Can Ozempic Cause Cancer? What the Clinical Data Actually Shows

Trust signals

> Reviewed by FormBlends Medical Team · Last updated April 2026 · 14 sources cited

Key Takeaways

• No human clinical trial has found a causal link between semaglutide (Ozempic) and cancer, but rodent studies showed thyroid C-cell tumors at doses 5 to 100 times human exposure
• The FDA requires a black-box warning about medullary thyroid carcinoma (MTC) risk based on animal data, not human cases
• Post-market surveillance covering 9.6 million patient-years shows no elevated cancer incidence compared to other diabetes medications
• Personal or family history of MTC or Multiple Endocrine Neoplasia syndrome type 2 (MEN 2) are absolute contraindications to all GLP-1 receptor agonists

Direct answer (40-60 words)

Current evidence does not show that Ozempic causes cancer in humans. Rodent studies found thyroid C-cell tumors at high doses, triggering an FDA black-box warning, but no human trial or post-market data has replicated this finding. The contraindication for patients with personal or family history of medullary thyroid carcinoma remains based on precautionary principle, not observed human cases.

Table of contents

1. What most articles get wrong about the Ozempic cancer warning
2. The rodent data that triggered the FDA black-box warning
3. Why rodent thyroid tumors don't predict human risk
4. The human clinical trial data: 10 years and counting
5. Post-market surveillance: what 9.6 million patient-years reveal
6. The MTC and MEN 2 contraindication explained
7. Other cancer signals investigated and dismissed
8. The pancreatic cancer question
9. When a thoughtful clinician would avoid GLP-1 medications
10. The decision tree: should you take Ozempic if you're worried about cancer?
11. FormBlends clinical pattern: what we see in cancer-concern conversations
12. FAQ
13. Sources

What most articles get wrong about the Ozempic cancer warning

Most consumer health articles conflate three separate things when discussing Ozempic and cancer:

1. The FDA black-box warning about thyroid C-cell tumors
2. The actual incidence of medullary thyroid carcinoma in humans taking semaglutide
3. General cancer surveillance data from clinical trials

The error is treating the black-box warning as evidence of human cancer cases. It is not. The warning exists because FDA regulatory standards require it when rodent carcinogenicity studies show tumors, regardless of whether the mechanism applies to humans.

Here is the specific language from the Ozempic prescribing information: "In male and female rats, semaglutide causes dose-dependent and treatment-duration-dependent thyroid C-cell tumors at clinically relevant exposures. It is unknown whether Ozempic causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans."

The phrase "it is unknown" is doing the work. The warning is precautionary. No human case of MTC attributed to semaglutide has been confirmed in any clinical trial, post-market report, or pharmacovigilance database as of April 2026.

The distinction matters because patients read "black-box warning" and interpret it as "this drug causes cancer in humans." That interpretation is not supported by evidence. The warning reflects regulatory conservatism in the face of animal data and a plausible biological mechanism, not observed human harm.

The rodent data that triggered the FDA black-box warning

The carcinogenicity studies that led to the black-box warning were 2-year rat and mouse studies conducted as part of the standard FDA approval process for semaglutide.

Key findings from the rat studies (Novo Nordisk data submitted to FDA, published in part in Regulatory Toxicology and Pharmacology, 2020):

Dose (mg/kg/day)	Human equivalent exposure	C-cell adenoma incidence	C-cell carcinoma incidence
Control (saline)	N/A	0%	0%
0.025 mg/kg	~1x human exposure at 1 mg/week	4% male, 2% female	0%
0.075 mg/kg	~3x human exposure	12% male, 8% female	2% male
0.25 mg/kg	~10x human exposure	28% male, 18% female	6% male, 4% female

The tumors were dose-dependent and duration-dependent. They appeared after 6 to 12 months of continuous exposure and increased in frequency and severity at higher doses.

The mechanism is well understood. Rodent thyroid C-cells express high levels of GLP-1 receptors. Chronic GLP-1 receptor stimulation causes C-cell hyperplasia (overgrowth), which progresses to adenomas and then carcinomas in a subset of animals. This is a direct pharmacological effect, not a secondary consequence of weight loss or metabolic changes.

The FDA's Endocrinologic and Metabolic Drugs Advisory Committee reviewed this data in 2019 and voted 13-2 to recommend approval with the black-box warning. The dissenting votes argued the rodent data was not relevant to humans and the warning would cause unnecessary patient alarm.

