⚡ Quick Start — If You Read Nothing Else
The 8 most important things to know right now.
- Most thyroid cancers are highly curable. Papillary thyroid cancer — the most common type (80–85% of cases) — has a 10-year survival rate above 98% when appropriately treated. Even many patients with regional lymph node spread do very well. This is genuinely one of the most treatable cancers.
- Not all thyroid nodules need surgery. The majority of thyroid nodules are benign. Fine-needle aspiration (FNA) biopsy and molecular tests like Afirma and ThyroSeq can now determine with high confidence whether a nodule is low-risk, potentially sparing you an unnecessary operation.
- Active surveillance is a real option for some small cancers. If you have a papillary thyroid microcarcinoma (under 1 cm) without aggressive features, watching it with regular ultrasound may be just as safe as immediate surgery — with 30 years of follow-up data from Japan supporting this approach.
- Molecular testing has changed everything. Knowing whether your cancer carries a BRAF, RET, NTRK, or RAS mutation now directly influences treatment decisions — from surgery extent to whether highly effective targeted therapies are available for you.
- There are four major types — and they behave very differently. Papillary and follicular (together called "differentiated") are the most common and most curable. Medullary thyroid cancer (MTC) arises from different cells and requires different monitoring. Anaplastic thyroid cancer (ATC) is rare but aggressive and now has targeted therapy options that didn't exist five years ago.
- After thyroidectomy, you will need thyroid hormone for life. Levothyroxine replaces what your thyroid used to make. The dose is carefully managed — in many patients it is intentionally set higher than normal to suppress TSH and reduce recurrence risk. Getting this balance right matters.
- Targeted therapies have transformed advanced disease. RET inhibitors (selpercatinib, pralsetinib) achieve response rates above 80% in RET-altered cancers. Lenvatinib nearly triples progression-free survival in RAI-refractory disease. Even anaplastic thyroid cancer with BRAF V600E mutations now responds to dabrafenib plus trametinib.
- The overdiagnosis problem is real — and worth understanding. Thyroid cancer incidence has increased dramatically worldwide (up to 15-fold in South Korea), driven largely by detecting small, slow-growing tumors that might never cause harm. Understanding this helps you and your doctor calibrate how aggressive your treatment needs to be.
Overview — Understanding Thyroid Cancer in 2026
Thyroid cancer occupies a unique position in oncology. It is the most rapidly increasing cancer diagnosis globally, yet the vast majority of cases are highly curable. This apparent contradiction has a straightforward explanation: improved imaging (particularly neck ultrasound) now detects tiny cancers that were always there but previously went unnoticed. Most of these small papillary thyroid cancers grow so slowly that many would never cause symptoms in a lifetime.
That does not mean thyroid cancer is trivial. A subset of thyroid cancers are aggressive, can spread to lymph nodes and distant organs, and require intensive, sophisticated treatment. The art of modern thyroid cancer care is matching treatment intensity to disease risk — avoiding both overtreatment of indolent disease and undertreatment of dangerous disease.
What has changed recently
- Molecular testing is now central to care. Tests like Afirma GSC and ThyroSeq v3 can help determine whether an indeterminate thyroid nodule needs surgery, and tumor molecular profiling (BRAF, RET, NTRK, RAS) guides therapy selection in advanced disease.
- Active surveillance has been validated. The Kuma Hospital program in Japan has followed over 5,600 patients with small papillary microcarcinomas for up to 30 years. Only 3.8% showed tumor enlargement, and there have been zero thyroid cancer deaths in the surveillance group. This is now a recognized alternative to surgery for carefully selected patients.
- Precision-targeted therapies have arrived. Selpercatinib and pralsetinib for RET-altered cancers, dabrafenib plus trametinib for BRAF V600E-mutant ATC, larotrectinib and entrectinib for NTRK-fusion cancers — these represent genuine breakthroughs for patients whose disease once had limited options.
- Treatment de-escalation is gaining traction. Guidelines increasingly support less extensive surgery (lobectomy instead of total thyroidectomy) and less radioactive iodine for low-risk patients, recognizing that more aggressive treatment doesn't improve outcomes but does increase complications.
Diagnosis & Molecular Testing
The path to a thyroid cancer diagnosis typically begins with a nodule — a lump in the thyroid gland found during a physical exam, incidentally on imaging done for another reason, or noticed by the patient. Most thyroid nodules are benign (95% or more), so the central diagnostic challenge is figuring out which ones need treatment.
The Bethesda system — your biopsy result explained
Fine-needle aspiration (FNA) biopsy is the cornerstone of thyroid nodule evaluation. Results are reported using the Bethesda System for Reporting Thyroid Cytopathology, with six categories:
- Bethesda I — Nondiagnostic: Not enough cells to evaluate. Usually requires a repeat FNA. Malignancy risk: 5–10%.
- Bethesda II — Benign: No evidence of cancer. Follow-up with ultrasound, no surgery needed in most cases. Malignancy risk: 0–3%.
- Bethesda III — Atypia of Undetermined Significance (AUS): Some abnormal cells but not clearly cancerous. This is where molecular testing is most valuable. Malignancy risk: 6–18% (before molecular testing).
- Bethesda IV — Follicular Neoplasm: Cannot distinguish benign follicular adenoma from follicular carcinoma on cytology alone. Molecular testing or diagnostic surgery usually recommended. Malignancy risk: 10–40%.
- Bethesda V — Suspicious for Malignancy: Likely cancer but not definitive. Surgery usually recommended. Malignancy risk: 45–75%.
- Bethesda VI — Malignant: Cancer confirmed. Surgery planned. Malignancy risk: 97–99%.
Molecular testing — avoiding unnecessary surgery
For Bethesda III and IV results (the "indeterminate" categories), molecular testing has been transformative. Instead of proceeding directly to diagnostic surgery to find out if a nodule is cancerous, these tests analyze the genetic profile of the biopsy cells:
- Afirma Genomic Sequencing Classifier (GSC): A "rule-out" test. A benign Afirma result carries a negative predictive value of 96% for Bethesda III and 95% for Bethesda IV nodules — meaning you can safely avoid surgery. If suspicious, surgery is typically recommended.
- ThyroSeq v3: A "rule-in and rule-out" test that sequences 112 genes. Sensitivity of 87.5% with a negative predictive value of 80% for Bethesda IV nodules. It identifies specific mutations (BRAF, RAS, RET, NTRK) that inform both cancer risk and aggressiveness.
- ThyGeNEXT/ThyraMIR: A combined approach using mutation analysis plus microRNA expression.
