8787 A Case of Indolent Medullary Thyroid Cancer with Sporadic HRAS Mutation and Prolonged Stability

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Abstract Disclosure: M. Lozano: None. A. Pinero-Pilona: None. Background: Medullary thyroid cancer (MTC) is a rare neuroendocrine tumor that is derived from calcitonin-producing C-cells that accounts for the smallest portion (<5%) of thyroid cancer. Most of these cases are attributed to mutations in the RET oncogene. Of the remainder, approximately 70% of MTC cases without a RET mutation have been attributed to RAS gene mutations. We report a case of a patient who presented with a thyroid nodule present and stable for years and was found to have MTC with a HRAS mutation. Clinical Case: A 73-year-old Caucasian male with a history of metastatic squamous cell carcinoma (SCC) of the neck, orthostatic hypotension, pacemaker implantation, and coronary artery disease with prior stenting presented to the clinic for evaluation after an abnormal thyroid biopsy. His SCC was diagnosed 16 years ago and was treated with surgery and cetuximab. It was a poorly differentiated squamous cell carcinoma with 2 of 7 lymph nodes positive for malignancy. Fifteen years ago, as part of the evaluation for his SCC, the patient had CAT and PET scans that showed a small nodule with increased uptake in the right lower neck in the thyroid bed (2.7 SUVs) measuring about 1.4 cm in diameter. No further interventions were done back then, and the patient was unaware of the mass until his records were reviewed. The patient was more recently noted to have the incidental thyroid nodule 2 months prior to clinic evaluation after routine carotid ultrasound. The gland was described to be homogeneous; in the mid to inferior portion of the right lobe, there was a 1.2 cm TR5 nodule of which biopsy was recommended. Fine needle aspiration biopsy showed a follicular lesion of unknown significance Bethesda category 3 using AFIRMA GCS RNA molecular analysis. Subsequently, gene sequencing classification was performed and abnormal: results were positive for HRAS mutation. Sonography in the office showed a right-sided, slightly hypoechoic, taller-than-wide vascular nodule with well-preserved borders and intermediate risk of malignancy. No abnormal lymphadenopathy was observed regionally in the central or lateral neck. The patient then underwent total thyroidectomy with modified right level 3 dissection. The right mid-superior nodule was consistent with MTC without tumor necrosis and without lymphatic, perineural, or extrathyroidal extension, but there was angioinvasion of at least 3 vessels. Preoperative calcitonin was elevated at 71 pg/mL and the level was undetectable (<2 pg/mL) 8 weeks post operatively (n<=10 pg/mL). The patient was deemed cured based on these biochemical studies and is recovering uneventfully on supplemental levothyroxine. Conclusion: Given the predominant association of MTC with RET, it is worth noting this case of a sporadic HRAS mutation in a patient with prior SCC. This case illustrates an indolent MTC without aggressive behavior that stayed stable in size and without metastasis for 15 years. Presentation: 6/1/2024