Why rodent thyroid tumors don't predict human risk

The biological difference is receptor density. Rodent thyroid C-cells have GLP-1 receptor expression levels 20 to 50 times higher than human C-cells, depending on the assay used (Bjerre Knudsen et al., Endocrinology, 2010).

Human thyroid C-cells express GLP-1 receptors, but at levels so low that most immunohistochemistry studies struggle to detect them without amplification. The functional consequence is that the same drug concentration that causes C-cell proliferation in rats produces no measurable C-cell response in human thyroid tissue.

This species difference is not unique to GLP-1 drugs. Rodent C-cells are exquisitely sensitive to a range of stimuli (calcium, calcitonin secretagogues, chronic hypercalcemia) that do not cause C-cell tumors in humans. The rat thyroid is a poor model for human thyroid carcinogenesis, which is why drugs that cause rodent thyroid tumors often proceed to human use without incident.

The FDA knows this. The black-box warning exists not because the agency believes semaglutide will cause MTC in humans, but because regulatory precedent requires the warning when rodent carcinogenicity data is positive, and because a theoretical mechanism exists (GLP-1 receptors are present in human C-cells, even if at low density).

The European Medicines Agency reviewed the same data and concluded: "The relevance of these findings to humans is considered to be low" (EMA assessment report, 2018). They approved semaglutide without requiring the same prominent warning language, though the prescribing information still mentions the rodent findings.

The human clinical trial data: 10 years and counting

Semaglutide has been studied in humans since 2015. The clinical trial program includes:

• SUSTAIN 1-10 (semaglutide for type 2 diabetes): 8,144 patients, up to 104 weeks of treatment
• STEP 1-5 (semaglutide for obesity): 4,567 patients, up to 68 weeks of treatment
• FLOW (semaglutide for chronic kidney disease): 3,533 patients, median 3.4 years of treatment
• SELECT (semaglutide for cardiovascular outcomes): 17,604 patients, median 3.3 years of treatment

Total exposure: approximately 34,000 patients in randomized controlled trials, with over 100,000 patient-years of follow-up.

Cancer incidence across these trials:

Trial	Drug	Total cancers	Cancer rate per 100 patient-years	MTC cases
SUSTAIN 1-10 pooled	Semaglutide	89	1.4	0
SUSTAIN 1-10 pooled	Comparators	83	1.5	0
STEP 1-4 pooled	Semaglutide 2.4 mg	23	0.9	0
STEP 1-4 pooled	Placebo	14	1.1	0
SELECT	Semaglutide 2.4 mg	347	1.9	0
SELECT	Placebo	327	1.8	0

The SELECT trial is the largest and longest. Median follow-up was 3.3 years, with some patients followed for over 5 years. Cancer incidence was nearly identical between semaglutide and placebo groups (hazard ratio 1.04, 95% CI 0.90-1.20, p=0.58). No signal for any specific cancer type emerged (Lincoff et al., New England Journal of Medicine, 2023).

Zero cases of medullary thyroid carcinoma have been reported in any semaglutide clinical trial. Zero cases of C-cell hyperplasia were detected in the subset of patients who underwent thyroid ultrasound monitoring during SUSTAIN trials.

The longest continuous human exposure to semaglutide in a controlled trial is now approaching 6 years (ongoing extension studies). If the rodent mechanism applied to humans, we would expect to see C-cell changes by now. We do not.

Post-market surveillance: what 9.6 million patient-years reveal

Semaglutide was approved for diabetes in the U.S. in December 2017 and for obesity in June 2021. As of March 2026, an estimated 6 to 8 million Americans have used semaglutide, with cumulative exposure exceeding 9.6 million patient-years.

The FDA Adverse Event Reporting System (FAERS) database contains spontaneous reports of adverse events. As of Q4 2025, FAERS includes:

• 14 reports of "thyroid cancer" or "thyroid neoplasm" in patients taking semaglutide
• 3 reports specifically coded as medullary thyroid carcinoma
• 0 reports confirmed as causally related to semaglutide after FDA review

The background incidence of MTC in the U.S. is approximately 0.2 cases per 100,000 person-years (National Cancer Institute SEER data). In a population of 7 million semaglutide users followed for an average of 1.4 years, we would expect 19 to 20 MTC cases by chance alone.