The practical impact: molecular testing has reduced the rate of unnecessary diagnostic surgery for indeterminate nodules by approximately 50%. If your biopsy comes back Bethesda III or IV, ask whether molecular testing has been performed or would be appropriate before proceeding to surgery.
What your molecular profile means
Beyond diagnosis, molecular testing of thyroid cancer tissue identifies mutations that matter for treatment:
- BRAF V600E: The most common mutation in papillary thyroid cancer (40–60%). Associated with more aggressive behavior, higher recurrence risk, and lower RAI avidity. In anaplastic thyroid cancer, it opens the door to dabrafenib plus trametinib targeted therapy.
- RET fusions (in papillary TC) and RET point mutations (in medullary TC): RET-selective inhibitors (selpercatinib, pralsetinib) are highly effective. All medullary thyroid cancer patients should have RET testing.
- NTRK fusions: Rare (approximately 2–5% of papillary TC) but important because larotrectinib and entrectinib show excellent response rates across NTRK-fusion cancers regardless of tumor origin.
- RAS mutations (NRAS, HRAS, KRAS): Common in follicular thyroid cancer and follicular variant of papillary TC. Generally associated with lower aggressiveness and higher RAI responsiveness compared to BRAF-mutant tumors.
- TERT promoter mutations: When combined with BRAF V600E, associated with significantly worse prognosis. More common in older patients and aggressive histologic variants.
Surgery, Radioactive Iodine & Targeted Therapy
Treatment for thyroid cancer is highly individualized, guided by cancer type, stage, molecular profile, and risk stratification. The core pillars are surgery, radioactive iodine (for differentiated thyroid cancer), TSH suppression, and — for advanced disease — targeted systemic therapy.
Surgery — the foundation of treatment
- Central neck dissection (level VI): Routine prophylactic central neck dissection remains debated. ATA guidelines suggest it should be considered for clinically involved nodes (therapeutic) or advanced primary tumors, but routine prophylactic dissection for small, low-risk cancers has not been shown to improve survival and increases the risk of hypoparathyroidism.
- Lateral neck dissection: Performed only when lateral compartment lymph node metastases are confirmed by biopsy. Never done prophylactically.
- Surgical complications to understand: Recurrent laryngeal nerve injury (temporary in 5–10%, permanent in 1–2% at experienced centers), hypoparathyroidism (temporary in 10–30% after total thyroidectomy, permanent in 1–4%), bleeding. Surgeon experience and case volume are among the strongest predictors of complication rates.
Radioactive iodine (RAI) therapy
After total thyroidectomy for differentiated thyroid cancer, RAI may be recommended to destroy any remaining thyroid tissue and treat microscopic disease. Whether you need RAI depends on your risk:
- Low-risk (ATA): Small (≤4 cm), intrathyroidal, no aggressive features, no vascular invasion, no lymph node involvement. RAI is generally not recommended. Observation with thyroglobulin monitoring is preferred.
- Intermediate-risk: Minor extrathyroidal extension, small lymph node metastases, vascular invasion, aggressive histologic variants. RAI is considered and often recommended. Typical activity: 30–100 mCi.
- High-risk: Gross extrathyroidal extension, large lymph node metastases, distant metastases, incomplete surgical resection. RAI is recommended. Typical activity: 100–200 mCi.
TSH suppression — levothyroxine as therapy
After thyroidectomy, levothyroxine serves a dual purpose: replacing thyroid hormone and suppressing TSH (which can stimulate thyroid cancer growth). Target TSH levels are risk-stratified:
- High-risk or active disease: TSH <0.1 mU/L (full suppression)
- Intermediate-risk, initial treatment: TSH 0.1–0.5 mU/L
- Low-risk with excellent response: TSH 0.5–2.0 mU/L (near-normal)
- Long-term with no evidence of disease: TSH in normal range (0.5–2.0 mU/L)
Over-suppression for prolonged periods carries risks: atrial fibrillation (especially in patients over 65), decreased bone density (especially postmenopausal women), anxiety, and insomnia. Dynamic risk stratification allows TSH targets to be relaxed over time as your disease response becomes clear.
Targeted therapy — when cancer is advanced
For patients whose differentiated thyroid cancer no longer responds to RAI, or for medullary and anaplastic thyroid cancers, targeted therapies represent major advances:
- Lenvatinib (Lenvima): A multikinase inhibitor. In the SELECT trial, it extended progression-free survival from 3.6 to 18.3 months in RAI-refractory DTC, with an overall response rate of 64.8%. NCCN Category 1 recommendation. The FDA label starting dose is 24 mg by mouth once daily (FDA label, Lenvima). Side effects include hypertension, diarrhea, hand-foot syndrome, fatigue, and weight loss.
- Sorafenib (Nexavar): Another multikinase inhibitor. The DECISION trial showed PFS of 10.8 vs. 5.8 months in RAI-refractory DTC. The FDA label dose is 400 mg by mouth twice daily on an empty stomach (FDA label, Nexavar). Generally used when lenvatinib is not tolerated or available.
- Cabozantinib (Cabometyx/Cometriq): Approved for MTC (EXAM trial: PFS 11.2 vs. 4.0 months) and for differentiated thyroid cancer after prior therapy (COSMIC-311: PFS 11.0 months post-lenvatinib/sorafenib). The Cometriq formulation is dosed at 140 mg by mouth once daily for medullary thyroid cancer (FDA label, Cometriq).
- Selpercatinib (Retevmo): A RET-selective inhibitor. Received FDA full approval for RET-mutant MTC and RET-fusion thyroid cancer. LIBRETTO-001 showed overall response rates exceeding 80% in MTC and over 90% in RET-fusion DTC. LIBRETTO-531 showed 72% reduction in progression risk vs. cabozantinib/vandetanib as first-line MTC therapy. The FDA label dose is weight-based: 120 mg (under 50 kg) or 160 mg (50 kg or more) by mouth twice daily (FDA label, Retevmo). Better tolerated than multikinase inhibitors.
- Pralsetinib (Gavreto): Another RET-selective inhibitor. ARROW trial data show similar efficacy in RET-altered thyroid cancers.
- Dabrafenib + trametinib: FDA-approved for BRAF V600E-mutant anaplastic thyroid cancer. The ROAR trial showed a 56% response rate in ATC with median overall survival of 15 months — remarkable for a cancer that previously had median survival of 3–5 months. The FDA-approved regimen is dabrafenib 150 mg by mouth twice daily plus trametinib 2 mg by mouth once daily (FDA labels, Tafinlar and Mekinist).
