Pathophysiology of cancer-associated hypercalcemia

Gregory R. Mundy

Research output: Contribution to journalArticlepeer-review

46 Scopus citations


During the past decade, specific mediators of bone destruction in hypercalcemia of malignancy have been identified and characterized. These humoral factors include parathyroid hormone-related protein, transforming growth factor alpha, and cytokines such as interleukin-1 and tumor necrosis factor. In metastatic hypercalcemia associated with breast cancer, prostaglandin secretion by tumor cells may be one of the important factors. Among the osteoclast activating factors associated with hypercalcemia in patients with myeloma, lymphotoxin plays a central but probably not exclusive role. Alterations of renal function in hematologic hypercalcemia may potentiate bone destruction that usually occurs in the presence of impaired rates of glomerular filtration. Further research is required to determine the relative contributions of bone and kidney to the pathogenesis of hypercalcemia of malignancy.

Original languageEnglish (US)
Pages (from-to)10-15
Number of pages6
JournalSeminars in Oncology
Issue number2 SUPPL. 5
StatePublished - Apr 1990

ASJC Scopus subject areas

  • Hematology
  • Oncology


Dive into the research topics of 'Pathophysiology of cancer-associated hypercalcemia'. Together they form a unique fingerprint.

Cite this