Evidence map›Paper›PMID 34389035›Full record

ArticleThyroid research2021

Development of metastatic poorly differentiated thyroid cancer from a sub-centimeter papillary thyroid carcinoma in a young patient with a germline MET mutation - association or random chance?

Klara Johansson, Adam Stenman, Johan O Paulsson, Na Wang, Catharina Ihre-Lundgren, Jan Zedenius, C Christofer Juhlin

Open access · goldAbstract read
In one paragraph

Article in Thyroid research, 2021. 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, top 85% 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

1 citing paper in PubMed, 0 citations in OpenAlex.

  1. Identification and assessment ofOncology letters · 2026
    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

7 authors at 2 institutions in 2 countries.

Klara Johansson *Department of Oncology-Pathology, Karolinska Institutet, BioClinicum J6:20, Visionsgatan 4, SE-17164, Solna, Sweden.
Adam Stenman *Department of Oncology-Pathology, Karolinska Institutet, BioClinicum J6:20, Visionsgatan 4, SE-17164, Solna, Sweden.
Johan O PaulssonDepartment of Oncology-Pathology, Karolinska Institutet, BioClinicum J6:20, Visionsgatan 4, SE-17164, Solna, Sweden.
Na WangDepartment of Oncology-Pathology, Karolinska Institutet, BioClinicum J6:20, Visionsgatan 4, SE-17164, Solna, Sweden.
Catharina Ihre-LundgrenDepartment of Breast, Endocrine Tumors and Sarcoma, Karolinska University Hospital, Stockholm, Sweden.
Jan ZedeniusDepartment of Breast, Endocrine Tumors and Sarcoma, Karolinska University Hospital, Stockholm, Sweden.
C Christofer JuhlinDepartment of Oncology-Pathology, Karolinska Institutet, BioClinicum J6:20, Visionsgatan 4, SE-17164, Solna, Sweden. christofer.juhlin@ki.se.ORCID http://orcid.org/0000-0002-5945-9081
Karolinska University Hospital · SEKarolinska Institutet · SE

Funding

Cancerfonden Junior Clinical Investigator AwardSvenska Sällskapet för Medicinsk Forskning Stora Etableringsanslaget
6 · The paper itself

Abstract

backgroundThyroid cancer dedifferentiation is an unusual observation among young patients and is poorly understood, although a recent correlation to DICER1 gene mutations has been proposed. CASE PRESENTATION: A 28-year old patient presented with a sub-centimeter cytology-verified primary papillary thyroid carcinoma (PTC) and a synchronous lateral lymph node metastasis. Following surgery, histopathology confirmed a 9 mm oxyphilic PTC and a synchronous metastasis of poorly differentiated thyroid carcinoma (PDTC). Extensive molecular examinations of both lesions revealed wildtype DICER1 sequences, but identified a somatic ETV6-NTRK3 gene fusion and a MET germline variant (c.1076G > A, p.Arg359Gln). MET is an established oncogene known to be overexpressed in thyroid cancer, and this specific alteration was not reported as a single nucleotide polymorphism (SNP), suggestive of a mutation. Both the primary PTC and the metastatic PDTC displayed strong MET immunoreactivity. A validation cohort of 50 PTCs from young patients were analyzed using quantitative real-time PCR, revealing significantly higher MET gene expression in tumors than normal thyroid controls, a finding which was particularly pronounced in BRAF V600E mutated cases. No additional tumors apart from the index case harbored the p.Arg359Gln MET mutation. Transfecting PTC cell lines MDA-T32 and MDA-T41 with a p.Arg359Gln MET plasmid construct revealed no obvious effects on cellular migratory or invasive properties, whereas overexpression of wildtype MET stimulated invasion.

conclusionsThe question of whether the observed MET mutation in any way influenced the dedifferentiation of a primary PTC into a PDTC metastasis remains to be established. Moreover, our data corroborate earlier studies, indicating that MET is aberrantly expressed in PTC and may influence the invasive behavior of these tumors.

Indexed as

MET mutationMET overexpressionPapillary thyroid cancerPoorly differentatied thyroid carcinoma

Identifiers

PMID34389035
PMCPMC8364030
OpenAlexW3190115688

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.