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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The adenylate cyclase activity and the binding of 125I-labeled thyroid-stimulating hormone (TSH) of normal and tumor rat thyroid plasma membranes were compared. No significant difference in the basal and fluoride-sensitive adenylate cyclase activity between normal and tumor plasma membranes was observed. Thyroid plasma membranes responded to TSH, whereas the enzyme from the tumor plasma membranes was TSH insensitive. Thyroid plasma membranes boud 125I-TSH. Tumor plasma membranes bound 125I-TSH poorly. At the highest concentration of unlabeled TSH used, 80% of the 125I-TSH that was bound to thyroid plasma membranes was displaced, whereas only 10% of the 125I-TSH bound to tumor plasma membranes was displaced. Therefore, it seems likely that the failure of this tumor to respond to TSH is due to an alteration in the functional unit of membrane adenylate cyclase at the level of the receptor subunit.
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PMID:Diminished binding of thyroid-stimulating hormone in a transplantable rat thyroid tumor as a possible cause of hormone unresponsiveness. 17 Oct 62

Studies of TSH release and production were performed in short term monolayer cultures of transplantable, thyroid hormone responsive, thyrotropin (TSH) producing mouse pituitary tumors. These tumors contained large amounts of TSH, small amounts of growth hormone (GH) and no detectable luteinizing hormone (LH), indicating that the predominant hormone product of tumor cells was TSH. The TSH content per tumor cell was similar to that of the normal pituitary where thyrotrophs represent a small fraction of the total cells, suggesting that the TSH content per tumor cell was less than that of the normal thyrotroph. There was a time dependent release and production of TSH by tumor cells in monolayer culture. Thyrotropin releasing hormone (TRH) increased the release into the media and the production of TSH in a dose dependent manner. Maximum effects were noted at 0.2 ng/ml. Thyroid hormones and somatostatin inhibited both basal and TRH induced effects on both TSH release and production. TSH release as induced by TRH was calcium dependent. TSH release was stimulated by ouabain (10(-3)M) and potassium (57 mM), agents known to promote cellular calcium uptake in a calcium dependent manner. These studies indicate that tumor derived cells function in monolayer culture in a similar fashion to normal thyrotrophs. Studies were conducted to test the hypothesis that TRH action is mediated by adenosine 3',5' monophosphate (cAMP). Dibutyryl cAMP (6 mM) and theophylline (10 mM) increased TSH release suggesting that cAMP is involved in TSH release. However, TRH had no detectable effect on tumor cell adenylate cyclase activity or levels of cAMP. In contrast, PGE1 (1-10 mug/ml) stimulated adenylate cyclase activity and elevated cellular levels of cAMP without increasing TSH release. Thus, we are unable to confirm the postulate that cAMP is the intracellular mediator of TRH action.
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PMID:Regulation of thyrotropin (TSH) release and production in monolayer cultures of transplantable TSH-producing mouse tumors. 17 85

The nuclear receptor affinity for L-triiodothyronine (L-T3), L-thyroxine (L-T4), L-triiodothyroacetic acid (triac), and D-triiodothyronine (D-T3) was compared to the potency of these thyroid hormone analogues in regulating thyrotropin (TSH) production and the number of membrane receptors for thyrotropin-releasing hormone (TRH) in mouse thyrotropic tumor cells in culture. L-T3 and triac were equally potent and D-T3 was one-sixth to one-fifth as potent in binding to the receptor and in regulating TSH production and TRH receptor number. L-T4 was the least potent analogue in each instance, but its relative receptor-binding affinity, measured after 3 h, was significantly less than its somewhat variable relative biological potency, measured after 48 h. The cells were shown to monodeiodinate L-[125I]T4 to L-[125I]T3 in a time-dependent manner, and the enhanced biological potency of L-T4 was ascribed to its conversion to L-T3. Thyroid hormones appear to regulate TSH production and the number of receptors for TRH in thyrotropic cells in culture through interaction with a nuclear receptor.
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PMID:Receptor affinity and biological potency of thyroid hormones in thyrotropic cells. 22 53

