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New Rochelle, NY, August 22, 2025—The American Thyroid Association has released new guidelines for the management of adult patients with differentiated thyroid cancer (DTC), the most prevalent cancer of the thyroid. The guidelines are published in the peer-reviewed journal Thyroid®, the official journal of the American Thyroid Association® (ATA®). Click here to read the article now.

The new guidelines, developed by an ATA task force led by Co-Chairs Matthew Ringel, MD, from The Ohio State University College of Medicine and Comprehensive Cancer Center, and Julie Ann Sosa, MD, from the University of California San Francisco, include input from a large, diverse complement of stakeholders. The panel included members from multiple specialties involved in thyroid cancer care, including a patient advocate and an expert in systematic reviews/meta-analyses/guidelines who educated and supported task force members. Jacqueline Jonklaas, MD, PhD, ATA President, noted that “ATA leadership is grateful to the task force members, ably lead by Drs. Ringel and Sosa, for this superlative clinical practice guideline that I believe will help set the standard of care for future generations of patients with thyroid cancer.”

These revised guidelines begin with the initial cancer diagnosis and continue with recommendations for staging and risk assessment; initial treatment decisions; assessment of treatment responses; monitoring approaches; diagnostic testing; and subsequent therapies based on the strength of evidence for response and consideration of side-effects and outcomes. Patient-reported outcomes, thyroid cancer survivorship, and identified areas of need for additional high-quality research are highlighted. “This thyroid cancer guideline continues the ATA’s leadership in providing high quality and evidence-based guidelines which provide thoughtful guidance to clinicians taking care of patients with thyroid cancer,” said Christopher McCabe, PhD, ATA Secretary and Chief Operating Officer.

About the Journal
Thyroid®, the official journal of the American Thyroid Association®, (ATA®) is an authoritative peer-reviewed journal published monthly online with open access options and in print. Led by Editor-in-Chief Anna M. Sawka, MD, PhD, University of Toronto, the Journal publishes original articles and timely reviews that reflect the rapidly advancing changes in our understanding of thyroid physiology and pathology, from the molecular biology of the cell to clinical management of thyroid disorders. Complete tables of content and a sample issue may be viewed on the Thyroid® website. The complete Thyroid Journal Program includes the highly valued abstract and commentary publication Clinical Thyroidology®, led by Editor-in-Chief Trevor E. Angell, MD and published monthly, and the groundbreaking videojournal companion VideoEndocrinology, led by Editor Catherine F. Sinclair, MD, FRACS. Complete tables of content and sample issues may be viewed on the Thyroid® website.

About the American Thyroid Association®
The American Thyroid Association® (ATA) is dedicated to transforming thyroid care through clinical excellence, education, scientific discovery and advocacy in a collaborative and diverse community. ATA® is an international professional medical society with over 1,800 members from 43 countries around the world. The ATA® promotes thyroid awareness and information through Clinical Thyroidology®, a resource that summarizes research for patients and families, and extensive, authoritative resources on thyroid disease and thyroid cancer in both English and Spanish. The ATA® website www.thyroid.org serves as a bonafide clinical resource for patients and the public who look for reliable thyroid-related information.

About the Publisher
Mary Ann Liebert, Inc. is a global media company dedicated to publishing and delivering impactful peer-reviewed research in biotechnology & life sciences, specialized clinical medicine, public health and policy, and technology & engineering. Since its founding in 1980, the company has focused on providing critical insights and content that empower researchers and clinicians worldwide to drive innovation and discovery.

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New Rochelle, NY, January 8, 2025—A new study found no evidence that glucagon-like peptide 1 receptor agonist (GLP1-RA) use is associated with an increased risk of thyroid cancer. The study is published in the peer-reviewed journal Thyroid^®, the official journal of the American Thyroid Association^®sup> (ATA^®). Click here to read the article now.

GLP1-Ras are incretin-based glucose-lowering medications that are commonly used to treat type 2 diabetes and obesity.

