It was initially thought to be secreted by the parathyroid gland but was shown by Iain Macintyre and his team at the Royal Postgraduate Medical School, London, to be secreted by parafollicular cells of the thyroid gland. Dr. Copp named the discovered hormone calcitonin because of its role in maintaining normal calcium tone. Medical significance
Calcitonin assay is used in identifying patients with nodular thyroid diseases. It is helpful in making an early diagnosis of medullary carcinoma of thyroid. A malignancy of the parafollicular cells, i.e. Medullary thyroid cancer, typically produces an elevated serum calcitonin level. Prognosis of MTC depends on early detection and treatment. Calcitonin also has significantly impacted molecular biology, as the gene encoding calcitonin was the first gene discovered in mammalian cells to be alternatively spliced, now known to be a ubiquitous mechanism in eukaryotes. Pharmacology
Calcitonin has clinically been used for metabolic bone disorders for more than 50 years. Salmon calcitonin is used for the treatment of:

Postmenopausal osteoporosis
Hypercalcaemia
Bone metastases
Pagets disease
Phantom limb painIt has been investigated as a possible non-operative treatment for spinal stenosis.The following information is from the UK Electronic Medicines Compendium

General characteristics of the active substance
Salmon calcitonin is rapidly absorbed and eliminated. Peak plasma concentrations are attained within the first hour of administration. Animal studies have shown that calcitonin is primarily metabolised via proteolysis in the kidney following parenteral administration. The metabolites lack the specific biological activity of calcitonin. Bioavailability following subcutaneous and intramuscular injection in humans is high and similar for the two routes of administration (71% and 66%, respectively).
It is believed that mutations to TP53 are responsible for the frequent therapy resistance and aggressive course of this disease. c-MYC Gene
In a small number of B-PLL cases, abnormalities in the c-MYC gene have been observed. It is considered a global amplifier and influences nearly all aspects of cellular activity. Among the number of genes it regulates, most are involved in cell growth, cell cycle progression, protein biosynthesis and apoptosis. Amplification of c-MYC has been reported in B-PLL patients and while the consequences are unclear, it is generally associated with poor clinical outcome. Biopsy
After physicians have identified an abnormality in the composition of the peripheral blood, biopsies (tissue samples) from a patients bone marrow and/or spleen are often recommended for confirmation. A bone marrow biopsy involves the removal of a small amount of tissue that is further analyzed for abnormalities, for B-PLL pathologists look for prolymphocytic infiltration where the hematopoietic stem cells of the bone marrow are replaced with prolymphocytes due to excess production. In 50% of reported cases, it was common for patients to be both anemic (lack healthy red blood cells in blood) and thrombocytopenic (deficiency of platelets in blood). Treatment
The rarity of B-PLL paired with its considerably fast progression compared to other leukemias has resulted in difficult production of effective treatments. This disease is currently incurable, treatments and therapy are guided to reduce prolymphocyte abundance in the blood and production by the bone marrow, treating symptoms and controlling progression.