Evidence map›Paper›PMID 38900279›Full record

ArticleInnere Medizin (Heidelberg, Germany)2024

[Thyroid carcinomas: the role of systemic therapies in internal medicine].

Tim Brandenburg, Matthias Kroiß

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Article in Innere Medizin (Heidelberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

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5 · Who and what money

Authors and funding

2 authors.

Tim BrandenburgKlinik für Endokrinologie, Diabetologie und Stoffwechsel, Universitätsklinikum Essen, Hufelandstraße 55, 45147, Essen, Deutschland. tim.brandenburg@uk-essen.de.
Matthias KroißMedizinische Klinik IV, Universitätsklinikum, Member of Endo-ERN and EURACAN, Ludwig-Maximilians-Universität München, Ziemssenstr. 5, 80336, München, Deutschland. matthias.kroiss@med.uni-muenchen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular pathogenesis of thyroid carcinoma is well studied and of importance for the treatment of advanced stages. Differentiated, poorly differentiated and anaplastic carcinomas originate in the follicular cells, while medullary carcinomas derive from the C‑cells. The prognosis of differentiated thyroid carcinoma is generally very favourable after surgery and radioiodine therapy. Where tumours progress and lose the ability to enrich iodine, curative treatment is usually not possible. A strategy of watchful waiting is often appropriate. Activating mutations in BRAF or gene fusions of RET and NTRK provide opportunities for targeted therapies. These may be applied with the aim of restoring iodine uptake (redifferentiation). In the absence of molecular therapy targets, multityrosine kinase inhibitors (MKI) are the therapy of choice. If anaplastic thyroid carcinoma is suspected, rapid diagnostic workup including molecular pathology is warranted. Surgery where possible and radiochemotherapy are essential components of therapy. In the presence of a BRAF mutation, inhibition of BRAF and MEK is effective, even if it is not approved in Germany. Where molecular targets are lacking, combination therapy with the MKI lenvatinib and immune checkpoint inhibition is highly effective. Mutations in RET are present in the vast majority of cases of medullary thyroid carcinoma. In aggressive advanced disease, selective RET inhibition has recently been approved as first-line therapy and often leads to an objective response and long-lasting disease stabilisation. In summary, thyroid carcinomas are among the tumour entities for which molecularly targeted therapies can be used most frequently. The involvement of specialised centres is advisable.

Indexed as

Thyroid NeoplasmsHumansMolecular Targeted TherapyMutationPhenylurea CompoundsPrognosisProtein Kinase InhibitorsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-retQuinolineslenvatinibPhenylurea CompoundsProtein Kinase InhibitorsProto-Oncogene Proteins B-rafProto-Oncogene Proteins c-retQuinolinesRET protein, humanMolecular targeted therapyRedifferentiationThyroid cancer, differentiatedThyroid cancer, medullaryThyroid carcinoma, anaplastic

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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.