A controversy exists in regard to thyroid function and breast cancer. Hypothyroidism has been suggested as being either protective from breast cancer or predisposing to the disease. It has been hypothesized that a deficiency in circulating thyroid hormones may hypersensitize the mammary glandular epithelium toward prolactin and estrogens, thus aiding the development of breast neoplasia. On the other hand, thyroid hormone replacement therapy has been connected with an increased risk of breast cancer, but this has been contested. At this time the American Thyroid Association recommends that, if indicated, hypothyroid patients should take their thyroid hormone medication. Hyperthyroidism has been associated with a decreased risk of breast cancer. Also, in hyperthyroid patients with inoperable breast cancer, the malignant growth is thought to be slowed. However, this, too has been disputed. Moreover, hyperthyroidism has been connected with the development of breast cancer in premenopausal women. At present no role of thyroid hormone in the pathobiology of breast cancer can be defined. It seems that the "thyroid-breast cancer controversy" can only be resolved by a prospective study preferably on postmenopausal women correlating thyroid (T3, T4, PBI), pituitary (TSH, TRH, Prolactin), and adrenocortical (androgens) function tests with the clinical examination of thyroid, breast, and genital apparatus and determination of the estrogen status (vaginal smear, plasma estrogens) as well.
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PMID:Thyroid disease in relation to breast cancer. 36 55

Medullary thyroid carcinoma (MTC) is a distinctive neoplasm which is derived from the calcitonin-producing intrathyroidal C-cell system and which develops commonly in untreated rats of various strains. Thyroid glands of Long-Evans rats ranging in age from 3 months to 3 years showed a spectrum of C-cell proliferative abnormalities. As compared to 3-month-old control rats, thyroids from 9- to 12-month-old animals exhibited mild diffuse C-cell hyperplasia (CCH). Thyroids from animals ranging from 1 to 3 years of age exhibited progressively more severe C-cell abnormalities including severe diffuse CCH, nodular CCH, and/or MTC. In contrast to the normal basal serum calcitonin levels in controls and in animals with mild diffuse CCH, animals with severe diffuse CCH, nodular CCH, or MTC had elevated basal serum calcitonin values. Nodular CCH was characterized by the replacement and enlargement of individual follicles by C-cells. Larger foci of nodular CCH were characterized by similar changes in multiple adjacent follicles or by an irregular expansion of individual follicles. MTC was characterized by penetration of the follicular basal lamina by C-cells with extension into the adjacent thyroid stroma. In addition to the high incidence of thyroidal C-cell abnormalities, diffuse and/or nodular parathyroid hyperplasia was commonly found. There was no evidence of chronic renal failure in these animals, and the serum calcium levels were within normal limits. Although the stimulus for the initial C-cell proliferation remains unknown, the appearance of MTC is preceded by relatively prolonged phases of CCH. These findings are essentially identical with those noted in human familial MTC and indicate that the rat provides a useful model system for studying the regulation of C-cell proliferation during the processes of neoplastic development and progression.
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PMID:C-cell hyperplasia and medullary thyroid carcinoma in the rat. An immunohistochemical and ultrastructural analysis. 43 Oct 34

Surgery is the primary form of therapy in the management of malignant thyroid disease. A near-total thyroidectomy is the preferred approach. Radioactive iodine is used for supplementary ablation therapy and for definitive therapy in differentiated tumors of papillary or follicular cell type. Thyroid-stimulating hormone (TSH) is administered in conjunction with radioactive iodine therapy, since tumor uptake appears to be directly related to endogenous TSH levels. Therapeutic doses of radioactive iodine range from 100 to 200 mCi of 131 I depending on tumor distribution. Adequate thyroid hormone replacement therapy resulting in the suppression of TSH is of considerable value in the prevention of tumor recurrence. Due to the possibility of late recurrence, patients should be followed for indefinite periods by means of diagnostic imaging studies at 1-2 yr intervals. Despite 30 yr of experience, the therapeutic efficacy of radioactive iodine remains controversial. However, in recent years, there has been mounting evidence indicating increased survival and decreased tumor recurrence in radioactive iodine-treated patients. External radiation therapy is reserved for anaplastic carcinoma and lymphoma, and adenocarcinomas that are refractory to radioactive iodine. Chemotherapy experience is limited; however, some reduction in the size of metastatic lesions has been observed after the administration of adriamycin.
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PMID:Treatment of malignant thyroid disease. 48 55

