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The cellular basis of metastatic bone disease in patients with lung cancer
Author(s) -
Cramer Stewart F.,
Fried Lawrence,
Carter Kimbroe J.
Publication year - 1981
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(19811215)48:12<2649::aid-cncr2820481217>3.0.co;2-s
Subject(s) - medicine , pathology , lung cancer , cancer , lung , stromal cell
Abstract Histologic patterns of tumor‐bone interaction were systematically evaluated in 80 cases of metastatic lung cancer involving bone. Patterns of tumor‐bone interaction varied with the histologic type of lung cancer, reflecting the biochemical and biologic differences among the different types of lung cancer. Evidence presented here suggests that destruction of bone by metastatic lung cancer is mediated neither by direct contact of tumor cells with bone matrix nor by release of diffusible substances that lyse bone matrix. Among indirect mechanisms, the most prevalent and important was the activation of bone‐lining cells by metastatic tumor. Epidermoid carcinomas in particular were associated with histologic patterns of classical bone remodelling, including osteoblastic, osteoclastic, and osteocytic activity. Adenocarcinomas showed a particularly high association with microfractures and manifested a stromal pattern consistent with release of prostaglandins. Ischemic necrosis of bone due to compression of vessels by expanding tumor mass is also a common and important mechanism. Correlation of histologic patterns with reported data on the frequency of bone metastases and syndromes of ectopic hormone production provides insight into the mechanism(s) of paraneoplastic hypercalcemia in patients with lung cancer.