Fig.20.17Capsularinvasioninfollicularcarcinoma.Evaluatingtheintegrityofthecapsuleiscriticalindistinguishingfollicularadenomasfromfollicularcarcinomas.(A)Inadenomas,afibrouscapsule,usuallythinbutoccasionallymoreprominent,surroundstheneoplasticfolliclesandnocapsularinvasionisseen;compressednormalthyroidparenchymausuallyispresentexternaltothecapsule(top). (B)Bycontrast,follicularcarcinomasdemonstratecapsularinvasionthatmaybeminimal,asinthiscase,orwidespread,withextensionintolocalstructuresoftheneck.
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Anaplastic carcinomas grow with wild abandon despite therapy. Metastases to distant sites are common, but in most cases death occurs in less than 1 year as a result of aggressive local growth and compromise of vital structures in the neck.
Medullary carcinomas of the thyroid are neuroendocrine tumors derived from the parafollicular cells, or C cells, of the thyroid. Like normal C cells, medullary carcinomas secrete calcitonin, measurement of which plays an important role in the diagnosis and postoperative follow-up of patients. In some cases, the tumor cells elaborate other polypeptide hormones such as somatostatin, serotonin, and vasoactive intestinal peptide. Medullary carcinomas arise sporadically in about 70% of cases. The remaining 30% are familial, occurring in the setting of multiple endocrine neoplasia (MEN) syndrome 2A or 2B, or familial medullary thyroid carcinoma without an associated MEN syndrome, as discussed later. Both familial and sporadic medullary forms are associated with gain-of-function driver mutations in the RET receptor tyrosine kinase. Sporadic medullary carcinomas, as well as familial cases without an associated MEN syndrome, occur in adults, with a peak incidence in the fifth and sixth decades. Cases associated with MEN-2A or MEN-2B, by contrast, tend to occur in younger patients, including children.
MORPHOLOGYMedullarycarcinomasmayariseasasolitarynoduleormaymanifestasmultiplelesionsinvolvingbothlobesofthethyroid.Multicentricityisparticularlycommoninfamilialcases.Largerlesionsoftencontainareasofnecrosisandhemorrhageandmayextendthroughthecapsuleofthethyroid.Onmicroscopicexamination,medullarycarcinomasarecomposedofpolygonaltospindle-shapedcells,whichmayformnests,trabeculae,andevenfollicles.Amyloiddeposits,derivedfromalteredcalcitoninmolecules,arepresentintheadjacentstromainmanycases(
Fig.20.18 )andareadistinctivefeature.Calcitoninisreadilydemonstrablebothwithinthecytoplasmofthetumorcellsandinthestromalamyloidbyimmunohistochemicalmethods.OneofthecharacteristicfeaturesoffamilialmedullarycarcinomasisthepresenceofmulticentricCcellhyperplasiainthesurroundingthyroidparenchyma,afeatureusuallyabsentinsporadiclesions.FociofCcellhyperplasiaarebelievedtorepresenttheprecursorlesionsfromwhichmedullarycarcinomasarise.