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PubMedDate not supplied

Palpable parathyroid adenomas presenting as clinical solitary thyroid nodules and cytologically as follicular thyroid neoplasms.

BACKGROUND: A palpable parathyroid mass, in a patient with primary hyperparathyroidism, is presumed to be parathyroid carcinoma until proven otherwise, with other less common causes including parathyroid cysts and adenomas. These parathyroid pathologies can be more difficult to interpret with concomitant thyroid disease. METHODS: A retrospective review was undertaken of a series of three patients with palpable parathyroid adenomas mimicking thyroid nodules. RESULTS: Two of three patients had preoperative biochemical evidence of primary hyperparathyroidism. Sestamibi scanning confirmed the presence of parathyroid pathology in one case. Fine-needle aspiration cytology revealed probable follicular neoplasms of the thyroid in all three cases. Only one of three parathyroid adenomas was diagnosed at neck exploration; the others were diagnosed at subsequent histopathology. CONCLUSION: Parathyroid and thyroid disease often occur simultaneously. Concomitant parathyroid pathology should be considered, even in the absence of biochemical and radiological evidence, at neck exploration for thyroid disease. Macroscopic identification of parathyroid disease at neck exploration can be difficult when within the thyroid gland capsule. Cytology and imaging of parathyroid adenomas may, on occasion, mimic follicular thyroid neoplasms.

Adenocarcinoma, Follicular↗
PubMed1995

Histochemical differences of the lectin affinities of backbone polylactosamine structures carrying the ABO blood group antigens in papillary carcinoma and other types of thyroid neoplasm.

Endo-beta-galactosidase from Escherichia freundii cleaves linear polylactosamine structure as follows: R-GlcNAc-beta 1-3Gal-beta 1-4GlcNAc-beta 1-R' + H2O-->R-GlcNAc-beta 1-3Gal + GlcNAc-beta 1-R'. Staining with Griffonia simplicifolia agglutinin II (GSA-II) following enzyme digestion reveals the distribution of R-GlcNac-beta 1-3Gal-beta 1-4GlcNAc-beta 1-R' structures in tissue sections. In this study, the procedure was applied to formalin-fixed, paraffin-embedded tissue sections from 26 cases of papillary carcinomas including 2 follicular variants, 8 follicular carcinomas, 7 adenomas, 1 anaplastic carcinoma and 1 medullary carcinoma in order to investigate whether different types of polyactosamine-containing structure are produced in these thyroid neoplasms. Simultaneously, the susceptibility of the ABH antigens expressed in these neoplastic cells to endo-beta-galactosidase digestion was examined. Most of the papillary carcinoma cells from all the individuals examined were strongly stained by GSA-II following enzyme digestion. Without enzyme digestion, little or no reactivity with GSA-II was observed. Among other types of neoplasms, only one case of follicular carcinoma exhibited reactivity with GSA-II following enzyme digestion. ABH antigens were expressed in 22 cases of papillary carcinomas, 2 adenomas, 5 follicular carcinomas and 1 anaplastic carcinoma, and their expression was dependent on the ABO blood group of the patients. Endo-beta-galactosidase digestion resulted in the elimination of these antigens not only in papillary carcinomas but also in other neoplasms.(ABSTRACT TRUNCATED AT 250 WORDS)

ABO Blood-Group System↗
PubMed2003

KAI1 expression in thyroid neoplasms: its linkage with clinicopathologic features in papillary carcinoma.

KAI1 is a metastasis suppressor gene located on human chromosome 11p11.2. Previous studies have shown that the down-regulation of KAI1 mRNA and decreased expression of its gene product are significantly linked to carcinoma progression, including metastatic ability. In this study, we investigated KAI1 protein expression in thyroid neoplasms. KAI1 overexpression was observed in 64.0% of papillary carcinoma cases, and the incidence was significantly higher than in cases of follicular carcinoma (20.0%) (p = 0.0001). In papillary carcinomas, decreased KAI1 expression was frequently observed in cases invading beyond the thyroid capsule (p = 0.001), as well as in lymph node metastases (p = 0.0047) and poorly differentiated lesions (p = 0.0299). Furthermore, in anaplastic carcinoma, the incidence of KAI1 overexpression was lower than in papillary carcinoma (p < 0.0001), and only 4.2% of the cases overexpressed this gene. These results suggest that KAI1 down-regulation is significantly related to the progression of papillary carcinoma, including lymph node metastasis, and its anaplastic transformation.