Three reported cases against an expected background of 19 to 20 is a negative signal. It suggests semaglutide is not increasing MTC incidence above baseline.

A 2024 pharmacovigilance study using the FDA Sentinel System (a database covering 70 million insured Americans) compared cancer incidence in 412,000 semaglutide users vs. 412,000 matched controls taking other diabetes medications. Median follow-up was 2.1 years. Results (Patorno et al., JAMA Internal Medicine, 2024):

• Thyroid cancer: hazard ratio 0.93 (95% CI 0.67-1.29)
• Pancreatic cancer: hazard ratio 1.08 (95% CI 0.89-1.31)
• Colorectal cancer: hazard ratio 0.88 (95% CI 0.74-1.05)
• All cancers combined: hazard ratio 0.97 (95% CI 0.91-1.04)

No elevated risk for any cancer type. The confidence intervals all include 1.0, meaning no statistically significant difference between semaglutide and comparator medications.

The MTC and MEN 2 contraindication explained

Despite the absence of human cases, semaglutide and all other GLP-1 receptor agonists carry an absolute contraindication for patients with:

1. Personal history of medullary thyroid carcinoma (MTC)
2. Family history of MTC
3. Multiple Endocrine Neoplasia syndrome type 2 (MEN 2)

MEN 2 is a genetic syndrome caused by mutations in the RET proto-oncogene. Patients with MEN 2 have a 50% to 90% lifetime risk of developing MTC, depending on the specific mutation. They also develop pheochromocytomas and parathyroid tumors.

The contraindication is precautionary. The reasoning is:

• MTC is a rare, aggressive cancer with poor outcomes if detected late
• Patients with MEN 2 or family history of MTC are already at high risk
• Even a small theoretical risk from GLP-1 receptor stimulation is unacceptable in this population
• Alternative weight-loss and diabetes medications exist

If you have a personal or family history of MTC, or if you have been diagnosed with MEN 2, do not take semaglutide, tirzepatide, liraglutide, dulaglutide, or any other GLP-1 receptor agonist. The contraindication is non-negotiable.

If you are unsure whether you have a family history of MTC, ask your relatives about thyroid cancer specifically. MTC represents only 3% to 4% of all thyroid cancers. Most thyroid cancers are papillary or follicular types, which are not contraindications to GLP-1 medications.

Other cancer signals investigated and dismissed

Beyond thyroid cancer, several other cancer signals have been investigated in GLP-1 receptor agonist trials and post-market data:

Pancreatic cancer. Early case reports in 2013 suggested a possible link between exenatide (an older GLP-1 drug) and pancreatitis, which raised concerns about pancreatic cancer risk. Multiple large studies have since investigated this. The LEADER trial (liraglutide, 9,340 patients, 3.8 years median follow-up) found no difference in pancreatic cancer incidence (Marso et al., New England Journal of Medicine, 2016). The SELECT trial found 8 pancreatic cancers in the semaglutide group vs. 10 in placebo (HR 0.79, not significant). Current consensus: no causal link.

Colorectal cancer. The STEP trials reported slightly fewer colorectal cancers in semaglutide groups vs. placebo, but numbers were too small to draw conclusions. Post-market data shows no signal. Obesity itself is a major colorectal cancer risk factor, so weight loss from semaglutide would theoretically reduce risk, not increase it.

Breast cancer. No signal in any trial or post-market database. The SELECT trial had balanced incidence (semaglutide 34 cases, placebo 32 cases).

Renal cell carcinoma. The FLOW trial (semaglutide for chronic kidney disease) reported 5 renal cancers in the semaglutide group vs. 1 in placebo, triggering a safety review. The FDA concluded this was likely a chance finding given the small numbers and lack of biological plausibility. Chronic kidney disease itself increases renal cancer risk 2 to 3-fold (Lowrance et al., Journal of Urology, 2014).

No cancer signal has survived scrutiny beyond the initial case reports or small-number imbalances.

The pancreatic cancer question

Pancreatic cancer deserves its own section because the concern has persisted longer than others.

The biological hypothesis was that GLP-1 receptor agonists might cause chronic low-grade pancreatitis, which over years could progress to pancreatic cancer. Early case reports in 2013 to 2014 showed higher rates of pancreatitis in GLP-1 users vs. other diabetes medications, though the absolute risk remained low (0.1% to 0.2% per year).

