Figure 11. A diffuse cytoplasmic staining pattern for high molecular weight cytokeratins and cytokeratin-19 are the hallmark of papillary carcinomas of all types.
An unusual variant of papillary carcinoma is the hyalinizing trabecular tumour. This tumour was originally described by pioneers such as Zipkin in 1905 (109), Masson in 1922 (110), and Ward et al. in 1982 (111). The terminology "hyalinizing trabecular adenoma" (HTA) was defined by Carney et al. in 1987 (112). This lesion has also been designated "paraganglioma-like adenoma of thyroid" (PLAT) by Bronner et al (113) because of its unusual histologic pattern (Figure 12). Since the original descriptions, a malignant counterpart, hyalinizing trabecular carcinoma (HTC), has been described (114-116) and both HTA and HTC are now incorporated under the umbrella of hyalinizing trabecular tumors (HTT). Their main importance lies in the fact that they are sometimes mistaken for other entities such as paraganglioma or medullary carcinoma (112). Immunohistochemical stains for neuroendocrine markers will easily discriminate between HTT and paraganglioma or medullary carcinoma. However, it was noted that many features of HTT were also seen in papillary carcinoma; both lesions are of thyroid follicular epithelial origin and therefore both express thyroglobu-lin; several cases of HTT have been reported in patients with Hashimoto's thyroiditis or who have had a history of neck irradiation (117); HTT can co-exist with papillary carcinoma (5); HTT can often exhibit papillary carcinoma-like histologic features such as
psammoma-body formation, and characteristic nuclear changes including elongation, hypochromasia, grooves and pseudoinclusions (112). Based on these observations, a number of authors have hypothesized that these two entities are related and may in fact share a similar pathogenesis (118). These lesions are generally well delineated tumors characterised architecturally by trabecular and nesting architecture and elongated tumor cells which can have abundant pale eosinophilic cytoplasm and scattered "yellow bodies" (112,113,117,119). There is perivascular hyaline fibrosis and the cyto-plasmic hyaline is usually identified as cytoplasmic filaments of cytokeratin. Occasional cases are immunoreactive for S100 protein. Most importantly, the tumour cells harbour large clear nuclei with irregular and elongated contours, grooves and inclusions as well as micronucleoli, features of papillary carcinoma. Application of ret/PTC analysis identified rearrangements in these lesions at a rate identical to that found in other papillary carcinomas (120,121) and many pathologists now consider this to be a variant of papillary carcinoma. However, some continue to maintain that these are distinct lesions (122,123) .
The diffuse sclerosis variant occurs in young individuals and often presents as goitre without a specific mass lesion (124-127). This tumour microscopically involves thyroid
lymphatics, exhibits squamous metaplasia and forms numerous psammoma bodies, giving it a very gritty appearance when examined grossly. These tumours almost always have lymph node metastases at presentation and 25% have lung metastases as well. It is interesting that about 10% of the paediatric thyroid cancers that occurred following the Chernobyl nuclear accident in 1986 were of the diffuse sclerosis type (128).
An unusual variant of papillary thyroid carcinoma known as the cribriform-morular variant has been identified in patients who harbour mutations of the APC gene that is responsible for familial adenomatous polyposis (FAP) syndrome (25,62,129). These lesions have unusual architecture as their name implies; they exhibit intricate admixtures of cribriform, follicular, papillary, trabecular, and solid patterns of growth (Figure 13), with morular or squamoid areas. Cribriform structures are prominent. The tumor cells are generally cuboidal or tall, with nuclear pseudostratification. Vascular and capsular invasion are common in these lesions, and while they may exhibit lymph node metastasis, there are no data to suggest that they have worse outcomes than other conventional forms of papillary carcinoma. They harbour ret/PTC gene rearrangements and do not exhibit loss of heterozygosity of the normal allele of the APC gene to explain an independent mechanism of tumorigenesis. Alterations in the APC
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