{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,10]],"date-time":"2025-10-10T12:34:55Z","timestamp":1760099695487},"reference-count":41,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2004,2,19]],"date-time":"2004-02-19T00:00:00Z","timestamp":1077148800000},"content-version":"vor","delay-in-days":3277,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[1995,3]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Humoral hypercalcemia of malignancy (HHM) is a common paraneoplastic syndrome mediated by tumor\u2010derived parathyroid hormone\u2010related peptide (PTHRP), which bears structural and functional similarities to PTH. Thus the clinical features of HHM are very similar to those of primary hyperparathyroidism (1\u00b0 HPT), a prototype of humoral hypercalcemia caused by PTH. On the other hand, HHM syndrome differs from 1\u00b0 HPT in several aspects, including serum 1,25(OH)<jats:sub>2<\/jats:sub>D levels, acid\u2010base balance, and bone remodeling process, the reason of which remains largely unknown. We approached these questions using a unique animal model of HHM, nude rats implanted with PTHRP\u2010overproducing human carcinomas. In this review we will summarize the results and discuss the implications in understanding the disease mechanism.<\/jats:p>","DOI":"10.1002\/jcb.240570303","type":"journal-article","created":{"date-parts":[[2005,5,28]],"date-time":"2005-05-28T22:07:11Z","timestamp":1117318031000},"page":"384-391","source":"Crossref","is-referenced-by-count":11,"title":["Humoral hypercalcemia of malignancy: Some enigmas on the clinical 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