Evidence map›Paper›PMID 40887557›Full record

ArticleEndocrine pathology2025

Progression of Follicular Thyroid Carcinomas to Anaplastic Thyroid Carcinomas: Molecular and Clinicopathologic Characteristics with Comparison to Papillary Thyroid Carcinoma-Derived Anaplastic Thyroid Carcinomas.

Toru Odate, Tetsuo Kondo, Ryohei Katoh, Koichi Ito, Toshihide Ueno, Yasushi Yatabe, Taisuke Mori

Abstract readComparative Study
PubMed Publisher
In one paragraph

Article in Endocrine pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Multimodal spectrum of approach in poorly differentiated thyroid carcinoma (an updated analysis).Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    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

7 authors.

Toru OdateDepartment of Pathology, University of Yamanashi, Yamanashi, Japan.
Tetsuo KondoDepartment of Pathology, University of Yamanashi, Yamanashi, Japan.
Ryohei KatohDepartment of Pathology, Ito Hospital, Tokyo, Japan.
Koichi ItoDepartment of Surgery, Ito Hospital, Tokyo, Japan.
Toshihide UenoDivision of Cellular Signaling, National Cancer Center Research Institute, Tokyo, Japan.
Yasushi YatabeDepartment of Diagnostic Pathology, National Cancer Center Hospital, Tokyo, Japan.
Taisuke MoriDepartment of Diagnostic Pathology, National Cancer Center Hospital, Tokyo, Japan. tamori@ncc.go.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although anaplastic thyroid carcinomas (ATCs) typically arise from papillary thyroid carcinomas (PTCs), follicular thyroid carcinomas (FTCs) can also progress to ATCs; however, histologically confirmed FTC-derived ATCs are relatively uncommon and remain poorly characterized. To clarify this phenomenon, we analyzed eight FTC-derived ATCs and compared them with 11 PTC-derived ATCs. Whole-exome sequencing (WES) was conducted on the differentiated thyroid carcinoma (DTC) and ATC components within the same tumors to examine mutational profiles; three additional cases underwent FoundationOne® testing. The demographic features were similar between FTC- and PTC-derived ATCs. Histologically, spindle-cell morphology was more common in FTC-derived ATCs (3/8), whereas PTC-derived ATCs exhibited squamoid (5/11) and giant cell features (5/11), including osteoclast-like cells. WES was successfully performed on both the ATC and FTC components in seven of the eight FTC-derived ATCs. Common alterations included TERT promoter (5/7), NRAS (4/7), and HRAS (2/7) mutations in both components. TP53 mutations were observed only in the ATC component (5/7). EIF1AX mutations co-occurred with TERT and HRAS mutations in two cases. PTEN mutations were found in two FTCs with solid/trabecular patterns but were absent in the corresponding ATC components. One tumor harbored a DGCR8 p.E518K mutation that was retained during progression. By contrast, PTC-derived ATCs consistently showed concurrent BRAF and TERT promoter mutations (11/11). Immunohistochemistry for BRAF V600E, RAS Q61R, p53, PTEN, and MTAP showed high concordance with the corresponding mutation status. These findings revealed significant histological and genetic differences between FTC- and PTC-derived ATCs, providing new insights into the molecular basis of FTC dedifferentiation into ATC.

Indexed as

Adenocarcinoma, FollicularThyroid Cancer, PapillaryThyroid Carcinoma, AnaplasticThyroid NeoplasmsAdultAgedAged, 80 and overDisease ProgressionFemaleHumansMaleMiddle AgedMutationAnaplastic thyroid carcinomaFollicular thyroid carcinomaMutationPapillary thyroid carcinomaProgression

Identifiers

PMID40887557

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.