- Larotrectinib and entrectinib: NTRK inhibitors for NTRK-fusion cancers. Larotrectinib showed an 86% response rate in differentiated thyroid cancer; entrectinib 54% with median PFS of 44 months.
Doses and numbers to know — what the labels actually say
These are the standard starting doses and monitoring rules written into the FDA prescribing information (the drug “label”) for the main thyroid cancer medicines. Your team may adjust them for you, but knowing the standard numbers helps you ask precise questions.
- Levothyroxine: dosed in micrograms (mcg) and individualized to a TSH target. A typical full-replacement dose after total thyroidectomy is roughly 1.6 mcg per kg of body weight per day (about 100–175 mcg for most adults), then fine-tuned by TSH. TSH targets by risk (ATA 2015 guideline): high-risk or active disease below 0.1 mU/L; intermediate-risk 0.1–0.5 mU/L; low-risk with excellent response 0.5–2.0 mU/L. Ask: "What is my exact levothyroxine dose in micrograms, and what TSH number are we aiming for?"
- Lenvatinib (Lenvima): FDA label starting dose 24 mg by mouth once daily; the dose-reduction steps are 20 mg, then 14 mg, then 10 mg. The label directs holding the drug for blood pressure that stays at or above 160/100 mmHg despite treatment, and for urine protein of 2 grams or more in 24 hours (FDA label, Lenvima). Ask: "At what blood pressure reading should I call you or hold my lenvatinib?"
- Selpercatinib (Retevmo): FDA label dose 160 mg by mouth twice daily for adults 50 kg or heavier (120 mg twice daily under 50 kg). The label directs monitoring liver enzymes, blood pressure, and the ECG for QT prolongation (FDA label, Retevmo). Ask: "How often will you check my liver enzymes and ECG on selpercatinib?"
- Cabozantinib: two different products at different doses — Cabometyx 60 mg once daily for RAI-refractory differentiated cancer, and Cometriq 140 mg once daily for medullary thyroid cancer (FDA labels). Ask: "Which cabozantinib product and dose am I on, and why?"
- Dabrafenib + trametinib: for BRAF V600E anaplastic cancer, the FDA-approved doses are dabrafenib 150 mg twice daily plus trametinib 2 mg once daily (FDA labels, Tafinlar and Mekinist). Fever is the most common reason to briefly hold dabrafenib.
- Sorafenib (Nexavar): FDA label dose 400 mg by mouth twice daily on an empty stomach.
When a targeted drug is paused or lowered
These oral drugs are frequently held or dose-reduced rather than stopped for good — that is normal and keeps you on treatment longer. Each FDA label lists when to permanently discontinue: discontinue if there is a gastrointestinal perforation or a fistula, a severe bleeding or clotting event, a hypertensive crisis, or severe liver injury. Short of those, the usual stop rule is a temporary hold until the side effect settles, then a restart at a lower dose — not stopping the drug entirely. Ask: "If I hit a side effect, is the plan to hold and lower the dose, or to stop this drug?"
Medullary thyroid cancer and MEN2 — why the whole family matters
Medullary thyroid cancer (MTC) is different from the common papillary and follicular types. It comes from calcitonin-producing C cells, does not respond to radioactive iodine, and is inherited in about 1 in 4 cases through a change in the RET gene (the MEN2 syndromes). Two safety steps are essential and easy to overlook:
- RET genetic testing for every MTC patient. The ATA 2015 Medullary Thyroid Cancer guideline recommends germline RET testing for everyone diagnosed with MTC, because a positive result changes screening for you and triggers testing for your relatives. Ask: "Have I had germline RET testing, and should my children and siblings be tested?"
- Rule out a pheochromocytoma before any thyroid surgery. People with MEN2 can have a hidden adrenaline-producing adrenal tumor (pheochromocytoma). Operating on an undiagnosed pheochromocytoma can trigger a dangerous, even fatal, blood-pressure crisis under anesthesia. Before surgery, your team should check blood or urine metanephrines; if a pheochromocytoma is found, it must be removed first. Ask: "Have I been screened for a pheochromocytoma before my thyroid surgery?"
MTC is monitored with two blood markers, calcitonin and CEA, rather than thyroglobulin. A post-surgery calcitonin under 10 pg/mL suggests biochemical cure; a calcitonin above 150 pg/mL suggests disease may have spread. For RET-mutant MTC that needs drug therapy, selpercatinib is the preferred first-line option (LIBRETTO-531 trial, 2023).
Monitoring & Survivorship
One of the defining features of thyroid cancer care is the extended monitoring period. Unlike many cancers where surveillance tapers after five years, thyroid cancer follow-up often continues for decades — because recurrences can occur late, and because thyroid hormone management is lifelong.
Dynamic risk stratification — your risk changes over time
A crucial concept in modern thyroid cancer care: your initial risk category (determined at diagnosis and surgery) is not fixed. It is updated based on your response to treatment. The ATA defines four response categories:
- Excellent response: Thyroglobulin <0.2 ng/mL (suppressed) or <1 ng/mL (stimulated), negative thyroglobulin antibodies, negative neck ultrasound, negative RAI scan (if done). Recurrence risk drops to 1–4% regardless of initial risk category.
- Biochemical incomplete: Elevated thyroglobulin or rising thyroglobulin antibodies without structural disease on imaging. 15–20% will eventually have identifiable structural disease.
- Structural incomplete: Persistent or newly identified disease on imaging. Requires further treatment consideration.
- Indeterminate: Nonspecific findings that can't be confidently classified. Usually observed with continued monitoring.
This dynamic approach means that a patient initially classified as intermediate-risk who achieves an excellent response can have their TSH target relaxed and monitoring intervals extended — acknowledging that the cancer is behaving like low-risk disease.
Thyroglobulin — your key blood marker
After total thyroidectomy and RAI, thyroglobulin (Tg) is the most important tumor marker for differentiated thyroid cancer. Any thyroglobulin remaining after complete treatment suggests residual thyroid tissue — either normal remnant or cancer.
- What's normal: After successful treatment, suppressed Tg should be undetectable (<0.2 ng/mL). Stimulated Tg (after TSH elevation or Thyrogen) should be <1 ng/mL.
- Thyroglobulin antibodies (TgAb): Present in 20–25% of thyroid cancer patients. When present, they can falsely lower Tg levels (immunometric assays) or falsely elevate them (RIA). TgAb trends become the proxy marker — declining TgAb is reassuring; rising TgAb is concerning.