Professor Anton Pottegård, from the University of Southern Denmark, and coauthors, analyzed databased from six countries, comparing patients with type 2 diabetes between 2007 and 2023 for the risk of thyroid cancer among GLP1-RA users compared with dipeptidyl peptidase-4 inhibitors (DPP-4is). The investigators examined data from 92,497 users of GLP1-RA and 2,484,408 users of DPP-4i.

“In this large multisite study, utilizing data from six population-based databases, we found no evidence that GLP1-RA use is associated with an increased risk of thyroid cancer with follow-up ranging from 1.8-3.0 years, providing some reassurance to patients and clinicians about the short-term safety of these drugs,” concluded the investigators.

In an associated Commentary titled “Thyroid Cancer Risk with GLP-1 Receptor Agonists: Evidence, Knowledge Gaps, and the Path Forward,” Juan Brito, MD, from the Mayo Clinic, and coauthors, stated the following: this study “stands out for its large scale and robust methodology. The inclusion of six population-based cohorts from diverse geographical settings enhances the generalizability of the findings.” The authors also remarked that, “The median follow-up period of 1.8 to 3.0 years is insufficient to evaluate long-term risks.” In addition, “the study’s focus on populations with type 2 diabetes may limit is applicability to non-diabetic populations, a growing group of GLP-1RA users, particularly for obesity management.”

About the Journal

Thyroid^®, the official journal of the American Thyroid Association^®, (ATA^®) is an authoritative peer-reviewed journal published monthly online with open access options and in print. Led by Editor-in-Chief Anna M. Sawka, MD, PhD, University of Toronto, the Journal publishes original articles and timely reviews that reflect the rapidly advancing changes in our understanding of thyroid physiology and pathology, from the molecular biology of the cell to clinical management of thyroid disorders. Complete tables of content and a sample issue may be viewed on the Thyroid^®website. The complete Thyroid Journal Program includes the highly valued abstract and commentary publication Clinical Thyroidology^®, led by Editor-in-Chief Trevor E. Angell, MD and published monthly, and the groundbreaking videojournal companion VideoEndocrinology, led by Editor Catherine F. Sinclair, MD, FRACS. Complete tables of content and sample issues may be viewed on the Thyroid^® website.

About the American Thyroid Association^®

The American Thyroid Association^® (ATA) is dedicated to transforming thyroid care through clinical excellence, education, scientific discovery and advocacy in a collaborative and diverse community. ATA^® is an international professional medical society with over 1,800 members from 43 countries around the world. The ATA^® promotes thyroid awareness and information through Clinical Thyroidology^®, a resource that summarizes research for patients and families, and extensive, authoritative resources on thyroid disease and thyroid cancer in both English and Spanish. The ATA^® website www.thyroid.org serves as a bonafide clinical resource for patients and the public who look for reliable thyroid-related information.

About the Publisher

Mary Ann Liebert, Inc. is a global media company dedicated to creating, curating, and delivering impactful peer-reviewed research and authoritative content services to advance the fields of biotechnology and the life sciences, specialized clinical medicine, and public health and policy. For complete information, please visit the Mary Ann Liebert, Inc. website.

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Award Winner: Theodora Pappa, MD, PhD, Brigham and Women’s Hospital; Dana-Farber Cancer Institute, Winchester, MA

Award Winning Paper: GLP-1 Receptor Agonists and the Risk of Thyroid Cancer

Published in: Clinical Thyroidology®

The 2023 Rosalind Franklin Society (RFS) Awards in Science, recognize outstanding peer-reviewed research by women and underrepresented minorities in STEM. The anthology of award winners is available digitally on the Rosalind Franklin Society website and in print.

RFS, in partnership with Mary Ann Liebert, Inc., launched this prestigious annual award for the best paper by a woman or under-represented minority in science in each of the publisher’s more than 100 peer-reviewed journals to highlight the important contributions of these scientists and provide role models and mentors for younger scientists following in their footsteps.

