Mechanisms of cancer-induced hypercalcemia.
Lab Invest. 1992 Dec; 67(6):680-702.LI

Abstract

Cancer-associated hypercalcemia is due to the: (a) elaboration of systemically-acting humoral factors by neoplasms which alter calcium metabolism in bone, kidney, and intestine; or (b) stimulation of bone resorption at sites of tumor metastasis to bone. It is likely that both mechanisms occur in the same patient with certain neoplasms. There are many humoral factors that can be produced by tumors, secreted into the circulation, and have distant effects which induce hypercalcemia. The stimulation of increased osteoclastic bone resorption is a principal feature of humoral hypercalcemia of malignancy, but the kidney also plays an important role. In addition, intestinal absorption of calcium may be a factor in the pathogenesis of hypercalcemia in certain neoplasms. Parathyroid hormone-related protein plays a dominant role in the pathogenesis of HHM. PTHrP alone is able to induce nearly all of the clinical signs of HHM in experimental animals, but other humoral factors, such as cytokines, can interact with PTHrP to contribute to the development of hypercalcemia. Neoplasms which metastasize widely to bone and induce local osteoclastic bone resorption, such as multiple myeloma, also are capable of inducing hypercalcemia. Based upon existing data it is not clear what percentage of neoplasms which metastasize to bone and stimulate local bone resorption also are capable of stimulating hypercalcemia by systemic factors. Future research is needed to delineate the systemic and local factors associated with CAH; to define interactions of humoral factors in the pathogenesis of hypercalcemia; and to investigate the regulation of transcription, translation, modification, and secretion of hypercalcemia-inducing factors in normal and neoplastic tissues.

Authors+Show Affiliations

Rosol TJ

Department of Veterinary Pathobiology, Ohio State University, Columbus.

Capen CC

No affiliation info available

MeSH

AnimalsBiological FactorsBone ResorptionHumansHypercalcemiaNeoplasmsParaneoplastic Syndromes

Pub Type(s)

Journal Article

Research Support, Non-U.S. Gov't

Research Support, U.S. Gov't, P.H.S.

Review

Language

eng

PubMed ID

1460860

Citation

Rosol, T J., and C C. Capen. "Mechanisms of Cancer-induced Hypercalcemia." Laboratory Investigation; a Journal of Technical Methods and Pathology, vol. 67, no. 6, 1992, pp. 680-702.

Rosol TJ, Capen CC. Mechanisms of cancer-induced hypercalcemia. Lab Invest. 1992;67(6):680-702.

Rosol, T. J., & Capen, C. C. (1992). Mechanisms of cancer-induced hypercalcemia. Laboratory Investigation; a Journal of Technical Methods and Pathology, 67(6), 680-702.

Rosol TJ, Capen CC. Mechanisms of Cancer-induced Hypercalcemia. Lab Invest. 1992;67(6):680-702. PubMed PMID: 1460860.

* Article titles in AMA citation format should be in sentence-case

TY - JOUR T1 - Mechanisms of cancer-induced hypercalcemia. AU - Rosol,T J, AU - Capen,C C, PY - 1992/12/1/pubmed PY - 1992/12/1/medline PY - 1992/12/1/entrez SP - 680 EP - 702 JF - Laboratory investigation; a journal of technical methods and pathology JO - Lab Invest VL - 67 IS - 6 N2 - Cancer-associated hypercalcemia is due to the: (a) elaboration of systemically-acting humoral factors by neoplasms which alter calcium metabolism in bone, kidney, and intestine; or (b) stimulation of bone resorption at sites of tumor metastasis to bone. It is likely that both mechanisms occur in the same patient with certain neoplasms. There are many humoral factors that can be produced by tumors, secreted into the circulation, and have distant effects which induce hypercalcemia. The stimulation of increased osteoclastic bone resorption is a principal feature of humoral hypercalcemia of malignancy, but the kidney also plays an important role. In addition, intestinal absorption of calcium may be a factor in the pathogenesis of hypercalcemia in certain neoplasms. Parathyroid hormone-related protein plays a dominant role in the pathogenesis of HHM. PTHrP alone is able to induce nearly all of the clinical signs of HHM in experimental animals, but other humoral factors, such as cytokines, can interact with PTHrP to contribute to the development of hypercalcemia. Neoplasms which metastasize widely to bone and induce local osteoclastic bone resorption, such as multiple myeloma, also are capable of inducing hypercalcemia. Based upon existing data it is not clear what percentage of neoplasms which metastasize to bone and stimulate local bone resorption also are capable of stimulating hypercalcemia by systemic factors. Future research is needed to delineate the systemic and local factors associated with CAH; to define interactions of humoral factors in the pathogenesis of hypercalcemia; and to investigate the regulation of transcription, translation, modification, and secretion of hypercalcemia-inducing factors in normal and neoplastic tissues. SN - 0023-6837 UR - https://www.unboundmedicine.com/medline/citation/1460860/Mechanisms_of_cancer_induced_hypercalcemia_ DB - PRIME DP - Unbound Medicine ER -

Tags

Mechanisms of cancer-induced hypercalcemia.Lab Invest. 1992 Dec; 67(6):680-702.LI