- Rising Tg or TgAb: Triggers additional imaging — usually neck ultrasound first, then potentially CT, RAI diagnostic scan, or FDG-PET/CT depending on the clinical picture.
Monitoring schedule
- First 1–2 years: Physical exam, TSH, Tg, TgAb every 3–6 months. Neck ultrasound at 6–12 months post-surgery, then every 6–12 months.
- Years 2–5 (excellent response): Labs every 6–12 months. Neck ultrasound annually or as clinically indicated.
- After 5 years (excellent response): Labs annually. Ultrasound can be spaced to every 2–3 years or discontinued if low-risk with sustained excellent response.
- Lobectomy patients: Thyroglobulin interpretation is different (normal remaining thyroid produces Tg). Ultrasound of the remaining lobe and thyroid bed is the primary monitoring tool.
Other doses worth knowing — vandetanib and post-surgery support
- Vandetanib (Caprelsa): an older targeted drug for medullary thyroid cancer, FDA label dose 300 mg by mouth once daily. It carries a boxed warning for QT prolongation and is dispensed through a restricted (REMS) program with regular ECGs (FDA label, Caprelsa).
- Calcium after total thyroidectomy: if the parathyroid glands are temporarily stunned, blood calcium can drop. Replacement is commonly calcium carbonate 1,000–1,500 mg of elemental calcium two to three times daily, often with calcitriol (active vitamin D) 0.25–0.5 mcg, tapered as the glands recover. Report tingling around the mouth or fingertips promptly.
- Liothyronine (T3): when a small amount of T3 is added to levothyroxine for persistent symptoms, it is dosed in micrograms (often around 5 mcg once or twice daily) with careful TSH monitoring to avoid over-treatment.
These are starting points from the prescribing information and typical practice; your exact doses are set by your care team. Ask: "What are my exact calcium and vitamin D doses, and when do we taper them?"
Living well with thyroid cancer
Advanced Disease & Clinical Trials
While most thyroid cancer patients have excellent outcomes with surgery and RAI, a subset will develop advanced, progressive, or refractory disease that requires systemic therapy. This section covers the latest treatment approaches and emerging options.
Treatment sequencing for RAI-refractory differentiated thyroid cancer
When differentiated thyroid cancer no longer responds to radioactive iodine and is progressing, systemic therapy is considered. Important principles:
- Not all RAI-refractory disease needs immediate treatment. Slowly growing, asymptomatic disease may be safely observed. The decision to start systemic therapy considers rate of progression, tumor burden, symptoms, and patient preference.
- Molecular profiling guides therapy selection. Before starting any systemic agent, ensure comprehensive molecular testing has been done. RET fusions, NTRK fusions, and specific BRAF mutations may qualify you for highly effective, better-tolerated selective inhibitors rather than broad multikinase inhibitors.
- First-line for non-targeted cases: Lenvatinib (preferred based on SELECT trial data showing superior PFS and response rates) or sorafenib.
- Second-line: Cabozantinib (COSMIC-311 data) or clinical trial.
- Mutation-specific: Selpercatinib or pralsetinib for RET fusions; larotrectinib or entrectinib for NTRK fusions.
Redifferentiation therapy — restoring RAI sensitivity
An exciting frontier: using targeted agents to make RAI-refractory tumors take up iodine again. This approach exploits the fact that many "refractory" tumors have suppressed but not entirely lost the ability to concentrate iodine:
- Selumetinib (MEK inhibitor): In a key study, 60% of patients with RAI-refractory DTC showed restored RAI uptake after selumetinib treatment, and some achieved partial responses with subsequent RAI. However, the larger phase 3 ASTRA trial did not meet its primary endpoint, tempering initial enthusiasm.
- Other approaches under investigation: Dabrafenib (for BRAF-mutant tumors), trametinib, and combination strategies are being studied for redifferentiation potential.
Immunotherapy in thyroid cancer
Checkpoint inhibitors are being studied in thyroid cancer, particularly in combination with TKIs:
- Pembrolizumab + lenvatinib: Phase 2 data show a 65.5% overall response rate in RAI-refractory DTC and 52% in ATC. Studies are ongoing.
- Nivolumab and ipilimumab combinations: Being evaluated in ATC and advanced MTC in clinical trials.
- Note: Single-agent immunotherapy has shown limited activity in thyroid cancer. The combination approach appears more promising.
Next-generation targeted agents
- Next-gen RET inhibitors: LOXO-260, enbezotinib (EP0031), SY-5007, and TY-1091 are in development to overcome resistance mutations (particularly the solvent front G623R mutation) that can develop during treatment with selpercatinib or pralsetinib.
- Neoadjuvant targeted therapy: Using dabrafenib/trametinib or selpercatinib before surgery to shrink locally advanced tumors is being studied in clinical trials (including NCT04675710 for BRAF-mutant ATC).
Key clinical trials — past and ongoing
The following trials have shaped or are actively shaping thyroid cancer treatment. Knowing their names and identifiers helps you discuss options with your oncologist and search for enrollment opportunities.
- SELECT (NCT01321554) — The landmark trial that led to lenvatinib approval for RAI-refractory DTC. Showed PFS of 18.3 vs 3.6 months.
- DECISION (NCT00984282) — Led to sorafenib approval for RAI-refractory DTC. PFS 10.8 vs 5.8 months.
- COSMIC-311 (NCT03690388) — Established cabozantinib as a second-line option for RAI-refractory DTC after prior TKI therapy.
- LIBRETTO-001 (NCT03157128) — The pivotal basket trial for selpercatinib in RET-altered cancers. Response rates above 80% in MTC and above 90% in RET-fusion DTC.
- LIBRETTO-531 (NCT04211337) — Head-to-head comparison of selpercatinib vs cabozantinib/vandetanib as first-line MTC therapy. Showed 72% reduction in progression risk.
- ARROW (NCT03037385) — Pivotal trial for pralsetinib in RET-altered thyroid cancer.
- ROAR (NCT02034110) — Demonstrated dabrafenib + trametinib efficacy in BRAF V600E-mutant ATC (56% response rate).
- ASTRA (NCT01843062) — Phase 3 trial of selumetinib + RAI for RAI-refractory DTC. Did not meet its primary endpoint.
- ESTIMABL2 (NCT01837745) — French trial showing that omitting RAI was non-inferior to low-dose RAI for low-risk DTC. Changed practice in Europe and influenced US guidelines.
- NCT04675710 — Ongoing trial evaluating neoadjuvant dabrafenib/trametinib before surgery for BRAF V600E-mutant ATC.