The post Theodora Pappa, MD, PhD, awarded 2023 Rosalind Franklin Society (RFS) Award in Science for her outstanding work in Clinical Thyroidology® appeared first on American Thyroid Association.

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The post Radioactive iodine treatment for children with low-risk thyroid cancer – to give or not to give? – Clinical Thyroidology® for the Public appeared first on American Thyroid Association.

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The post Is removal of thyroid tissue through incisions made in the mouth safe and effective for treating thyroid cancer? – Clinical Thyroidology® for the Public appeared first on American Thyroid Association.

Kaniksha Desai, MD, interviews Anupam Kotwal, MD, about his journey from doctor to patient and how he managed his thyroid cancer diagnosis.

Editorial Collaboration Medscape & American Thyroid Association^®
August 10, 2023

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Sarimar Agosto Salgado, MD
Moffitt Cancer Center
Tampa, Florida
September 23, 2022

The mainstays of therapy for differentiated thyroid cancer cases include surgery, selective use of radioactive iodine (RAI) based on risk of tumor recurrence, and TSH suppression therapy with levothyroxine[1]. Although most patients have a favorable prognosis, a subset develop distant metastases (<10%), of which approximately two-thirds result in radioactive iodine refractory differentiated thyroid cancer (RAIR-DTC) [2]. Depending on the extent of metastatic disease, active surveillance under TSH suppression and localized therapies, including surgery, radiation, ablative therapies, and bone modulating agents for bone metastases, may assist in controlling the disease. Nevertheless, patients may require long-term systemic treatment for progressive RAIR-DTC. Evaluation for systemic therapy includes radiographic staging (including brain imaging), tumor testing for targetable mutations, comprehensive laboratories, cardiac function assessment, and close monitoring of comorbidities such as hypertension, diabetes, etc.

Initial systemic therapies approved for RAIR-DTC included multikinase inhibitors (MKIs) Lenvatinib and Sorafenib, which target multiple tumorigenic kinase pathways, including vascular endothelial growth factor receptors. Lenvatinib demonstrated impressive response rates of 65% and survival improvement in patients 65 years and older, leading to FDA approval in 2015 [3-5]. However, since tumors almost inevitably develop resistance mechanisms, additional therapies are being studied to expand the management options for RAIR-DTC; for example, Cabozantinib has recently been approved as a second line MKI [6].

Improved understanding of the molecular pathogenesis of thyroid cancer, coupled with increasingly comprehensive molecular testing platforms, has led to new insights. In fact, molecular testing has developed over time into an informative tool for prognostic and therapeutic implications. For example, BRAF V600E is the most common alteration in papillary thyroid cancer (PTC), present in at least 60% of cases [7]. BRAF inhibitors alone (e.g., Dabrafenib) or in combination with a MEK inhibitor (e.g., Trametinib) have shown overall responses between 42-54% in RAIR-DTC [8, 9]. A recent FDA approval in the summer of 2022, supported dabrafenib and trametinib combination for unresectable or metastatic BRAF V600E solid tumors with progression despite prior treatments. In addition, recently approved selective inhibitor options include Selpercatinib and Pralsetinib for RET fusion-driven thyroid cancer, and Larotrectinib and Entrectinib for tumors harboring NTRK fusions. Together, both MKI’s and selective inhibitors have brought a ray of hope for patients with RAIR-DTC[10]. However, practice variability still exists in terms of a) timing of initiation of systemic therapy, b) the definition criteria for RAI-refractory thyroid cancer, and c) decision regarding the first line of therapy when a targetable mutation is present.

