Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THYROID NEOPLASMS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2000

Thyroid transcription factor-1, thyroglobulin, cytokeratin 7, and cytokeratin 20 in thyroid neoplasms.

Thyroid transcription factor-1 (TTF-1), a member of the NKx2 family of homeodomain transcription factors, is a mediator of thyroid-specific transcription of the thyroglobulin (TG) gene. The combined immunohistochemical profile of TTF-1, TG, cytokeratin 7 (CK7), and cytokeratin 20 (CK20) in neoplasms of the thyroid gland and their metastases to other sites has not been defined previously. Formalin-fixed tissue of 43 thyroid tumors, including 31 carcinomas and 12 adenomas, and 16 metastasic lesions were immunostained using monoclonal antibodies to TTF-1, TG, CK7, and CK20. Immunoreactivity of the primary tumors (adenomas and carcinomas) for TTF-1 was seen in 32 cases (74%), TG 32 (74%), and CK7 34 (79%), whereas none (0%) showed positivity for CK20. The distribution of reactivity in the 31 carcinomas for TTF-1, TG, and CK7, respectively was papillary (8/8), (8/8), and (8/8); poorly differentiated (6/7), (4/7), and (6/7); oncocytic (Hürthle) cell (2/6), (6/6), and (4/6); follicular (4/4), (3/4), and (3/4); medullary (1/2), (0/2), and (1/2). One of four anaplastic carcinomas was focally immunoreactive showing positivity for TTF-1 only. Of the six follicular adenomas, five were positive for TTF-1, six for TG, and six for CK7. Among the six oncocytic cell adenomas, five were reactive for TTF-1, five for TG, and all six for CK7. Twelve (75%) of the 16 metastatic tumors were positive for TTF-1, 10 (63%) for TG, 15 (94%) for CK7, and none (0%) for CK20. In summary, TTF-1 and TG are demonstrable by immunohistochemistry in the majority of thyroid neoplasms. Compared with TG, an antibody to TTF-I is a similarly sensitive marker for thyroid tumors. Moreover, TTF-1 is a more sensitive marker for poorly differentiated carcinomas and metastasis. In most cases, its nuclear pattern of immunoreactivity facilitates interpretation. Thyroid tumors are CK7+/CK20-. The panel of antibodies for TG, TTF-1, CK7, and CK20 is useful when the thyroid origin of a metastatic tumor is a consideration.

Adenoma↗
PubMed2000

Advances in the diagnosis and management of thyroid neoplasms.

Thyroid cancers are still the most common endocrine cancers. They are dominated by well-differentiated carcinomas, including papillary carcinoma, follicular carcinoma, and medullary thyroid carcinoma. Diagnosis is based on fine-needle aspiration cytologic examination. Recently, reverse transcription polymerase chain reaction for the detection of cancer-specific mRNA was shown to be a useful adjunct in both initial diagnosis and detection of recurrent disease. In addition, positron emission tomography has become a valuable tool for staging and surveillance of thyroid cancer. Given the gradual perfection of surgical technique and reduction in complication rates, near-total and total thyroidectomy should be offered to patients with well-differentiated carcinoma. For medullary thyroid carcinoma, near-total and total thyroidectomy with routine central and bilateral functional neck dissection are recommended. So far, no effective treatment exists for anaplastic thyroid carcinoma.

Carcinoma, Medullary↗
PubMedDate not supplied

Molecular biology of thyroid neoplasms.

Thyroid tumorigenesis proceeds through the progressive accumulation of alterations in genes involved in the regulation of cell proliferation and differentiation accompanying the acquisition of phenotypic, biological and clinical characteristics of increasing malignancy and dedifferentiation. The molecular alterations specific to thyrocyte carcinogenesis are examined. Ras mutations seem to represent an early occurrence in thyroid tumorigenesis being common to both benign and malignant follicular tumors; they would represent the early mutational events able to enhance the cell proliferation. Subsequent alterations in several genes will probably result in the determination of a follicular or papillary phenotype. In particular, mutational events activating ret, met and trk thyrokinase receptors direct the tumor growth and development towards the papillary type. Progression towards a follicular phenotype would instead occur in two stages: first there is the loss of function of genes on chromosome 11q13 which may direct the tumor cell towards the phenotype of follicular adenoma, second, there is the inactivation of the probable suppressor oncogene on chromosome 3p which might be fundamental in the transition from adenoma to follicular carcinoma. Undifferentiated or anaplastic tumors are characterized by the presence of p53 gene mutations.