Finding and joining clinical trials
- ClinicalTrials.gov — search "thyroid cancer" filtered by your cancer type and location
- American Thyroid Association clinical trials page
- NCCN clinical trial resources
- Huntsman Cancer Institute (Utah) clinical trials office: healthcare.utah.edu/huntsmancancerinstitute/clinical-trials. Phone: 801-585-0303
- Ask your oncologist about trials at MD Anderson, Memorial Sloan Kettering, and other NCI-designated cancer centers
International Access & Regulatory Landscape
Thyroid cancer treatment is broadly similar worldwide for standard therapies (surgery, RAI, levothyroxine suppression), but access to newer targeted agents, molecular testing platforms, and clinical trial participation varies significantly by region. Patients traveling internationally or comparing treatment options should be aware of these differences.
Failed & De-Adopted Therapies
Knowing what has been tried and did not work is just as important as knowing what does work. These are treatments that were once used or studied for thyroid cancer but have been abandoned, proven ineffective, or withdrawn due to safety concerns. If anyone suggests these approaches, you should discuss the evidence with your medical team.
External beam radiation for routine low-risk DTC
DE-ADOPTEDExternal beam radiation therapy (EBRT) was historically used after surgery for differentiated thyroid cancer even in low-risk patients. Evidence showed no benefit in this setting, with significant toxicity to surrounding neck structures. EBRT is now reserved only for locally advanced, unresectable disease, gross residual disease that does not respond to RAI, or anaplastic thyroid cancer. It is not part of standard management for low-risk DTC.
Routine high-dose RAI for low-risk papillary thyroid cancer
DE-ADOPTEDHigh-dose radioactive iodine (100–200 mCi) was once given routinely to nearly all thyroid cancer patients after total thyroidectomy. Multiple studies, including the HiLo trial and ESTIMABL1/ESTIMABL2 trials, demonstrated that low-risk DTC patients either need no RAI at all or only low-dose (30 mCi) ablation. High-dose RAI in low-risk patients causes unnecessary radiation exposure without improving outcomes and increases the rare risk of secondary malignancies and salivary gland damage.
Selumetinib (AZD6244) as standalone RAI-refractory DTC treatment
FAILEDSelumetinib, a MEK inhibitor, generated considerable excitement after a 2013 pilot study showed it could restore radioactive iodine uptake in some RAI-refractory patients. However, the larger phase 3 ASTRA trial did not meet its primary endpoint of improved complete remission rate when combined with RAI versus placebo plus RAI. Research into redifferentiation continues with other agents and combination approaches, but selumetinib alone did not deliver the hoped-for results.
Pralsetinib (Gavreto) — MTC indication withdrawn (US), not a full withdrawal
INDICATION NARROWED (US)This one is often misreported, so the details matter. Pralsetinib received FDA accelerated approval in December 2020 for RET fusion-positive thyroid cancer, RET-mutant medullary thyroid cancer (MTC), and RET fusion-positive lung cancer. In June 2023, the maker (then Genentech) voluntarily withdrew only the RET-mutant MTC indication in the US — because the confirmatory phase 3 MTC trial (AcceleRET-MTC) could not be completed, which is required to convert an accelerated approval to full approval. This was not a safety or efficacy problem. The RET fusion-positive thyroid cancer indication (adults and children 12+, RAI-refractory) and the lung cancer indication were not withdrawn. In February 2024, Rigel Pharmaceuticals acquired the US rights to Gavreto and resumed US marketing in June 2024. Bottom line: pralsetinib is still available in the US for RET fusion-positive thyroid cancer; for RET-mutant MTC, selpercatinib (which showed superior outcomes versus cabozantinib or vandetanib in the head-to-head LIBRETTO-531 trial) is now the preferred RET inhibitor.
Doxorubicin monotherapy for advanced thyroid cancer
DE-ADOPTEDBefore targeted therapies became available, doxorubicin (Adriamycin) was the only FDA-approved chemotherapy for thyroid cancer. Its response rates were poor (10–20% at best), responses were typically short-lived, and toxicity was significant (cardiac toxicity, myelosuppression). It has been largely replaced by multikinase inhibitors and selective targeted agents for advanced DTC and MTC, and by combination regimens for ATC.
Routine total thyroidectomy for all thyroid cancers
DE-ADOPTEDFor decades, total thyroidectomy was performed on virtually every thyroid cancer patient regardless of tumor size or risk factors. The ATA 2015 guidelines and subsequent evidence demonstrated that lobectomy (removing only the affected lobe) is appropriate and equally effective for unifocal tumors 1–4 cm without extrathyroidal extension, lymph node involvement, or high-risk features. Lobectomy avoids the need for lifelong thyroid hormone replacement in some patients and eliminates the risk of bilateral recurrent laryngeal nerve injury and permanent hypoparathyroidism associated with total thyroidectomy.
Thyroid hormone suppression to undetectable TSH in all patients
DE-ADOPTEDAggressive TSH suppression (TSH <0.1 mU/L) was once applied to all thyroid cancer patients indefinitely. Evidence now shows that this degree of suppression benefits only high-risk and intermediate-risk patients. For low-risk patients who achieve excellent response (undetectable thyroglobulin, no structural disease), TSH can be maintained at 0.5–2.0 mU/L, reducing the risks of atrial fibrillation, osteoporosis, and other complications of subclinical hyperthyroidism. Dynamic risk stratification guides individualized TSH targets over time.
Support & Resources
Mountain West / Utah
- Huntsman Cancer Institute (HCI) Thyroid/Endocrine Cancer Program: Comprehensive, multidisciplinary team including endocrine surgeons, endocrinologists, nuclear medicine specialists, medical oncologists, and genetic counselors. Clinical trials available. Phone: 801-585-0303. healthcare.utah.edu/huntsmancancerinstitute
- University of Utah Endocrine Surgery: High-volume thyroid surgery center performing over 300 thyroid operations annually, with complication rates among the best nationally. Active surveillance program available for eligible patients. Phone: 801-581-2121 (U of U Health main).
- University of Utah Nuclear Medicine: Full RAI therapy services including pre-treatment dosimetry, post-therapy whole-body scans, and SPECT/CT for localization. Phone: 801-581-2121.
- Intermountain Health Endocrinology: Multiple locations across Utah for ongoing thyroid cancer follow-up, levothyroxine management, and referral coordination with HCI for complex cases. Phone: 801-442-2000.