Selective targeted therapies balance efficacy and tolerability, leading to new potential approaches to manage advanced thyroid cancer. A promising new strategy leverages the discovery that BRAF V600E mutations can lead to alteration-dysfunction in the sodium-iodine symporter and contribute to the development of RAIR-DTC. A short course of BRAF-inhibitor therapy may result in redifferentiation in BRAF-altered tumors; this is a promising approach to resensitize tumors to RAI, allowing for discontinuation of systemic therapy post-RAI and thereby limiting the toxicities of long-term chemotherapy [11, 12]. Similar capacity for redifferentiation has been reported in RAS altered, NTRK, or RET fusion-driven thyroid cancers after the treatment with a MEK inhibitor, Larotrectinib, and Selpercatinib, respectively [13-16]. Further studies are needed to determine the optimal candidates by molecular signature, standardization of protocols, and appropriate timing to implement a redifferentiation approach.

As an oncologic endocrinologist, given the evolving landscape of therapeutic options for RAIR-DTC, it is essential to highlight the importance of timely evaluating patients with advanced thyroid cancer. High-risk thyroid cancer patients should be referred to expert multidisciplinary patient-centered teams; this ensures patients receive a comprehensive assessment to delineate treatment plans and incorporate the use of precision oncology.

References:
1. Haugen, B.R., et al., 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid, 2016. 26(1): p. 1-133.
2. Fullmer, T., M.E. Cabanillas, and M. Zafereo, Novel Therapeutics in Radioactive Iodine-Resistant Thyroid Cancer. Front Endocrinol (Lausanne), 2021. 12: p. 720723.
3. Schlumberger, M., et al., Lenvatinib versus placebo in radioiodine-refractory thyroid cancer. N Engl J Med, 2015. 372(7): p. 621-30.
4. Brose, M.S., et al., Effect of Age on the Efficacy and Safety of Lenvatinib in Radioiodine-Refractory Differentiated Thyroid Cancer in the Phase III SELECT Trial. J Clin Oncol, 2017. 35(23): p. 2692-2699.
5. Brose, M.S., et al., Sorafenib in radioactive iodine-refractory, locally advanced or metastatic differentiated thyroid cancer: a randomised, double-blind, phase 3 trial. Lancet, 2014. 384(9940): p. 319-28.
6. Brose, M.S., et al., Cabozantinib for radioiodine-refractory differentiated thyroid cancer (COSMIC-311): a randomised, double-blind, placebo-controlled, phase 3 trial. Lancet Oncol, 2021. 22(8): p. 1126-1138.
7. Landa, I., et al., Genomic and transcriptomic hallmarks of poorly differentiated and anaplastic thyroid cancers. J Clin Invest, 2016. 126(3): p. 1052-66.
8. Shah, M.H., et al., Results of randomized phase II trial of dabrafenib versus dabrafenib plus trametinib in BRAF-mutated papillary thyroid carcinoma. Journal of Clinical Oncology, 2017. 35(15_suppl): p. 6022-6022.
9. Busaidy, N.L., et al., Dabrafenib Versus Dabrafenib + Trametinib in BRAF-Mutated Radioactive Iodine Refractory Differentiated Thyroid Cancer: Results of a Randomized, Phase 2, Open-Label Multicenter Trial. Thyroid, 2022.
10. Cabanillas, M.E., M. Ryder, and C. Jimenez, Targeted Therapy for Advanced Thyroid Cancer: Kinase Inhibitors and Beyond. Endocr Rev, 2019. 40(6): p. 1573-1604.
11. Dunn, L.A., et al., Vemurafenib Redifferentiation of BRAF Mutant, RAI-Refractory Thyroid Cancers. J Clin Endocrinol Metab, 2019. 104(5): p. 1417-1428.
12. Rothenberg, S.M., et al., Redifferentiation of iodine-refractory BRAF V600E-mutant metastatic papillary thyroid cancer with dabrafenib. Clin Cancer Res, 2015. 21(5): p. 1028-35.
13. Groussin, L., J. Clerc, and O. Huillard, Larotrectinib-Enhanced Radioactive Iodine Uptake in Advanced Thyroid Cancer. N Engl J Med, 2020. 383(17): p. 1686-1687.
14. Lee, Y.A., et al., NTRK and RET fusion-directed therapy in pediatric thyroid cancer yields a tumor response and radioiodine uptake. J Clin Invest, 2021. 131(18).
15. Ho, A.L., et al., Selumetinib-enhanced radioiodine uptake in advanced thyroid cancer. N Engl J Med, 2013. 368(7): p. 623-32.
16. Jaber, T., et al., Targeted Therapy in Advanced Thyroid Cancer to Resensitize Tumors to Radioactive Iodine. J Clin Endocrinol Metab, 2018. 103(10): p. 3698-3705.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