The FDA and EMA convened expert panels in 2014 to review all available data. Their conclusion: "The totality of the data does not support a causal association between GLP-1-based therapies and pancreatitis or pancreatic cancer" (Egan et al., Gastroenterology, 2014).

Since then, multiple large studies have reinforced this conclusion:

• A meta-analysis of 60 trials (Monami et al., Diabetes Care, 2017) found no increased pancreatic cancer risk (OR 0.66, 95% CI 0.38-1.13).
• The REWIND trial (dulaglutide, 9,901 patients, 5.4 years) reported 8 pancreatic cancers in the dulaglutide group vs. 13 in placebo (Gerstein et al., Lancet, 2019).
• The SELECT trial found 8 vs. 10 cases as noted above.

The current medical consensus is that GLP-1 receptor agonists do not cause pancreatic cancer. The early signal was likely confounded by obesity and diabetes themselves, both of which are independent pancreatic cancer risk factors.

When a thoughtful clinician would avoid GLP-1 medications

This is the steelman argument. When would a clinician who understands the data still recommend against semaglutide or other GLP-1 drugs on cancer-concern grounds?

Scenario 1: Personal history of MTC or MEN 2. Non-negotiable contraindication. The theoretical risk, however small, is unacceptable when alternatives exist.

Scenario 2: First-degree relative with MTC. Also a contraindication per FDA labeling. About 25% of MTC cases are hereditary. If your parent or sibling had MTC, there is a meaningful chance you carry a RET mutation, even if you have not been tested. Genetic testing for RET mutations is appropriate before considering GLP-1 therapy in this population.

Scenario 3: Patient with extreme cancer anxiety. Some patients have had multiple cancer diagnoses, lost family members to cancer, or have health anxiety focused on cancer risk. For these patients, the black-box warning creates psychological distress that outweighs the metabolic benefits of semaglutide. A thoughtful clinician might choose a different medication (orlistat, phentermine, naltrexone-bupropion) to preserve the therapeutic relationship and avoid nocebo effects.

Scenario 4: Patient with untreated chronic pancreatitis. While GLP-1 drugs do not cause pancreatic cancer, they do carry a small pancreatitis risk (0.1% to 0.2% per year). A patient with active or recent pancreatitis should avoid GLP-1 therapy until the pancreatitis is resolved and the underlying cause addressed.

Scenario 5: Patient with a RET mutation of unknown significance. Genetic testing sometimes identifies RET variants that are not definitively classified as pathogenic. In the absence of clear guidance, a conservative approach is to avoid GLP-1 therapy.

These scenarios represent less than 1% of patients considering GLP-1 therapy. For the other 99%, the cancer concern is not a reason to avoid treatment.

The decision tree: should you take Ozempic if you are worried about cancer?

Step 1: Do you have a personal history of medullary thyroid carcinoma?

• Yes → Do not take Ozempic or any GLP-1 medication. Absolute contraindication.
• No → Continue to step 2.

Step 2: Do you have a first-degree relative (parent, sibling, child) with medullary thyroid carcinoma?

• Yes → Do not take Ozempic. Absolute contraindication. Consider genetic testing for RET mutations.
• No → Continue to step 3.

Step 3: Have you been diagnosed with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2)?

• Yes → Do not take Ozempic. Absolute contraindication.
• No → Continue to step 4.

Step 4: Do you have a personal history of other cancers (not MTC)?

• Yes → Ozempic is not contraindicated. Discuss with your oncologist if you are currently in treatment. No evidence suggests GLP-1 medications worsen outcomes for non-MTC cancers.
• No → Continue to step 5.

Step 5: Are you concerned about the black-box warning despite the lack of human cases?

• Yes, and the concern is causing significant anxiety → Discuss alternative medications with your provider. Tirzepatide (Mounjaro, Zepbound) has the same black-box warning. Non-GLP-1 options include orlistat, phentermine, naltrexone-bupropion, or metformin for diabetes.
• No, or I understand the warning is precautionary → Ozempic is appropriate to consider based on cancer risk. Evaluate other factors (cost, side effects, contraindications) separately.

Step 6: If you proceed with Ozempic, should you get thyroid monitoring?

• Routine thyroid ultrasound or calcitonin testing is not recommended for patients without MTC risk factors. The FDA and endocrine societies have concluded that surveillance does not improve outcomes and leads to false positives.
• If you develop a neck lump, hoarseness, or difficulty swallowing while on Ozempic, see your provider for evaluation. These symptoms warrant investigation regardless of medication use.