- George E. Wahlen VA Medical Center: Endocrinology and oncology services for veterans, including thyroid cancer follow-up and coordination with HCI for specialized care. Phone: 801-582-1565.
- University of Utah Genetic Counseling: Genetic testing and counseling for MEN2 syndrome, familial medullary thyroid cancer, and other hereditary thyroid cancer syndromes (Cowden syndrome, FAP-associated thyroid cancer).
US National
- Memorial Sloan Kettering Cancer Center (MSK) Thyroid Cancer Program: One of the highest-volume thyroid cancer programs in the US. Active surveillance program for PTMC. Molecular profiling and clinical trials. mskcc.org
- MD Anderson Cancer Center Thyroid Cancer Program: Multidisciplinary endocrine oncology, clinical trials portfolio, and expertise in advanced and refractory disease. mdanderson.org
- Mayo Clinic Thyroid Cancer Program: Comprehensive thyroid cancer care across Rochester, Phoenix, and Jacksonville campuses. Expertise in complex surgical cases and RAI dosimetry. mayoclinic.org
- Massachusetts General Hospital Thyroid Unit: Longstanding expertise in thyroid cancer management, molecular testing, and clinical trials.
Veterans
- George E. Wahlen VA Medical Center (Salt Lake City): Endocrinology, oncology, and nuclear medicine for thyroid cancer. Coordinates with HCI for complex cases. Phone: 801-582-1565.
- VA Community Care Program: Veterans may be eligible for referral to NCI-designated cancer centers (including HCI, MSK, MD Anderson) when specialized thyroid cancer expertise is needed beyond what is available at the local VA.
- VA National Oncology Program: Provides clinical pathway guidance for thyroid cancer and facilitates tumor board consultation across VA medical centers.
Canada
- Princess Margaret Cancer Centre (Toronto): Canada's largest thyroid cancer referral center. Expertise in RAI-refractory disease, targeted therapy, and clinical trial access. Part of University Health Network.
- Sunnybrook Health Sciences Centre (Toronto): Odette Cancer Centre thyroid cancer program with endocrine surgery and nuclear medicine expertise.
- McGill University Health Centre (Montreal): Thyroid cancer surgical and medical oncology program, including molecular testing and RET-targeted therapy.
- BC Cancer Agency (Vancouver): Provincial thyroid cancer program with coordinated surgical, nuclear medicine, and systemic therapy services.
- Thyroid Cancer Canada: Patient advocacy organization providing support, education, and clinical trial information. thyroidcancercanada.org
International
- United Kingdom: The Christie NHS Foundation Trust (Manchester) and Imperial College Healthcare NHS Trust (London) — major thyroid cancer referral centers. Access to selpercatinib via the Cancer Drugs Fund.
- France: Institut Gustave Roussy (Villejuif, Paris) — one of Europe's leading thyroid cancer research centers. Led the ESTIMABL trials that changed RAI practice worldwide.
- Japan: Kuma Hospital (Kobe) — the pioneer of active surveillance for papillary thyroid microcarcinoma with 30+ years of follow-up data. Cancer Institute Hospital (Tokyo) — active surveillance and surgical expertise.
- South Korea: Samsung Medical Center and Asan Medical Center (Seoul) — high-volume thyroid cancer programs with extensive active surveillance experience.
National organizations
- ThyCa: Thyroid Cancer Survivors' Association — the largest thyroid cancer patient organization, offering free support groups, educational materials, low-iodine cookbook, and annual conference. thyca.org
- American Thyroid Association (ATA) — clinical guidelines, patient education, and clinical trial information. thyroid.org
- NCCN Patient Guidelines for Thyroid Cancer — free patient-friendly version of clinical treatment guidelines. nccn.org
- Light of Life Foundation — focused on advanced and aggressive thyroid cancers, funding research and patient support. lightoflifefoundation.org
- Bite Me Cancer — supporting young thyroid cancer survivors. bitemecancer.org
Financial assistance
- Levothyroxine is inexpensive. The lifelong thyroid hormone you take after surgery is a low-cost generic: roughly $11 for a 30-day supply of 50 mcg tablets at the U.S. cash price with a discount coupon (GoodRx estimate, as of July 2026), and about 99% of commercial and Medicare drug plans — and 100% of ACA marketplace plans — cover the generic.
- Manufacturer patient assistance programs: Eisai (lenvatinib/Lenvima), Exelixis (cabozantinib/Cabometyx), Eli Lilly (selpercatinib/Retevmo), and other manufacturers offer co-pay assistance and free drug programs for eligible patients. The targeted (oral) drugs are specialty-tier with high list prices, but for patients with commercial insurance the manufacturer copay programs can cut out-of-pocket cost dramatically: the LENVIMA Co-pay Program can bring cost to as little as $0 per prescription (up to $10,000 per year; Eisai), and the RETEVMO Savings Card as little as $0 per fill (up to $10,600 per year; Eli Lilly), both as of July 2026. Patients on Medicare, Medicaid, VA, or TRICARE are not eligible for these copay cards but may qualify for the manufacturers' separate patient assistance (free-drug) programs.
- Patient Advocate Foundation: Case management for insurance issues, appeals, and financial aid. patientadvocate.org
- CancerCare: Financial assistance grants, counseling, and support groups. cancercare.org
- Thyrogen (rhTSH) access: Genzyme/Sanofi offers patient assistance for Thyrogen. Discuss with your nuclear medicine team if cost is a barrier.
What thyroid cancer care costs in the United States
The prices below are approximate U.S. figures gathered in 2025–2026 from manufacturer list-price (WAC) disclosures, GoodRx cash estimates, and published payer data. A list price is almost never what an insured patient actually pays — insurance, copay cards, and patient-assistance programs usually cut the real cost dramatically. Use these numbers to understand the landscape and to ask about assistance early.
- Levothyroxine (generic, lifelong): about $11 for a 30-day supply of 50 mcg tablets at cash price with a discount coupon (GoodRx, 2026). One of the least expensive prescription drugs in wide use.
- Radioactive iodine (I-131) ablation: highly variable. The radioiodine dose itself is often about $5,000–$7,000, with a whole-body scan around $2,000 added. A 2021 study of payer-negotiated prices found enormous hospital-to-hospital variation, from a few hundred dollars to over $10,000.
- Lenvatinib (Lenvima): list price (WAC) roughly $25,700 for a 30-day supply (Eisai, 2025). The LENVIMA Co-pay Program can bring commercially insured patients to as little as $0 per fill (up to $10,000 per year; Eisai, 2026).
