK.
C SwantonCancer evolution and genome instability laboratory, Francis Crick Institute, London, UK.
D BonnetHaematopoietic Stem Cell Laboratory, Francis Crick Institute, London, UK.
T R KurzawinskiDepartment of Endocrinology, Great Ormond Street Hospital, London, UK.
L IzattClinical Genetics Service, Guy's and St Thomas' NHS Foundation Trust, London, UK.
N Q McDonaldSignalling and Structural Biology Laboratory, Francis Crick Institute, London, UK. neil.mcdonald@crick.ac.uk.
W GreyProteoStem Lab, Centre for Blood Research, York Biomedical Research Institute, Department of Biology, University of York, York, UK. William.grey@york.ac.uk.

Funding

Cancer Research UK CC20268Children's Cancer and Leukaemia Group LPT2021B44European Hematology Association RG112European Research Council PROTEUS, 835297Indian National Science Academy BCRF-22-157Leukaemia UK 2021/JGF/002Mark Foundation For Cancer Research 21-029-ASPMedical Research Council CC2068Medical Research Council MR/X007146/1Rosetrees Trust ID16584Royal Society RSRP\R\210001UK Research and Innovation EP/Z534298/1Wellcome Trust CC2041Wellcome Trust CC2068
6 · The paper itself

Abstract

Multiple Endocrine Neoplasia Type 2 (MEN2) is an autosomal dominant disease caused by pathogenic variants in the receptor tyrosine kinase RET, with strong genotype-phenotype correlations. The development and progression of these tumours are not always predictable even within families with the same RET pathogenic variant, demonstrating a need for better understanding of the underlying molecular mechanisms. Precision molecular medicine is not widely used and the standard of care remains prophylactic thyroidectomy. This absence of curative approaches is exacerbated by the lack of novel therapeutic markers/targets. In this study, we investigated the functional kinome of 24 familial MEN2 patients. We identified MEN2 subtype and RET pathogenic variant-specific alterations in signalling pathways including mTOR, PKA, NF-κB and focal adhesions, which were validated in patient thyroid tissue. Overall, our study of MEN2 functional kinomes uncovers novel specific drivers of MEN2 disease and its pathogenic variant subtypes, identifying new potential therapeutic targets for MEN2.

Identifiers

PMID40316714
PMCPMC12048619

What Socratic 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 Socratic graph.