{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T16:11:01Z","timestamp":1789747861864,"version":"4.0.1"},"reference-count":52,"publisher":"Bioscientifica","issue":"1","license":[{"start":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T00:00:00Z","timestamp":1787702400000},"content-version":"vor","delay-in-days":237,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["journals.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The AGK::BRAF fusion is a recurrent oncogenic alteration in sporadic pediatric papillary thyroid carcinoma (PTC), frequently associated with multifocal disease and pulmonary metastasis. However, the molecular and cellular consequences of AGK::BRAF expression in thyroid follicular cells remain poorly defined. Here, we investigated the biological effects of AGK::BRAF in PCCL3 thyroid cells and compared them with those induced by clinically established pediatric PTC oncogenic drivers, including RET\/PTC1, RET\/PTC3, ETV6::NTRK3, BRAF V600E, and wild-type BRAF. AGK::BRAF-expressing cells exhibited the most robust MAPK\/ERK activation, characterized by markedly enhanced ERK and MEK phosphorylation relative to all other oncogenic drivers analyzed. By contrast, STAT3 and AKT signaling remained comparatively modest and did not show consistent oncogene-specific activation patterns. Functionally, AGK::BRAF expression induced features of thyroid dedifferentiation, including reduced sodium\u2013iodide symporter (NIS) expression and impaired iodide uptake. Concomitantly, AGK::BRAF-expressing cells exhibited increased frequencies of micronuclei and chromatin bridges, together with disruption of three-dimensional telomere architecture, including reduced telomere signal number and intensity, altered spatial organization, and increased nuclear volume. Three-dimensional structured illumination microscopy (3D-SIM) further demonstrated chromatin remodeling, characterized by increased chromatin condensation accompanied by enlarged interchromatin spaces. Collectively, these findings suggest that AGK::BRAF is a dominant oncogenic driver of sustained MAPK\/ERK signaling coupled to thyroid dedifferentiation, nuclear architectural remodeling, telomere dysfunction, and genomic instability. These coordinated molecular and structural alterations provide a mechanistic basis for the aggressive clinical course observed in AGK::BRAF-driven pediatric PTC.<\/jats:p>","DOI":"10.1530\/eo-25-0096","type":"journal-article","created":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T13:47:08Z","timestamp":1787752028000},"update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-15","source":"Crossref","is-referenced-by-count":0,"title":["<i>AGK::BRAF<\/i>\n                    fusion activates MAPK signaling, promotes genomic instability, and reduces NIS expression in thyroid cancer cells"],"prefix":"10.1530","volume":"6","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7452-5756","authenticated-orcid":true,"given":"Luiza","family":"Sisdelli","sequence":"first","affiliation":[{"name":"Genetic Basis of Thyroid Tumors Laboratory, Division of Genetics, Department of Morphology and Genetics, Escola Paulista de Medicina, Universidade Federal de S\u00e3o Paulo 1 , , ,","place":["S\u00e3o Paulo, SP, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7395-3342","authenticated-orcid":true,"given":"Welbert Gomes","family":"Rocha","sequence":"additional","affiliation":[{"name":"Genetic Basis of Thyroid Tumors Laboratory, Division of Genetics, Department of Morphology and Genetics, Escola Paulista de Medicina, Universidade Federal de S\u00e3o Paulo 1 , , ,","place":["S\u00e3o Paulo, SP, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0626-5352","authenticated-orcid":true,"given":"D\u00e9bora Mota","family":"Dias Thomaz","sequence":"additional","affiliation":[{"name":"Genetic Basis of Thyroid Tumors Laboratory, Division of Genetics, Department of Morphology and Genetics, Escola Paulista de Medicina, Universidade Federal de S\u00e3o Paulo 1 , , ,","place":["S\u00e3o Paulo, SP, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roxane","family":"Hatanaka","sequence":"additional","affiliation":[{"name":"Genetic Basis of Thyroid