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Osteoclast‐mediated osteolysis in bone metastasis from renal cell carcinoma
Author(s) -
Aoki Jun,
Yamamoto Itsuo,
Hino Megumu,
Shigeno Chohei,
Kitamura Nobuyasu,
Sone Teruki,
Shiomi Kazuki,
Konishi Junji
Publication year - 1988
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/1097-0142(19880701)62:1<98::aid-cncr2820620118>3.0.co;2-8
Subject(s) - bone resorption , osteolysis , medicine , renal cell carcinoma , osteoclast , bone metastasis , resorption , pathology , in vitro , calcitonin , metastasis , prostaglandin e2 , carcinoma , endocrinology , cancer research , cancer , chemistry , surgery , receptor , biochemistry
Osteolytic characteristics of bone metastasis from renal cell carcinoma were morphologically and biochemically investigated. First, undecalcified ground sections of bone metastases were made from four patients with renal cell carcinoma. Second, renal cell carcinoma cell line (RCC‐K 1 ) was established from one of the four patients, and its effect on bone resorption in vitro was examined. Marked proliferation and activation of osteoclasts around the tumor cells was histologically demonstrated. Conditioned medium from the RCC‐K 1 cells contained potent bone‐resorbing activity in vitro. The activity was reduced to basal level by calcitonin, but was not blocked by indomethacin. The activity was lost after dialysis (MW cutoff 3500), while it was retained after 2 weeks of storage. Levels of prostaglandin E 2 and 1,25‐dihydroxyvitamin D of the RCC‐K 1 ‐conditioned medium were insufficient to cause bone resorption in vitro. The conditioned medium did not stimulate cAMP accumulation in rat osteoblastic cells. These results suggest that renal cell carcinoma causes bone destruction through the stimulation of osteoclasts by locally secreting an unknown humoral factor or factors.