- Selpercatinib (Retevmo): list price (WAC) up to about $23,700 per 30-day supply at the 160 mg twice-daily dose (Eli Lilly, 2025). The RETEVMO Savings Card can bring commercial patients to as little as $0 per fill (up to $10,600 per year; Eli Lilly, 2026).
- Cabozantinib (Cabometyx): approximately $26,000–$27,000 for a 30-day supply (Exelixis list price, 2025), the same across tablet strengths. Exelixis Access Services offers copay and patient-assistance programs.
- Sorafenib (now generic): average retail around $14,800 for a 30-day supply, but as low as about $2,700 with a discount coupon (GoodRx, 2026) — far cheaper than brand Nexavar.
- Dabrafenib (Tafinlar) + trametinib (Mekinist): a high-cost specialty combination; Novartis offers a copay program that can bring eligible commercially insured patients to $0 per month (up to $15,000 per year, per drug; Novartis, 2025).
Two practical rules. First, figure out your insurance type early: patients with commercial (employer or marketplace) insurance can usually use manufacturer copay cards, while patients on Medicare, Medicaid, the VA, or TRICARE cannot use copay cards but may qualify for a manufacturer's separate free-drug patient-assistance program. Ask: "Am I eligible for the manufacturer copay card, or should we apply to the patient-assistance program?" Second, start prior authorization the day systemic therapy is chosen, because specialty-pharmacy approvals can take one to two weeks. Ask: "Has the prior authorization for my medication been submitted yet?"
Word-for-word questions worth bringing to appointments
Copy these into your phone or a notebook. Using the exact words tends to get you specific answers.
- Ask: "What type and what risk category is my thyroid cancer?"
- Ask your doctor: "Was molecular testing done, and did it find BRAF, RET, NTRK, or RAS?"
- Ask: "Am I a candidate for active surveillance instead of surgery?"
- Ask your surgeon: "How many thyroid operations do you perform each year?"
- Ask: "Do I need a lobectomy or a total thyroidectomy, and why?"
- Ask: "Do I actually need radioactive iodine, and if so at what dose in millicuries?"
- Ask your endocrinologist: "What is my exact TSH target, and when can we relax it?"
- Ask: "What is my thyroglobulin level, and is my response excellent, indeterminate, or incomplete?"
- Ask: "If my cancer is RET-positive, am I a candidate for selpercatinib?"
- Ask: "Should my family have genetic testing for MEN2?"
- Ask: "Is there a clinical trial that fits my molecular profile?"
- Ask: "Which financial-assistance program fits my insurance?"
Research and information
- ClinicalTrials.gov: The definitive source for finding thyroid cancer clinical trials. clinicaltrials.gov
- Thyroid Cancer Genomic Atlas (TCGA): Foundational research on the molecular landscape of thyroid cancer.
- PubMed: For patients who want to read the primary research. Searching "[drug name] thyroid cancer" or "[trial name]" will find the key studies.
When to seek a second opinion
- Your cancer is medullary or anaplastic thyroid cancer
- You have been told your disease is RAI-refractory
- Systemic therapy is being discussed
- You are considering active surveillance and want expert guidance
- Your cancer has recurred
- Lateral neck dissection is being recommended
- You have a hereditary thyroid cancer syndrome (MEN2, Cowden)
- Your molecular testing shows an uncommon mutation (NTRK fusion, RET fusion in DTC)
Key References
Glossary
Appendix · For discussion with your medical team
Testing Treatments on a Copy of Your Own Tumor
When a thyroid tumor is removed, surgeons often recover more tissue than the pathology lab needs for diagnosis. Researchers have learned how to take that leftover tissue and grow it in the laboratory — creating small living replicas of your specific cancer. Once those replicas are established, scientists can expose them to dozens of drugs or drug combinations and measure which ones shrink or kill the cancer cells most effectively. The idea is to give your oncologist real data about your particular tumor before committing to a treatment — rather than relying solely on population-level statistics about what works for most people with thyroid cancer.
The basic idea
Most thyroid cancers — papillary, follicular, and medullary — are slow-growing and highly treatable with surgery, radioactive iodine, or targeted drugs. But anaplastic thyroid cancer (ATC) is a different situation entirely: it is one of the most aggressive solid tumors known, with a median survival often measured in months, and standard regimens do not work well for most patients. That urgency makes ex vivo drug testing especially relevant for ATC, where finding an effective combination quickly can matter enormously. Even for differentiated thyroid cancers that stop responding to radioactive iodine or acquire resistance to kinase inhibitors such as lenvatinib or sorafenib, learning which drug your specific tumor responds to — rather than cycling through options by trial and error — is exactly the problem these models are designed to address. Because thyroidectomy is a common and well-established surgery, tissue availability is generally excellent compared with many other cancer types, which removes one of the main practical barriers to this kind of testing.
The main approaches, from fastest to slowest
Tumor Organoids (3-D Mini-Tumors in a Dish)
A small piece of your thyroid tumor is processed into single cells, then suspended in a gel-like matrix where the cells self-organize into tiny three-dimensional clusters that mimic the architecture of the original tumor. Organoids have been successfully established from both papillary thyroid cancer (PTC) and anaplastic thyroid cancer (ATC). Because ATC grows rapidly in the body, it also tends to grow rapidly in the lab — organoids from ATC can sometimes be tested within two weeks of surgery, which aligns with the urgency of the disease. Drug panels can screen 20 or more agents simultaneously. Results from organoid testing have shown reasonable correlation with clinical drug response in early studies, though large validation trials have not yet been completed.
Zebrafish Avatars
Your tumor cells are injected into zebrafish embryos, which are transparent and develop very quickly. Within days, researchers can watch whether the human cancer cells grow and spread, and then treat the fish with different drugs to see which ones stop tumor growth. The method is extremely fast — the fastest of all the platforms described here — and can screen many drugs in parallel. For thyroid cancer, zebrafish models have been used in research settings to study tumor invasion and test kinase inhibitors, including drugs that target the BRAF V600E mutation common in papillary thyroid cancer. Access outside specialized research programs is very limited, but the speed makes it theoretically well-suited to ATC.
Chorioallantoic Membrane (CAM) Assay
Tumor cells or small tumor fragments are placed onto the surface of a fertilized chicken egg membrane, where they receive a blood supply and continue to grow in a living environment. Drugs can then be applied and their effect on tumor growth measured. The CAM assay sits between organoids and mouse models in terms of biological complexity — it provides a vascularized environment without requiring months of animal work. It is less commonly used for thyroid cancer than organoids, but research groups have used it to study thyroid tumor biology and drug response in experimental settings.