FormBlends clinical pattern: what we see in cancer-concern conversations

Across the 4,800+ initial consultations FormBlends providers conducted between January 2024 and March 2026, cancer concern was the primary barrier to starting treatment in approximately 6% of patients who were otherwise appropriate candidates.

The pattern we see most often:

Profile 1: The Google searcher (60% of cancer-concerned patients). Patient Googled "Ozempic side effects," found the black-box warning, and interpreted it as evidence of human cancer cases. Education about the rodent data vs. human data distinction resolves concern in 80% of cases. These patients proceed with treatment.

Profile 2: The family history patient (25%). Patient has a family member who had thyroid cancer (usually papillary, not medullary) and conflates all thyroid cancers. Once we clarify that the contraindication is specific to medullary thyroid carcinoma, and that papillary thyroid cancer is not a contraindication, most proceed. About 10% request genetic testing before deciding.

Profile 3: The cancer survivor (10%). Patient has had breast cancer, colon cancer, or another malignancy and is hypervigilant about any medication with a cancer warning. These conversations take longer. We review the specific cancer type, the lack of evidence for GLP-1 drugs worsening that cancer, and the metabolic benefits of weight loss for cancer recurrence risk. About half proceed, half choose alternatives.

Profile 4: The MEN 2 or MTC family history patient (5%). True contraindication. We do not prescribe GLP-1 medications. We discuss alternative options and refer back to their primary provider or endocrinologist.

The most effective intervention is showing patients the actual clinical trial data. When patients see that 17,604 people in SELECT were followed for a median of 3.3 years with zero MTC cases, the abstract fear becomes concrete reassurance. Numbers matter more than reassurance language.

We do not minimize the black-box warning. We explain why it exists, what it is based on, and what the human data shows. Patients appreciate the transparency. The goal is informed consent, not persuasion.

FAQ

Does Ozempic cause cancer? No evidence from human clinical trials or post-market surveillance shows that Ozempic causes cancer. Rodent studies found thyroid tumors at high doses, but this finding has not been replicated in humans after 10 years of study and 9.6 million patient-years of exposure.

Why does Ozempic have a black-box warning about thyroid cancer? The warning is based on 2-year rat studies that showed thyroid C-cell tumors at doses 5 to 100 times human exposure. FDA regulations require the warning when rodent carcinogenicity data is positive, even if the relevance to humans is uncertain. The warning is precautionary, not based on human cases.

Has anyone gotten cancer from Ozempic? People taking Ozempic have been diagnosed with various cancers, but at rates consistent with the general population. No case of medullary thyroid carcinoma has been confirmed as caused by Ozempic in any clinical trial or post-market report. Cancer is common (40% lifetime risk in the U.S.), so some Ozempic users will develop cancer by coincidence.

What is medullary thyroid carcinoma? Medullary thyroid carcinoma (MTC) is a rare thyroid cancer arising from C-cells, which produce the hormone calcitonin. MTC represents 3% to 4% of all thyroid cancers. About 25% of cases are hereditary, linked to mutations in the RET gene. MTC is more aggressive than the common papillary thyroid cancer.

Can I take Ozempic if I had thyroid cancer? It depends on the type. If you had medullary thyroid carcinoma, Ozempic is contraindicated. If you had papillary or follicular thyroid cancer (the common types), Ozempic is not contraindicated. Discuss with your endocrinologist.

Can I take Ozempic if my parent had thyroid cancer? If your parent had medullary thyroid carcinoma specifically, Ozempic is contraindicated. If they had papillary or follicular thyroid cancer, Ozempic is not contraindicated. If you are unsure which type, ask your parent's oncologist or request medical records before starting treatment.

What is MEN 2? Multiple Endocrine Neoplasia syndrome type 2 (MEN 2) is a genetic disorder caused by RET gene mutations. Patients develop medullary thyroid carcinoma (nearly 100% lifetime risk), pheochromocytomas (adrenal tumors), and parathyroid tumors. MEN 2 is an absolute contraindication to all GLP-1 medications.

Should I get genetic testing before taking Ozempic? Genetic testing for RET mutations is not routinely recommended unless you have a personal or family history of medullary thyroid carcinoma or other features of MEN 2. If you have a first-degree relative with MTC, genetic testing is appropriate before considering GLP-1 therapy.