Fifty patients with late-onset idiopathic immunoglobulin deficiency were studied and the frequency of various clinical associations and complications was observed. Men and women were equally affected, although the age at onset in men peaked in the third decade whereas it was more uniformly distributed in women. Sinobronchopulmonary infections were common and were caused by Haemophilus influenzae. Diplococcus pneumoniae, Streptococcus pyogenes and Staphylococcus aureus: bronchiectasis occurred in 28 per cent. Thirty patients (60 per cent) had diarrhea, which was often associated with steatorrhea, giardiasis, achlorhydria, abnormal Schilling tests and morphologic abnormalities on small bowel biopsy specimens, including nodular lymphoid hyperplasia; three patients had pernicious anemia. In the 20 patients without diarrhea these abnormalities were not observed except for giardiasis in one patient and achlorhydria in two patients. Cholelithiasis occurred in both groups in about a third of the patients tested. A high degree of susceptibility to neoplasia was noted. Thyroid abnormalities, including primary hypothyroidism and Graves' disease, were observed in six patients. Additional occasional findings were vitiligo, keratoconjunctivitis sicca and arthritis. Splenomegaly occurred in 14 (28 per cent) patients. The percentage of B lymphocytes in the blood was determined in 10 patients; it was normal or slightly decreased in eight patients and low in two patients.
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PMID:Idiopathic late-onset immunoglobulin deficiency. Clinical observations in 50 patients. 78 41

Many different classifications of thyroid tumors were employed during the last 50 years. In 1964 the WHO International Reference Centre for the Histological Classification of Thyroid Tumors was established, in 1974 the final version of "Histological Typing of Thyroid Tumours" was published by Chr. Hedinger in collaboration with L. H. Sobin and 11 pathologists in 9 countries ("WHO International Histological Classifications of Tumours No. 11").
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PMID:[Malignant struma. Pathological anatomy and functional properties. Discussion comments on the contribution of J. Thurner and G. Montano]. 97 30

The incidence of neoplastic disease was determined by a mail survey of 2,872 young adults given X-ray treatments in infancy and of their 5,005 nonirradiated siblings. Newly diagnosed benign and malignant neoplasms appeared more frequently in the irradiated subjects than in their siblings or the age- and sex-matched general population of upstate New York. Only thyroid neoplasms occurred in sufficient numbers to permit statistical analysis for the effects on incidence of sex, age, and dose, and of being in a high-risk group (sub-group C). Thyroid cancers developed earlier in life than did benign neoplasms, especially in boys; benign goiters occurred after smaller doses, predominantly in females. Females had a greater risk of developing thyroid cancer than males--2,3 times for females of all ages and 5 times for young adults. Except for young adult females, there was no definite age effect. The risk of cancer (but not of benign goiter) was proportional to the thyroid dose, with a linear risk coefficient of 2.5/year/million people exposed to 1 rad for the entire irradiated population and 4.0 for subgroup C. The high risk of thyroid cancer in subgroup C may be the result of the high percentage of Jews, who had a 3.4-fold greater risk than non-Jews. Young adult Jewish females had a 17-fold increased risk. An incidental observation was an apparent increased incidence of asthma and rare diseases with abnormal immunologic features in the irradiated population.
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PMID:Neoplasms in persons treated with x-rays in infancy: fourth survey in 20 years. 115 31

Thirty-eight patients with incidental thyroid carcinoma were reviewed. Thyroid lobectomy was adequate therapy in 15 to 17 patients. Both patients in whom lobectomy alone was inadequate had received prior irradiation. Five patients had antecedent head and neck irradiation, and in three of them, multicentric foci of tumor developed. Lobectomy alone was inadequate in three of these patients; they required thyroidectomy. A clinical recurrence developed in only two of 38 patients, and both of them had received previous irradiation. Reoperation in previously dissected areas was associated with an increased rate of complications. Lobectomy in nonirradiated and total thyroidectomy in irradiated patients cured the majority of patients suffering from incidental carcinoma of the thyroid.
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PMID:The treatment of incidental thyroid cancer. 125 86


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