Thyrocalcitonin: Hypocalcemic Hypophosphatemic Principle of the Thyroid Gland

Hirsch, Philip F.; Voelkel, Edward F.; Munson, Paul L.

doi:10.1126/science.146.3642.412

Cited by 306 publications

(101 citation statements)

References 8 publications

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“…60 The group of Armen Tashjian Jr studied a large kindred of MEN2A patients and discovered that the thyroid C-cells secreted calcitonin and that a calcium infusion stimulated release of calcitonin. This was an excellent provocative test for the early diagnosis of MTC.…”

Section: Biochemical Diagnosismentioning

confidence: 99%

RET gene mutations (genotype and phenotype) of multiple endocrine neoplasia type 2 and familial medullary thyroid carcinoma

Krampitz

Norton

2014

Cancer

114

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The rapid technical advances in molecular biology and accelerating improvements in genomic and proteomic diagnostics have led to increasingly personalized strategies for cancer therapy. Such an approach integrates the genomic, proteomic, and molecular information unique to the individual to provide an accurate genetic diagnosis, molecular risk assessment, informed family counseling, therapeutic profiling, and early preventative management that best fits the particular needs of each patient. The discovery of mutations in the RET proto-oncogene resulting in variable onset and severity of multiple endocrine neoplasia type 2 (MEN2) was the first step in developing direct genetic testing for at-risk individuals. Patients with germline RET mutations may undergo risk assessment and appropriate intervention based on specific mutations. Moreover, family members of affected individuals receive counseling based on understanding of the genetic transmission of the disease. Increasingly, clinicians are able to make therapeutic choices guided by an informative biomarker code. Improvements in detection and management of patients with MEN2 resulting from understanding of the RET proto-oncogene are evidence of the benefits of personalized cancer medicine. This review describes the discovery of the RET proto-oncogene, the association between genotype and phenotype, and the role of mutation analysis on diagnosis and treatment of MEN2. Cancer 2014;120:1920-31.

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Section: Biochemical Diagnosismentioning

confidence: 99%

RET gene mutations (genotype and phenotype) of multiple endocrine neoplasia type 2 and familial medullary thyroid carcinoma

Krampitz

Norton

2014

Cancer

114

View full text Add to dashboard Cite

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“…The remaining and the most probable explanation is that the thyrocalcitonin which leaked out during the surgical manipulation of the thyroid is responsible for this hypocalcemia. The magnitude of the Ca decrease in our cases was small when compared with that induced in rats by the electrocauterization of the thyroid (Hirsch et al, 1964). The concentration of thyrocalcitonin was reported much lower in the human than in the rat thyroid, although information is still scanty with the diseased thyroid (Aliapoulios et al, 1966).…”

mentioning

confidence: 74%

“…hypocalcemic-hypophosphatemic principlethyrocalcitonin-was extracted from the thyroid gland of various animals (Hirsch et al, 1964). A similar substance which induced hypocalcemia in rat was also extracted from the human thyroid (Aliapoulios et al, 1966).…”

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confidence: 99%

Transient Fall in Blood Calcium Level Following Thyroid Operations

et al. 1968

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“…Besides lowering serum Ca in various species (Hirsch et al, 1964;Munson and Hirsch, 1966), thyrocalcitonin is known to act on the bone inhibiting resorption (Raisz and Au, 1967;Aliapoulios et al, 1966). However, the action of thyrocalcitonin on other tissues has not yet been studied in detail, except for the possible action on the calcium content of the kidney and cutaneous calcinosis (Selye et al 1967).…”

Section: Discussionmentioning

confidence: 99%

Effect of Age and Thyrocalcitonin on Myocardial Changes Induced by Sodium Sulfaacetylthiazole

et al. 1968

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SYNOPSISNa-sulfaacetylthiazole, 0.5g/kg body weight, was injected into immature and adult rats to produce obstructive nephropathy. Necrotic changes in the myocardium were found in all of the 9 adult rats of about 120days of age, whereas no such changes occured in immature animals of about 40days of age. Thyrocalcitonin, 50 mMRC units a day injected subcutaneously for one week, completely inhibited the occurrence of such myocardial lesion in adult animals, as did parathyroidectomy performed one week previously. Serum calcium was decreased from the normal adult level in thyrocalcitonin treated or parathyroidectomized animals but not in untreated immature rats. Thyrocalcitonin appears to have some effect on cardiovascular system in addition to the known effect on the bone.

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Thyrocalcitonin: Hypocalcemic Hypophosphatemic Principle of the Thyroid Gland

Abstract: A factor that lowers serum calcium and inorganic phosphate in rats has been purified 500-fold from 0.1N HCl extracts of hog thyroid glands. It is distinct from thyroxine and triiodothyronine and appears to be a polypeptide.

Cited by 306 publications

References 8 publications

RET gene mutations (genotype and phenotype) of multiple endocrine neoplasia type 2 and familial medullary thyroid carcinoma

RET gene mutations (genotype and phenotype) of multiple endocrine neoplasia type 2 and familial medullary thyroid carcinoma

Transient Fall in Blood Calcium Level Following Thyroid Operations

Effect of Age and Thyrocalcitonin on Myocardial Changes Induced by Sodium Sulfaacetylthiazole

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