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Tumor necrosis factor-beta and hypercalcemia.

K Ishibashi·M Kodama·S Hanada·T Arima
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Abstract

Hypercalcemia in hematological malignancy is frequently encountered in lymphoid malignancies such as adult T-cell leukemia (ATL) and multiple myeloma and is difficult to manage. As a causative agent of hypercalcemia in ATL, tumor necrosis factor-beta (TNF-beta), previously known as lymphotoxin, has been carefully studied and reviewed here. Bone resorption studies showed the presence of activity in culture supernatants of HTLV-I infected cells. Enzyme linked immunosorbent assays (ELISA) for TNF-beta detected elevated TNF-beta in the sera of ATL patients with hypercalcemia. Immunostaining by monoclonal anti-TNF-beta antibody demonstrated the presence of TNF-beta in both HTLV-I infected cell lines and freshly isolated ATL cells. Furthermore biological TNF-beta activity assay including inhibition of anti-TNF-beta antibody confirmed the conventional documentation of TNF-beta activity in the sera and culture supernatants of HTLV-I infected cell lines. These studies showed that the TNF-beta secreted from ATL cells might be one of the factors contributing to the hypercalcemia in patients with ATL functioning as an osteoclast activating factor (OAF).

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AnimalsBone RemodelingBone ResorptionCytokinesEnzyme-Linked Immunosorbent AssayHumansHypercalcemiaLeukemia, T-CellLymphotoxin-alphaMultiple MyelomaJournal ArticleReview

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K Ishibashi, M Kodama, S Hanada, T Arima. 1992. Tumor necrosis factor-beta and hypercalcemia.. https://doi.org/10.3109/10428199209049796

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