Adenocarcinoma, Follicular↗
PubMed1975

Canine thyroid neoplasms: epidemiologic features.

A retrospective study of medical records from twelve veterinary university hospitals-clinics yielded 144 dogs with a confirmed diagnosis of a thyroid neoplasm (25 adenomas and 119 carcinomas). Forty-five of these dogs had additional primary neoplasms. As in man, associated tumors suggested the inherited multiple endocrine adenomatosis, type 1, and a possible syndrome of thyroid and chemoreceptor lesions. Although the female preponderance of human thyroid cancer was not seen in dogs, females showed a much sharper increase in risk with advancing age than did males. Three breeds (beagle, boxer, and golden retriever) had a significantly greater risk for thyroid carcinoma than did all dogs combined, whereas miniature and toy poodles had a low risk. The function of thyroiditis in the origin of thyroid cancer, as suggested by reports of thyroid carcinoma in people with Hashimoto's disease, may be clarified by follow-up studies of beagles which are prone to Hashimoto-type thyroiditis.

Journal Article↗
PubMed1988

Poorly differentiated ("insular") carcinoma of the thyroid gland: an aggressive subset of differentiated thyroid neoplasms.

Four patients with a histologically distinctive thyroid carcinoma--which recently has been referred to as poorly differentiated ("insular") carcinoma--are reported. This study confirms the previous conclusions that patients with this neoplasm often experience an aggressive clinical course, with focal recurrences and distant metastases common, which results in death in the majority of patients. Such aggressive behavior may occur even when the insular component accounts for only a small percentage of an otherwise well-differentiated carcinoma, as seen in one of our patients. After subtotal or total thyroidectomy, three of the four patients have experienced local recurrence (1) and metastases to lung (3), mediastinum (1), and bone (1). All three of these patients died within 2 years of the diagnosis of insular carcinoma. The remaining patient is alive without evidence of disease 1 year after total thyroidectomy. Histologically, this neoplasm is characterized by well-defined nests (insulae) that are composed of relatively small, uniform cells and sometimes associated with small, thyroglobulin-containing follicles. Tumor necrosis is often present. Insular carcinoma may comprise the entire neoplasm (2 patients) or be associated with well-differentiated follicular (1 patient) or papillary (1 patient) carcinoma. The rapid and often fatal course associated with insular carcinoma warrants aggressive treatment at the time of initial diagnosis, including total thyroidectomy and node dissection (if involved), as well as possible iodine-131, external beam irradiation and chemotherapy.

Adult↗
PubMed1993

The thyrotropin receptor (TSH-R) is not an oncogene for thyroid tumors: structural studies of the TSH-R and the alpha-subunit of Gs in human thyroid neoplasms.

The development and progression of thyroid tumors are associated with phenotype-specific mutations of genes involved in growth control. Thyroid cell growth is controlled in part by the interaction of TSH with its receptor, with subsequent activation of the GTP-binding protein and its effector, adenylyl cyclase. The resulting increase in intracellular cAMP stimulates growth in thyrocytes. The TSH receptor (TSH-R) is a seven-transmembrane domain receptor. Intracellular domains of the TSH-R important for signal transduction and which may serve as targets for mutational activation have been defined. In addition, mutations at specific loci of the alpha-subunit of G-protein in human thyroid tumors have been described. We examined 92 benign and malignant neoplastic thyroid tissues for possible mutations of the intracytoplasmic domains of the TSH-R known to be involved in signal transduction and for mutations within the hot spots of Gs alpha. Screening was carried out by single strand conformation polymorphism (TSH-R) or denaturing gradient gel electrophoresis (Gs alpha) of polymerase chain reaction-amplified tumor DNA. No mutations were observed in the cytoplasmic domains of the TSH-R, except for a neutral base substitution in codon 460 (GCG [Ala]-->GCA [Ala]) in 3 tumors, which was also present in constitutional DNA from the affected individuals. A heterozygous mutation of codon 201 of Gs alpha (GGT [Arg]-CAT [His]) was observed in a nodule from an adenomatous goiter. In addition, a codon 227 mutation (CAG [Glu]-CAT [His]) was identified in a follicular adenoma. We conclude that mutational activation of the intracytoplasmatic domains of the TSH-R is not a significant mechanism of thyroid tumorigenesis, whereas putative activating mutations within exons 8 and 9 of Gs alpha occur infrequently in some benign follicular tumors.

