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Detection of an Activating Mutation of the Thyrotropin Receptor in a Case of an Autonomously Hyperfunctioning Thyroid Insular Carcinoma¹

Hospital of the University of Pennsylvania Philadelphia, Pennsylvania 19104

We read with interest the recent report of an activating mutation of the thyrotropin receptor in a case of an autonomously hyperfunctioning thyroid carcinoma by Russo et al. (1). The depicted light microscopy in this case report is described as insular carcinoma, in both the thyroid primary and its lymph node metastasis.

As this report points out, only rarely have thyroid cancers been associated with clinical hyperthyroidism (2). There is no doubt the case reported by Russo et al. is indeed a thyroid malignancy and that the authors have elegantly documented tumor and its metastasis an activating thyrotropin mutation. However, the histopathologic diagnosis of this tumor as an insular carcinoma, i.e. a poorly differentiated malignancy, is not well-documented in this report. The pattern of growth and cytology of the tumor presented is not classical of an insular carcinoma; on the contrary, it may represent a solid growth pattern of a papillary carcinoma (3, 4, 5). The morphologic appearance in an insular carcinoma is usually characterized by large, well-formed nests of tumor cells, sharply demarcated from each other by artifactually created clefts, similar to those seen in carcinoid tumor. There are usually foci of necrosis, sparing the cellular nests around the blood vessels, giving rise to a peritheliomatous appearance (6). The cells of insular carcinoma usually lack prominent nucleoli, which the authors describe as one of the cytologic features in this case (although these are not illustrated in the photomicrographs). Insular carcinomas show significant mitotic activity (6), whereas in the reported case, "mitoses were rare." Hence in our opinion, this report falls short of providing convincing evidence of pathologic characteristics for a diagnosis of insular carcinoma of thyroid. We believe that reports in which a morphologic characterization of a tumor forms an integral part of the report (in this case the first documentation of a functioning, poorly differentiated thyroid carcinoma), should be corroborated by photomicrographs that clearly demonstrate the classic growth patterns and cytology for the tumor.

Footnotes

¹ Address correspondence to: Virginia A. Livolsi, MD, Department of Pathology and Laboratory Medicine, University of Pennsylvania Health System, 6 Founders Pavilion, 3400 Spruce Street, Philadelphia, Pennsylvania 19104-4283.

Received May 1, 1997.

References

1. Russo D, Tumino S, Arturi F, et al. 1997 Detection of an activating mutation of the thyrotropin receptor in a case of an autonomously hyperfunctioning thyroid insular carcinoma. J Clin Endocrinol Metab. 82:735–738.[Abstract/Free Full Text]
2. Mizukami Y, Michigishi T, Nonomura A, et al. 1994 Autonomously functioning (hot) nodule of the thyroid gland: a clinical and histopathologic study of 17 cases. Am J Clin Pathol. 101:29–35.[Medline]
3. LiVolsi V. 1992 Papillary neoplasms of the thyroid. Pathologic and prognostic features. Am J Clin Pathol. 97:426–34.[Medline]
4. Sakamoto A, Kasai N, Sugano H. 1983 Poorly differentiated carcinoma of the thyroid. A clinicopathologic entity for a high-risk group of papillary and follicular carcinomas. Cancer. 52:1849–1855.[CrossRef][Medline]
5. Nikiforov Y, Gnepp DR. 1994 Pediatric thyroid cancer after the Chernobyl disaster. Pathmorphologic study of 84 cases (1991–1992) from the Republic of Belarus. Cancer. 74:748–66.[CrossRef][Medline]
6. Carcangui ML, Zampi G, Rosai J. 1984 Poorly differentiated ("insular") thyroid carcinoma. A reinterpretation of Langhan’s "wuchernede Struma." Am J Surg Pathol. 8:655–668.[Medline]

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