Anaplastic carcinoma of the thyroid is an aggressive, rapidly fatal neoplasm that is generally believed to arise from the epithelium of the thyroid follicle. When differentiated carcinoma is not present, the diagnosis can be difficult and confusion with a sarcoma is frequently a problem. Ten anaplastic thyroid carcinomas have been examined by light and electron microscopy and compared with two biologically aggressive, solid follicular carcinomas. Ultrastructural study revealed evidence of epithelial differentiation in all the anaplastic carcinomas, confirming their origin from thyroid follicular cells. The study illustrates the value of electron microscopy in establishing the diagnosis of anaplastic carcinoma and in differentiating it from sarcoma.

Aged↗

PubMedDate not supplied

Adrenocortical carcinomas: an ultrastructural study of 22 cases.

Twenty-eight adrenocortical carcinomas from 22 patients have been studied by light and electron microscopy. The objective were to document the range of fine structure, to establish ultrastructural criteria for diagnosis, and to relate the morphology to the presence or lack of functional activity. The distinctive ultrastructural features of steroid-forming cells, smooth endoplasmic reticulum and tubular mitochondrial cristae, were only present in some cells of some of the cases. Sequential specimens (up to four) from a single patient demonstrated changes in the tumor cell morphology with progression, including marked accumulation of cytoplasmic glycogen.

Adrenal Cortex Neoplasms↗

PubMedDate not supplied

C-myc, N-myc, N-ras, and c-erb-B: lack of amplification or rearrangement in human medullary thyroid carcinoma and a derivative cell line.

We investigated the copy number and possible rearrangement of the four protooncogenes, c-myc, N-myc, N-ras, and c-erb-B, in DNA from seven untreated primary cancers or metastases of medullary thyroid carcinoma and an established human medullary thyroid carcinoma cell line, TT, using the Southern blotting technique. The purpose of this study was two-fold: 1) to examine whether protooncogene perturbations in medullary thyroid carcinoma could be considered as a prognostic marker; and 2) to determine whether the protooncogenes could have a possible role in medullary thyroid tumorigenesis. Neither amplification nor rearrangement of the protooncogenes was detectable in the DNA from any tumor samples or in the cell line. Our results suggest that DNA-evident amplification and rearrangement of the c-myc, N-myc, N-ras, and c-erb-B oncogenes may not be mechanisms through which these oncogenes become activated in this malignancy.

Carcinoma↗