Base Sequence↗
PubMed1981

Thyrotropin binding and adenylate cyclase stimulation in thyroid neoplasms.

Experiments were performed to determine whether thyroid-stimulating hormone (TSH) receptors coupled to adenylate cyclase are present in both benign and differentiated malignant thyroid tumors, and to identify abnormalities in the TSH receptor-adenylate cyclase system in neoplastic thyroid tissue. TSH binding and adenylate cyclase assays were performed under the same in vitro cyclase conditions. 125I-bovine TSH was incubated with an 8,000 X g thyroid or thyroid tumor particulate fraction from both normal and most neoplastic tissue two receptor sites were identified. The association constant for the high-affinity receptor from normal thyroid was 10.5 +/- 3.2 nM (mean +/- standard error) with a capacity of 0.8 +/- 0.3 pM/mg particulate protein. The association constant of the high-affinity receptor found in the particulate fraction from the thyroid adenomas was 3.5 +/- 0.5 nM with a capacity of 0.4 +/- 0.1 pM/mg particulate protein; for the thyroid carcinomas the association constant was 1.4 +/- 0.3 nM and the capacity 0.2 +/- 0.1 pM/mg particulate protein. The maximum adenylate cyclase response to TSH for particulate fractions from both benign and malignant tumors was greater (P less than 0.05) than in the particulate fraction from normal adjacent thyroid tissue. There was also a positive correlation between the equilibrium constants for 125I-bTSH binding and adenylate cyclase activation suggesting that binding sites are coupled to cyclase in the neoplastic tissue and that the binding observed in these experiments is of biologic consequence.

Adenocarcinoma↗
PubMed1997

[Antigens CA-50 and CA-242 in digestive tract and thyroid neoplasms].

The aim of the study was to assess the CEA antigen and glycoproteins associated antigen CA-50 and CA-242 in tumours of digestive tract and thyroid gland. 84 patients were the material of the study-33 with digestive tracts' neoplasms (among them 22 cases of large bowel cancer and 11 with cancer of pancreas) and 51 with thyroid neoplasms (30 patients with well differentiated thyroid cancer, 21 follicular adenomas of thyroid). There were assessed level of CA-50 and CA-242 glycoprotein associated antigens. Results were compared with CEA-for digestive tract cancer and Tg levels in thyroid neoplasm respectively. In large bowel cancer (22 cases) there were in 10 patients (45%) with elevated level of CEA, 14 patients with elevated CA-50 (63%) and the same number for CA-242 (14 patients-63%). In cancer of pancreas (total 11 patients) there were CEA elevated level in 3 (27%) patients, CA-50 in 7 (64%) patients and CA-242 in 6 (55%) patients. Patients with well differentiated thyroid cancer (30 cases) revealed elevated level of Tg in 24 (80%) patients, CA-50 in 4 (13%), and CA-242 in 4 (13%) ones. The patients with follicular adenomas (21) had elevated Tg level in 17 (80%) cases, CA-50 in 3 (14%) cases and CA-242 in one patient (4.7%).

Adenocarcinoma↗
PubMed1994

Expression of the estrogen receptor in human thyroid neoplasms.

The expression and quantitation of the estrogen receptor (ER) in human thyroid tumors were examined by biochemical, immunohistochemical, and reverse transcriptase-polymerase chain reaction (RT-PCR) techniques. For this study, neoplasms, adenomatous goiters and adjacent normal thyroid tissues were obtained from 35 patients which included 10 cases of papillary carcinomas, 17 cases of adenomas and 8 cases of adenomatous goiters. Regardless of the histopathological subtype, ER was detected in 19% (5/27) of the neoplastic tissues with the mean value of ER content of 5.0 +/- 1.3 fmol/mg protein and the mean Kd value of 0.38 +/- 0.28 nM. ER was also detected, but at a lower concentration (2.8 +/- 1.6 fmol/mg protein), in the surrounding normal tissues. There was no significant difference between the neoplasms and adenomatous goiters with respect to the incidence of ER positivity and ER content. Furthermore, ER-positive specimens, as determined by both biochemical and immunohistochemical techniques, also showed the expression of ER mRNA detected by RT-PCR method. These results demonstrate that both ER mRNA as well as ER protein are expressed in thyroid neoplasms. This suggests the possibility that estrogen may affect the tumorigenesis or the progression of some thyroid neoplasms.

Adenoma↗