Evidence map›Paper›PMID 41175860›Full record

ReviewEuropean thyroid journal2025

Somatic genetic alterations in the development and progression in thyroid tumors of follicular cells.

Giulia Calafato, Floriana Jessica Di Paola, Antonio De Leo, Thais Maloberti, Sara Coluccelli, Laura Poppi, Andrea Repaci, Erica Solaroli, Stefania Damiani, Stefano Chillotti and 4 more

Abstract readReview
In one paragraph

Review in European thyroid journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

14 authors.

Giulia CalafatoBiobank of Research, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Floriana Jessica Di PaolaBiobank of Research, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.ORCID 0000-0003-3110-3865
Antonio De LeoDepartment of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.
Thais MalobertiSolid Tumor Molecular Pathology Laboratory, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Sara ColuccelliSolid Tumor Molecular Pathology Laboratory, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Laura PoppiSolid Tumor Molecular Pathology Laboratory, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Andrea RepaciDivision of Endocrinology and Diabetes Prevention and Care, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Erica SolaroliEndocrinology Unit, Ospedale Maggiore, Bologna, Italy.
Stefania DamianiPathology Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Stefano ChillottiPathology Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Federico ChiarucciPathology Unit, Ospedale Maggiore, Bologna, Italy.
Kerry Jane RhodenDepartment of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.
Dario de BiaseSolid Tumor Molecular Pathology Laboratory, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Giovanni TalliniDepartment of Medical and Surgical Sciences (DIMEC), University of Bologna, Bologna, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Thyroid cancer is the most prevalent endocrine malignancy. Distinct genetic alterations drive the development and progression of thyroid tumors of follicular cells with remarkable genotype-phenotype correlation. In most tumors of follicular cell origin, the primary molecular events are RAS or RAS-like (follicular-patterned tumors) and BRAF p.V600E or BRAF V600E-like (conventional papillary carcinomas) alterations. Progression of thyroid tumors to advanced and less-differentiated carcinomas requires additional oncogenic alterations, including TP53 and TERT promoter mutation, and aberrant PI3K-PTEN-AKT signaling. Understanding the genetic landscape of thyroid carcinoma of follicular cells is essential to optimize clinical management and to identify molecular targets to treat cases with aggressive disease refractory to standard radioactive iodine therapy. What follows is a comprehensive and updated outline of the main somatic genetic and molecular alterations in thyroid carcinoma of follicular cells.

Indexed as

Adenocarcinoma, FollicularThyroid NeoplasmsDisease ProgressionHumansMutationPhosphatidylinositol 3-KinasesProto-Oncogene Proteins B-rafPTEN PhosphohydrolaseSignal TransductionTelomeraseTumor Suppressor Protein p53BRAF protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins B-rafPTEN PhosphohydrolasePTEN protein, humanTelomeraseTERT protein, humanTP53 protein, humanTumor Suppressor Protein p53anaplastic thyroid carcinomafollicular thyroid carcinomamolecular diagnosticspapillary thyroid carcinomapathways dysregulationspoorly differentiated thyroid carcinomathyroid cancerthyroid genetic alterationsthyroid tumors

Identifiers

PMID41175860
PMCPMC12579491

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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.