We invite you to submit any questions or comments regarding this blog post below, for potential response in a future blog or social media post.

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Iñigo Landa, PhD
Brigham and Women’s Hospital & Harvard Medical School
Boston, MA
May 20, 2022

Thyroid cancers are driven by a handful of genetic alterations. Papillary thyroid cancer (PTC), the most frequent thyroid tumor with excellent survival rates, primarily harbors mutations involving BRAF, RAS or RET genes, which in turn constitutively activate the MAPK pathway, a key process for cell proliferation (1). A subset of PTCs can evolve to more aggressive forms, namely poorly differentiated (PDTC) and anaplastic thyroid cancers (ATC), which account for most of the disease-associated morbidity and mortality (2, 3). TERT (telomerase reverse transcriptase) is one of the genes that is most often mutated as thyroid cancer progresses. Mutations in TERT occur in its promoter region, which is the non-coding portion of a gene acting as an on/off switch. The acquisition of a TERT promoter mutation (TPM) reactivates the expression of telomerase, a bona fide oncogene that is otherwise silenced in human adult cells.

TPMs were discovered in advanced melanomas in 2013 (4, 5), then found at high rates in certain tumor types, such as glioblastomas, bladder and hepatocellular carcinomas (6), and shortly after reported in thyroid carcinomas (7-10). Remarkably, TPMs display a stepwise increase across thyroid specimens, tracking with tumor virulence. Less than 10% of the mostly indolent PTCs harbor TPMs; this prevalence increases in high grade PTCs and PDTCs, rising to more than 70% in the highly aggressive ATCs (11-13). Within each tumor type, TPMs systematically associate with poor prognosis. They correlate with an increased frequency of metastasis, persistent disease and lower survival in PTC patients, particularly when they co- occur with BRAFV600E or RAS oncogenic mutations (14-16). In advanced disease, patients with TERT-mutant PDTCs develop more metastasis, whereas survival of ATC patients whose tumors carry TPMs is further diminished (12). Overall, TERT promoter mutations have become a promising biomarker of poor prognosis which is progressively being incorporated in the guidelines for the management of thyroid cancer patients (17, 18).

Telomerase reactivation, which in thyroid tumors mainly occur via the acquisition of TPMs, likely enhances several molecular functions of TERT, which are relevant for the biology of cancer cells. The best-known role of telomerase is its ability to prevent the critical shortening of chromosomal ends (called “telomeres”), thus circumventing the molecular clock for cells to stop dividing (19). There are, however, multiple non-telomeric TERT functions that likely favor cancer fitness (20, 21). The elucidation of which of these cellular processes are unleashed in aggressive thyroid tumors is a topic of great interest for research, and has the potential to unveil novel nodes for genotype-driven and mechanism-oriented therapeutic intervention for thyroid cancer patients harboring TPMs.

