15 research outputs found
Structural studies of the thyrotropin receptor and Gs alpha in human thyroid cancers: low prevalence of mutations predicts infrequent involvement in malignant transformation.
No full textStructural studies of the thyrotropin receptor and Gs alpha in human thyroid cancers: low prevalence of mutations predicts infrequent involvement in malignant transformation.
Full text linkSimilarities and differences in the phenotype of members of an Italian family with hereditary non-autoimmune hyperthyroidism associated with an activating TSH receptor germline mutation
No full textNon-hyperfunctioning nodules from multinodular goiters: A minor role in pathogenesis for somatic activating mutations in the TSH-receptor and Gsα subunit genes
No full textRecent developments in the investigation of thyroid regulation and thyroid carcinogenesis.
No full textSomatic and germline mutations of the TSH receptor and thyroid diseases.
No full textJournal ArticleReviewFLWINinfo:eu-repo/semantics/publishe
Mutations in the Thyrotropin Receptor Signal Transduction Pathway in the Hyperfunctioning Thyroid Nodules from Multinodular Goiters: A Study in the Turkish Population
No full textThyroid-hormone therapy and thyroid cancer: a reassessment
Get PDFExperimental studies and clinical data have demonstrated that thyroid-cell proliferation is dependent on thyroid-stimulating hormone (TSH), thereby providing the rationale for TSH suppression as a treatment for differentiated thyroid cancer. Several reports have shown that hormone-suppressive treatment with the L-enantiomer of tetraiodothyronine (L-T-4) benefits high-risk thyroid cancer patients by decreasing progression and recurrence rates, and cancer-related mortality. Evidence suggests, however, that complex regulatory mechanisms (including both TSH-dependent and TSH-independent pathways) are involved in thyroid-cell regulation. Indeed, no significant improvement has been obtained by suppressing TSH in patients with low-risk thyroid cancer. Moreover, TSH suppression implies a state of subclinical thyrotoxicosis. In low-risk patients, the goal of L-T-4 treatment is therefore to obtain a TSH level in the normal range (0.5-2.5 mU/1). Only selected patients with high-risk papillary and follicular thyroid cancer require long-term TSH-suppressive doses of L-T-4. In these patients, careful monitoring is necessary to avoid undesirable effects on bone and heart
