Calcium metabolism in cancer.Studies using calcium isotopes and immunoassays for parathyroid hormone and calcitonin

Coombes, R. Charles; Ward, M. K.; Greenberg, P. B.; Hillyard, C. J.; Tulloch, B.; Morrison, R.; Joplin, G. F.

doi:10.1002/1097-0142(197611)38:5<2111::aid-cncr2820380539>3.0.co;2-q

Cited by 60 publications

(9 citation statements)

References 25 publications

(2 reference statements)

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“…22 Other sources of calcium appear to be less important as demonstrated by isotope studies which typically show a decrease in intestinal absorption of calcium in these patients. 23 The decrease is presumably mediated by the low levels of 1,25-dihydroxy-vitamin D usually observed.24 Renal tubular calcium reabsorption also is usually decreased in most patients with paraneoplastic hypercal~emia.~~?~~…”

Section: Discussionmentioning

confidence: 99%

The spectrum of metabolic bone disease in lymphoblastic leukemia

Cohn

Morgan

Mallette

1987

Cancer

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Eight patients with childhood acute lymphoblastic leukemia (ALL) and hypercalcemia, osteopenia, or vertebral compression fractures seen at our institution during the last 12 years were evaluated for biochemical evidence of bone disease. Five patients were hypercalcemic, three had abnormal phosphorous levels, and four had elevated alkaline phosphatase values. Parathyroid hormone (PTH) was measured by a polyvalent radioimmunoassay in five patients and these levels were abnormally high in three patients. Four of these five patients also had PTH measured by a midregion-specific radioimmunoassay. One patient had a high PTH value. Two patients had low levels and one patient had a normal PTH level. Although these studies suggest diverse biochemical mechanisms may be contributing to the bone changes and hypercalcemia seen in childhood ALL, ectopic PTH production as well as ectopically produced fragments of PTH may have a role in mediating bone resorption and hypercalcemia.

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Section: Discussionmentioning

confidence: 99%

The spectrum of metabolic bone disease in lymphoblastic leukemia

Cohn

Morgan

Mallette

1987

Cancer

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“…In fact, malignant disease is thc most common cause of hypercalcacmia in hospitaliscd patients [177]. The cause is uncertain.…”

Section: Fluid and Electrolyte Disturbancesmentioning

confidence: 99%

“…The cause is uncertain. It has been suggested that, in patients with bone metastases, hypercalcaemia is due to the release of calcium following bone destruction [177]. It is clear, however, that hypcrcalcaemia can arise even when there is no direct bonc involvement when removal of the tumour may result in the return of serum calcium to within the normal rangc.…”

Section: Fluid and Electrolyte Disturbancesmentioning

confidence: 99%

“…Such effects are most common in squamous cell carcinomas of the bronchus or head and ncck, or in renal cancers [1781. This suggests a role for a circulating mediator such as parathyroid hormone (PTH), although intestinal absorption of calcium is not, in general, increased, and circulating PTH levels are elevated only in about 10% of hypcrcalcaemic cancer patients [177].…”

Section: Fluid and Electrolyte Disturbancesmentioning

confidence: 99%

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Malignant disease: nutritional implications of disease and treatment

Holmes

Dickerson

1987

Cancer Metast Rev

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Protein-energy malnutrition (PEM) is common in cancer patients and may develop into the syndrome known as 'cancer cachexia'. This is characterised by complex disturbances in carbohydrate, lipid, protein, and electrolyte metabolism. The aetiology is equally complex, with host and therapeutic factors contributing to the reduced food intake and effects on host tissues. Anorexia is of prime importance, differing in its cause from one patient to another and often presenting a barrier to successful nutritional support. Further research is necessary to elucidate the interaction of central and peripheral factors that may be involved in the aetiology of anorexia. Because of the interplay of biochemical, physiological, and psychological consequences of cancer, the nutritional support of the patient presents a considerable challenge to the caring professions.

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“…Accelerated net bone resorption is believed to be the source of the hypercalcemia in such patients (1,4,5), although understanding of the mechanisms whereby malignant cells alter the functions of normal bone cells remains incomplete. Direct osteolysis by tumor cells metastatic to bone may occur (6).…”

Section: Introductionmentioning

confidence: 99%

Humoral hypercalcemia of malignancy. Release of a prostaglandin-stimulating bone-resorbing factor in vitro by human transitional-cell carcinoma cells.

Bringhurst¹,

Bierer²,

Godeau³

et al. 1986

J. Clin. Invest.

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Secretion by tumor cells of circulating bone-resorbing factors may frequently underlie the hypercalcemia that occurs in patients with malignancy. Efforts to identify the responsible mediators have been hampered by a lack of available human tumor cell systems suitable for study of the pathogenesis of the humoral hypercalcemia syndrome. We have established a transitionalcell carcinoma (TCC) line in vitro from a patient with humoral hypercalcemia. These cells are tumorigenic and cause hypercalcemia in athymic nude mice. Culture medium conditioned by TCC cells contains potent bone-resorbing activity in vitro, the physical and biological properties of which are similar to those of bone-resorbing activity present in the original patient's urine. The bone-resorbing activity of the TCC factor is accompanied by increased prostaglandin release from bone and is blocked by indomethacin and calcitonin. The TCC-derived bone-resorbing activity coelutes with prostaglandin-stimulating activity during gel filtration with an approximate molecular weight of 15,000. This activity is nondialyzable, stable to concentrated urea and reducing agents, and destroyed by boiling. The TCC factor does not increase cyclic AMP production in bone or kidney bioassays and does not exhibit transforming growth factor activity. We conclude that a unique macromolecular factor released by TCC cells causes bone resorption by a mechanism dependent upon stimulation of bone cell cyclooxygenase, and that this factor is the probable cause of the hypercalcemia in vivo. The TCC cell line provides a new model for study of the human humoral hypercalcemia syndrome.

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Calcium metabolism in cancer.Studies using calcium isotopes and immunoassays for parathyroid hormone and calcitonin

Cited by 60 publications

References 25 publications

The spectrum of metabolic bone disease in lymphoblastic leukemia

The spectrum of metabolic bone disease in lymphoblastic leukemia

Malignant disease: nutritional implications of disease and treatment

Humoral hypercalcemia of malignancy. Release of a prostaglandin-stimulating bone-resorbing factor in vitro by human transitional-cell carcinoma cells.

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