Cell Division↗
PubMed2000

[Drug therapy of endocrine neoplasms. Part I: Thyroid neoplasms, adrenal neoplasms and parathyroid neoplasms].

BACKGROUND: The incidence of endocrine carcinomas is about 5.3 persons per 100,000 population. Most frequent are malignancies of the thyroid gland (about 89%). THERAPY: Because of low incidences and missing prospective studies as well as radiotherapy and chemotherapy resistance, general accepted therapy guidelines for endocrine carcinomas are still missing. Surgery and radionucleotide treatment is generally the first-line therapy. Hormonal active carcinomas can be additionally treated with special substances such as octreotide and mitotane. Chemotherapy is frequently not effective. Widely used substances are cyclophosphamide, cisplatin, doxorubicine, dacarbazine, vincristine and etoposide. This first part of the review will present medical therapies of thyroid carcinomas, adrenal carcinomas and parathyroid carcinomas. The second part in one of the next issues will focus on less frequent endocrine carcinomas of the gastrointestinal tract.

Adrenal Gland Neoplasms↗
PubMed1991

Ras oncogene mutations in benign and malignant thyroid neoplasms.

Current models for tumorigenesis propose that a series of genetic alterations occur during the progression from the normal cell to the malignant phenotype. Mutations in each of the three ras genes (K-ras, H-ras, and N-ras) have been identified in many human neoplasms, including thyroid cancer. In this study we examined genomic DNA from benign and malignant thyroid neoplasms for mutations that are known to activate the ras oncogenes (codons 12, 13, and 61). DNA from frozen surgically excised tissue (n = 8) and from formalin-fixed paraffin-embedded tissue (n = 30) was amplified by the polymerase chain reaction and screened for mutations using oligonucleotide-specific hybridization. No mutations were identified in follicular adenomas (n = 9). In follicular carcinomas, 2 of 14 tumors contained mutations (N-ras 61, Gln to Arg), and both of these patients had bone metastases. One of 15 papillary carcinomas had a ras mutation (H-ras 12, Gly to Ser). In contrast to other studies, we found that ras mutations are relatively uncommon in both benign and malignant thyroid neoplasms. Studies of larger numbers of tumors and comparisons of different patient populations will be required to assess a possible association of mutations in N-ras 61 with clinically aggressive follicular cancer.

Adenocarcinoma↗
PubMedDate not supplied

Horner's syndrome and thyroid neoplasms.

Although thyroid goiter is a common condition, it rarely results in Horner's syndrome. We report a case of a patient with an intrathoracic multinodular goiter complicated by Horner's syndrome. Benign thyroid disease was confirmed pathologically, and the patient's symptoms improved after surgery. In the literature, the major cause of Horner's syndrome is neoplasia, with malignant lesions being twice as frequent as benign tumors. An extensive review of the literature demonstrates a different repartition for thyroid neoplasia: including our case, 38 cases of Horner's syndrome secondary to a benign thyroid tumor are described, against only 8 cases caused by a thyroid carcinoma. We conclude that contrary to the commonly held opinion, Horner's syndrome is more often due to benign thyroid diseases than to thyroid malignancies.

Goiter, Nodular↗
PubMed2001

Real-time quantitative analysis of E-cadherin expression in ret/PTC-1-activated thyroid neoplasms.