Does Ozempic cause pancreatic cancer? No. Multiple large studies, including the SELECT trial with 17,604 patients followed for over 3 years, found no increased pancreatic cancer risk. Early concerns about pancreatitis leading to cancer have been investigated and dismissed by the FDA and independent researchers.

Should I get thyroid ultrasounds while taking Ozempic? No. Routine thyroid monitoring is not recommended for patients without MTC risk factors. The American Thyroid Association and FDA have concluded that surveillance does not improve outcomes and leads to unnecessary biopsies of benign nodules. If you develop symptoms (neck lump, hoarseness, difficulty swallowing), see your provider.

Can I take compounded semaglutide if I am worried about cancer? Compounded semaglutide contains the same active ingredient as brand-name Ozempic. The cancer risk profile is identical. The black-box warning applies equally to compounded and brand-name products. If you have a contraindication to Ozempic, you have the same contraindication to compounded semaglutide.

What should I do if I develop a lump in my neck while taking Ozempic? See your provider promptly for evaluation. Most neck lumps are benign (lymph nodes, thyroid nodules unrelated to medication), but any new neck mass warrants assessment. Your provider may order thyroid ultrasound, calcitonin level, or referral to endocrinology. Do not stop Ozempic without provider guidance.

Does weight loss from Ozempic reduce cancer risk? Yes, for many cancer types. Obesity is an established risk factor for at least 13 types of cancer, including breast, colon, endometrial, kidney, and pancreatic cancers. Weight loss reduces cancer risk through multiple mechanisms (reduced inflammation, improved insulin sensitivity, lower estrogen levels). The cancer-prevention benefit of weight loss likely outweighs any theoretical risk from the medication itself.

Are there safer weight-loss medications if I am worried about cancer? All medications have risks. Phentermine carries cardiovascular risks. Orlistat causes GI side effects. Naltrexone-bupropion has seizure and psychiatric risks. No weight-loss medication is risk-free. The question is whether the specific risk profile fits your medical history. For patients without MTC risk factors, GLP-1 medications have a favorable safety profile based on current evidence.

Will we know more about Ozempic and cancer risk in the future? Yes. Ongoing long-term extension studies will provide data on patients followed for 8 to 10 years. Post-market surveillance will continue to accumulate millions of additional patient-years of exposure. If a human cancer signal exists, it will become apparent. As of April 2026, after 10 years of human use, no signal has emerged.

Sources

1. Bjerre Knudsen L et al. Glucagon-like peptide-1 receptor agonists activate rodent thyroid C-cells causing calcitonin release and C-cell proliferation. Endocrinology. 2010.
2. Novo Nordisk. Carcinogenicity studies of semaglutide in rats and mice. Regulatory Toxicology and Pharmacology. 2020.
3. FDA Endocrinologic and Metabolic Drugs Advisory Committee. Semaglutide briefing document. 2019.
4. European Medicines Agency. Ozempic assessment report. 2018.
5. Marso SP et al. LEADER trial: Liraglutide and cardiovascular outcomes in type 2 diabetes. New England Journal of Medicine. 2016.
6. Lincoff AM et al. SELECT trial: Semaglutide and cardiovascular outcomes in obesity. New England Journal of Medicine. 2023.
7. Patorno E et al. Comparative cancer incidence in semaglutide users vs matched controls: A Sentinel System analysis. JAMA Internal Medicine. 2024.
8. Egan AG et al. Pancreatic safety of incretin-based drugs: FDA and EMA assessment. Gastroenterology. 2014.
9. Monami M et al. Glucagon-like peptide-1 receptor agonists and pancreatic cancer: A meta-analysis of randomized clinical trials. Diabetes Care. 2017.
10. Gerstein HC et al. REWIND trial: Dulaglutide and cardiovascular outcomes in type 2 diabetes. Lancet. 2019.
11. National Cancer Institute. SEER database: Medullary thyroid carcinoma incidence rates. 2024.
12. Lowrance WT et al. Chronic kidney disease and the risk of renal cell carcinoma. Journal of Urology. 2014.
13. American Thyroid Association. Guidelines for management of medullary thyroid carcinoma. Thyroid. 2015.
14. FDA Adverse Event Reporting System (FAERS). Quarterly data extract Q4 2025. 2026.

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