References:
1. Fagin JA, and Wells SA, Jr. Biologic and Clinical Perspectives on Thyroid Cancer. N Engl J Med. 2016;375(23):2307.
2. Nikiforov YE, and Nikiforova MN. Molecular genetics and diagnosis of thyroid cancer. Nat Rev Endocrinol. 2011;7(10):569-80.
3. Smallridge RC, and Copland JA. Anaplastic thyroid carcinoma: pathogenesis and emerging therapies. Clin Oncol (R Coll Radiol). 2010;22(6):486-97.
4. Huang FW, Hodis E, Xu MJ, Kryukov GV, Chin L, and Garraway LA. Highly recurrent TERT promoter mutations in human melanoma. Science. 2013;339(6122):957-9.
5. Horn S, Figl A, Rachakonda PS, Fischer C, Sucker A, Gast A, et al. TERT promoter mutations in familial and sporadic melanoma. Science. 2013;339(6122):959-61.
6. Killela PJ, Reitman ZJ, Jiao Y, Bettegowda C, Agrawal N, Diaz LA, Jr., et al. TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal. Proc Natl Acad Sci U S A. 2013;110(15):6021-6.
7. Landa I, Ganly I, Chan TA, Mitsutake N, Matsuse M, Ibrahimpasic T, et al. Frequent somatic TERT promoter mutations in thyroid cancer: higher prevalence in advanced forms of the disease. J Clin Endocrinol Metab. 2013;98(9):E1562-6.
8. Liu T, Wang N, Cao J, Sofiadis A, Dinets A, Zedenius J, et al. The age- and shorter telomere-dependent TERT promoter mutation in follicular thyroid cell-derived carcinomas. Oncogene. 2013.
9. Liu X, Bishop J, Shan Y, Pai S, Liu D, Murugan AK, et al. Highly prevalent TERT promoter mutations in aggressive thyroid cancers. Endocr Relat Cancer. 2013;20(4):603-10.
10. Vinagre J, Almeida A, Populo H, Batista R, Lyra J, Pinto V, et al. Frequency of TERT promoter mutations in human cancers. Nature communications. 2013;4:2185.
11. Cancer Genome Atlas Research N. Integrated genomic characterization of papillary thyroid carcinoma. Cell. 2014;159(3):676-90.
12. Landa I, Ibrahimpasic T, Boucai L, Sinha R, Knauf JA, Shah RH, et al. Genomic and transcriptomic hallmarks of poorly differentiated and anaplastic thyroid cancers. J Clin Invest. 2016;126(3):1052-66.
13. Pozdeyev N, Gay L, Sokol ES, Hartmaier RJ, Deaver KE, Davis SN, et al. Genetic analysis of 779 advanced differentiated and anaplastic thyroid cancers. Clin Cancer Res. 2018.
14. Melo M, Rocha AG, Vinagre J, Batista R, Peixoto J, Tavares C, et al. TERT promoter mutations are a major indicator of poor outcome in differentiated thyroid carcinomas. J Clin Endocrinol Metab. 2014:jc20133734.
15. Xing M, Liu R, Liu X, Murugan AK, Zhu G, Zeiger MA, et al. BRAF V600E and TERT promoter mutations cooperatively identify the most aggressive papillary thyroid cancer with highest recurrence. J Clin Oncol. 2014;32(25):2718-26.
16. Song YS, Lim JA, Choi H, Won JK, Moon JH, Cho SW, et al. Prognostic effects of TERT promoter mutations are enhanced by coexistence with BRAF or RAS mutations and strengthen the risk prediction by the ATA or TNM staging system in differentiated thyroid cancer patients. Cancer. 2016;122(9):1370-9.
17. Bible KC, Kebebew E, Brierley J, Brito JP, Cabanillas ME, Clark TJ, Jr., et al. 2021 American Thyroid Association Guidelines for Management of Patients with Anaplastic Thyroid Cancer. Thyroid. 2021;31(3):337-86.

Disclaimer:
The ideas and opinions expressed on the ATA Blogs do not necessarily reflect those of the ATA. None of the information posted is intended as medical, legal, or business advice, or advice about reimbursement for health care services. The mention of any product, service, company, therapy or physician practice does not constitute an endorsement of any kind by ATA. ATA assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the material contained in, posted on, or linked to this site, or any errors or omissions.

For more information on Thyroid Topics please visit: https://www.thyroid.org/thyroid-information/

We invite you to submit any questions or comments regarding this blog post below, for potential response in a future blog or social media post.

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