Papillary thyroid carcinoma (PTC), the most common variety of thyroid cancer, is found in a variety of morphologic variants, usually grows slowly, and is clinically indolent, although rare, aggressive forms, with local invasion or distant metastases, occur. Our group has previously demonstrated an association between Hashimoto thyroiditis and ret/PTC-1 activation, and have hypothesised that c-ret activation might be implicated in immune reaction to thyroid epithelium. The objective of this study was to examine expression of the cellular adhesion molecule, E-cadherin, in various thyroid tumor types and Hashimoto thyroiditis in the context of ret/PTC-1 positivity by using laser capture microdissection and TaqMan reverse transcription-polymerase chain reaction (RT-PCR). Variable down-regulation of E-cadherin among carcinomas was demonstrated, with anaplastic carcinomas showing little or no expression. Follicular thyroid carcinomas consistently had significantly decreased E-cadherin expression compared with papillary thyroid carcinomas. The ret/PTC-1-positive papillary thyroid carcinoma (PTCret+) and Hashimoto thyroiditis cases had consistently lower E-cadherin expression levels than the corresponding ret/PTC-1-negative papillary carcinomas (PTCret-), suggesting not only an association between ret activation and the loss of cellular adhesion but also, more significantly, an association between papillary thyroid carcinoma and Hashimoto thyroiditis.

Cadherins↗
PubMed2002

Genomic instability measurement in the diagnosis of thyroid neoplasms.

BACKGROUND: Clinically palpable thyroid nodules are present in approximately 10% of the population, although only 5% to 7% of these nodules harbor malignancy. Fine-needle aspiration has become one of the central tools in the diagnostic armamentarium of the surgeon/endocrinologist. There is, however, up to a 30% indeterminate diagnostic rate associated with this technique, resulting in unnecessary surgical interventions for patients harboring benign disease. A second issue of clinical importance is the unreliability of predicting outcomes based either on histologic findings alone or in combination with clinical staging. To address these diagnostic and clinical shortcomings, we have used measurement of genomic instability as a diagnostic and prognostic indicator for thyroid neoplasms. METHODS: Genomic instability of thyroid tissue samples was determined by inter-(simple sequence repeat) PCR, microsatellite instability analysis, and fluorescence in situ hybridization (FISH) on thyroid neoplasms from 22 patients. RESULTS: Inter-(simple sequence repeat) PCR detected genomic instability with an index range 0% to 1.9% (mean, 0.56%) in patients with benign disease, whereas in patients with malignant histologic findings the values ranged from 0% to 6.6% (mean, 2.9%). This difference between benign and malignant values was statistically significant (p =.004). There was no demonstrable microsatellite instability or loss of heterozygosity for six markers examined in this group. Losses of chromosomes 17 and X in benign disease and gains of chromosomes 7, 12, 17, and X in Hurthle cell carcinoma were observed, although not at a significant rate. CONCLUSIONS: Genomic instability as measured by inter-(simple sequence repeat) PCR was significantly higher for malignant diseases compared with benign thyroid tissues, but no such association was seen with aneuploidy or microsatellite instability.

Adolescent↗
PubMed1998

Cytofluorometric DNA analysis by stathmokinetic method of experimental thyroid neoplasms in rats.

Thyroid neoplasms were induced in rats by the intraperitoneal injection of N-bis(2-hydroxy-propyl)nitrosamine as a carcinogenic substance and by the oral administration of KCIO4 as a promoter. The nuclear DNA content was measured in tissue sections of the tumors by the stathmokinetic method with the use of vincristine, and was correlated with the histopathological findings in the process of tumorigenesis and progression. Histological examination showed various types of lesions were produced in 47 surviving rats. A diploid pattern was seen in 82 (92%) of 89 tumors and an aneuploid pattern in 7 (8%) of 89 tumors. Papillary carcinomas and mixed carcinomas only had a diploid pattern, while two of 17 follicular carcinomas and five of 13 anaplastic carcinomas had an aneuploid pattern. On the other hand, benign proliferative nodules only had a diploid pattern. DNA heterogeneity was noted in seven malignant tumors. In four of them it was associated with the histopathological evidence of change, but in three there was no histological difference between the aneuploid and diploid areas other than a difference in the mitotic index. Mitotic indices were significantly higher in the aneuploid than in the diploid areas. These findings suggest that changes in the DNA ploidy cause histological abnormalities and/or affect the mitotic index. It is hypothesized that a change occurs in some diploid cells in a region of a tumor, and that aneuploid cells develop from the diploid cells which then acquire high proliferative activity.

Aneuploidy↗