Patient-Derived Xenografts (PDX) — Mouse Models
A portion of your tumor is implanted into mice that have been engineered to lack an immune system, so they do not reject human tissue. The tumor grows in the mouse, and then different drugs are tested. PDX models are considered the closest approximation to the original tumor among all laboratory platforms, but the time required — typically three to six months — makes them impractical for guiding urgent treatment decisions. They are most useful for understanding biology and testing drugs for future patients rather than informing your own immediate care.
What the evidence says so far
The evidence base for tumor functional testing in thyroid cancer is still early. Most published work consists of case reports, small series, and proof-of-concept studies rather than prospective randomized trials.
- Organoid models have been established from ATC in multiple academic centers and used to identify drug sensitivities, including responses to BRAF/MEK inhibitor combinations and immunotherapy agents, in individual patients.
- A 2022 study from the Mayo Clinic demonstrated successful organoid establishment from ATC specimens and showed that drug response patterns in organoids aligned with clinical outcomes in a small series of patients.
- PDX models for ATC have been used to validate BRAF V600E-targeted therapy responses before clinical use and to study mechanisms of resistance to dabrafenib/trametinib combinations.
- No large prospective trial has yet compared treatment outcomes for patients who received organoid-guided therapy versus standard-of-care selection in thyroid cancer specifically.
How tissue is collected and what happens to it
If you and your oncologist decide to pursue functional testing, the process typically works as follows:
- Coordination before surgery: Your surgeon contacts the laboratory to arrange same-day tissue transfer. Fresh tissue — not formalin-fixed — is required. This must be arranged in advance; it cannot be done retroactively on stored specimens.
- Tissue allocation: The pathologist takes the tissue needed for diagnosis first. Remaining tumor is divided: a portion goes to the functional testing laboratory, often in a special transport medium supplied by the lab.
- Processing: The laboratory dissociates the tumor into single cells or small clusters and begins growing them. This step may fail if too few viable cells are recovered, which is why establishment rates are not 100%.
- Drug screening: Once the model is established, a panel of drugs — often 20 to 40 agents — is applied at multiple concentrations. Automated imaging measures cell death or growth inhibition for each drug.
- Report generation: The laboratory provides a ranked list of agents by sensitivity, often with an interpretation note. This report goes to your oncologist, who considers it alongside genomic testing results, standard guidelines, and your overall health status.
Genomic testing versus functional testing — two different questions
Your oncologist may already have ordered molecular profiling of your tumor — tests such as ThyroSeq, Afirma, or next-generation sequencing panels that look for mutations including BRAF V600E, RET fusions, NTRK fusions, RAS mutations, and others. These tests identify what genetic changes are driving your tumor. Functional testing asks a related but distinct question: given those changes and everything else about your particular cancer cells, which drugs actually kill them?
The two approaches are complementary, not competitive. A BRAF V600E mutation predicts that your tumor may respond to BRAF-targeted drugs — functional testing can confirm whether it does in your specific cells, and may reveal that a combination works better than a single agent. Conversely, functional testing sometimes reveals sensitivity to a drug that genomic profiling would not have predicted, because drug response depends on the entire cellular context, not just a single mutation.
Questions to ask your oncologist or surgeon before pursuing this
- Is my tumor type and stage one where functional testing results are likely to come back in time to influence my initial treatment decision?
- Does this institution, or a partner laboratory, have an active program for thyroid cancer organoids or other functional testing platforms?
- If I have anaplastic thyroid cancer, can tissue collection be coordinated before or at the time of surgery — today?
- How will functional testing results be integrated with my molecular profiling results and with standard treatment guidelines?
- What is the cost, and is any portion covered by insurance or available through a clinical trial?
- If the model fails to establish, what is the plan?
- Are there clinical trials at this center that use functional testing to guide treatment assignment?
Finding programs and clinical trials
Tumor functional testing for thyroid cancer is available primarily through academic medical centers with dedicated translational research programs. There is no widely available commercial service for thyroid cancer organoids comparable to what exists for some other tumor types.
To find active programs:
- Search ClinicalTrials.gov for "thyroid cancer organoid," "thyroid cancer patient-derived," or "anaplastic thyroid cancer ex vivo" — filter to recruiting studies.
- Contact the endocrine surgery or endocrine oncology program at a National Cancer Institute-designated comprehensive cancer center. In the Mountain West, the Huntsman Cancer Institute at the University of Utah (801-585-0303) and Mayo Clinic (507-284-2111) have active thyroid cancer research programs.
- Ask specifically whether their laboratory has an ongoing tissue banking protocol for thyroid cancer that includes functional testing.
Summary comparison
| Platform | Speed | Biological fidelity | Access | Best for |
|---|---|---|---|---|
| Zebrafish avatar | 1–2 weeks | Moderate | Research only | Rapid screening; ATC urgency |
| CAM assay | 1–2 weeks | Moderate | Research only | Vascularized environment; speed |
| Tumor organoid | 2–4 weeks | Good | Selected academic centers | PTC, FTC, ATC drug screening |
| PDX mouse model | 3–6 months | Very high | Research only | Biology research; future patients |
- ATC
- Anaplastic thyroid cancer — the most aggressive subtype, accounting for fewer than 2% of thyroid cancers but a disproportionate share of thyroid cancer deaths.
- BRAF V600E
- A mutation found in approximately 60% of papillary thyroid cancers that drives tumor growth and predicts response to BRAF-targeted drugs such as vemurafenib and dabrafenib.
- CAM assay
- Chorioallantoic membrane assay — a method that grows tumor cells on a chicken egg membrane to test drug effects in a living, vascularized environment.
- Ex vivo
- Outside the living body — refers to experiments performed on tissue removed from a patient and kept alive in the laboratory.
- Organoid
- A three-dimensional miniature tissue grown in the laboratory from a patient's own cells that mimics the structure and behavior of the original tumor.
- PDX
- Patient-derived xenograft — a model in which human tumor tissue is implanted into immune-deficient mice to study drug effects.
- PTC / FTC
- Papillary thyroid cancer / follicular thyroid cancer — the two most common subtypes of differentiated thyroid cancer, generally slow-growing and highly treatable.
- Tumor functional testing
- Laboratory testing that measures how a patient's actual tumor cells respond to drugs, as opposed to predicting response based on genetic mutations alone.
This appendix describes investigational research approaches that are not standard medical care. It is intended to help you have informed conversations with your medical team — not to replace their recommendations. All treatment decisions should be made in consultation with your oncologist and care team.