Tumors Laboratory, Division of Genetics, Department of Morphology and Genetics, Escola Paulista de Medicina, Universidade Federal de S\u00e3o Paulo 1 , , ,","place":["S\u00e3o Paulo, SP, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renata Elen","family":"Costa da Silva","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular and Translational Endocrinology, Division of Endocrinology, Escola Paulista de Medicina, Universidade Federal de S\u00e3o Paulo 2 , , ,","place":["S\u00e3o Paulo, SP, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1702-1281","authenticated-orcid":true,"given":"Guilherme","family":"Henrique","sequence":"additional","affiliation":[{"name":"Thyroid Physiology and Pathophysiology Laboratory, Universidade Federal de S\u00e3o Paulo 3 , , ,","place":["Diadema, SP, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9146-6583","authenticated-orcid":true,"given":"Caroline","family":"Serrano-Nascimento","sequence":"additional","affiliation":[{"name":"Thyroid Physiology and Pathophysiology Laboratory, Universidade Federal de S\u00e3o Paulo 3 , , ,","place":["Diadema, SP, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matheus","family":"Fabi\u00e3o","sequence":"additional","affiliation":[{"name":"University of Manitoba, CancerCare Manitoba Research Institute, CancerCare Manitoba 4 , ,","place":["Winnipeg, Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7217-5297","authenticated-orcid":true,"given":"Aline","family":"Rangel-Pozzo","sequence":"additional","affiliation":[{"name":"University of Manitoba, CancerCare Manitoba Research Institute, CancerCare Manitoba 4 , ,","place":["Winnipeg, Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5797-2201","authenticated-orcid":true,"given":"Sabine","family":"Mai","sequence":"additional","affiliation":[{"name":"University of Manitoba, CancerCare Manitoba Research Institute, CancerCare Manitoba 4 , ,","place":["Winnipeg, Canada"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0156-8274","authenticated-orcid":true,"given":"Janete Maria","family":"Cerutti","sequence":"additional","affiliation":[{"name":"Genetic Basis of Thyroid Tumors Laboratory, Division of Genetics, Department of Morphology and Genetics, Escola Paulista de Medicina, Universidade Federal de S\u00e3o Paulo 1 , , ,","place":["S\u00e3o Paulo, SP, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","published-online":{"date-parts":[[2026,8,26]]},"reference":[{"key":"2026091811431340200_bib1","doi-asserted-by":"crossref","first-page":"2638","DOI":"10.1002\/(SICI)1097-0142(19981215)83:12<2638::AID-CNCR31>3.0.CO;2-1","article-title":"A National Cancer Data Base report on 53,856 cases of thyroid carcinoma treated in the U.S., 1985-1995","volume":"83","author":"Hundahl","year":"1998","journal-title":"Cancer"},{"key":"2026091811431340200_bib2","doi-asserted-by":"crossref","first-page":"322","DOI":"10.1016\/S0753-3322(00)80056-6","article-title":"The epidemiology and etiology of differentiated thyroid carcinoma","volume":"54","author":"Busnardo","year":"2000","journal-title":"Biomed Pharmacother"},{"key":"2026091811431340200_bib3","doi-asserted-by":"crossref","first-page":"501","DOI":"10.1016\/S0140-6736(03)12488-9","article-title":"Thyroid 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2\u2032, 4, 4\u2032-tetrabromodiphenyl ether induces thyroid toxicity by targeting BRAF-mediated MEK-ERK-NIS pathway in human thyroid follicular epithelial cells","volume":"302","author":"Xie","year":"2025","journal-title":"Ecotoxicol Environ Saf"},{"key":"2026091811431340200_bib39","doi-asserted-by":"crossref","first-page":"12","DOI":"10.1186\/s12964-019-0322-x","article-title":"Low dose radiation regulates BRAF-induced thyroid cellular dysfunction and transformation","volume":"17","author":"Kaushik","year":"2019","journal-title":"Cell Commun Signal"},{"key":"2026091811431340200_bib40","doi-asserted-by":"crossref","first-page":"e27707","DOI":"10.1002\/pbc.27707","article-title":"AGK-BRAF is associated with distant metastasis and younger age in pediatric papillary thyroid carcinoma","volume":"66","author":"Sisdelli","year":"2019","journal-title":"Pediatr Blood 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