Radioimmunometric Demonstration of Immunoglobulin G on Cancer Cells Derived from Malignant Pleural Effusions

Abstract

Well-preserved viable cancer cells, lymphocytes and mesothelial cells were prepared from various human malignant and non-malignant pleural effusions by a Ficoll-Hypaque discontinuous gradient. Using ¹²⁵I-labelled protein A from Staphylococcus aureus as tracer, IgG was found on all cancer cells and also on apparently non-malignant mesothelial cells. Loss of cell surface IgG by overnight incubation, and fluctuation of surface IgG levels in the same patient occurred with cancer cells as well as with mesothelial cells. The IgG in vivo coat of cancer cells reflected the IgG levels of the sera rather than those of the pleural effusions. Binding of IgG from autologous and allogeneic sera and from supernatantsof acid and mild overnight elution of cancer cells and mesothelial cells did not indicate a cancer-specific uptake of IgG. Various unspecific modes of IgG uptake by cancer cells are discussed including the possibility of a non-immune mechanism. Modification and loss of antigens by metastatic cells have also been considered.

Chronic Exendin-4 Treatment Prevents the Development of Cancer Cachexia Symptoms in Male Rats Bearing the Yoshida Sarcoma

“…This indicates that tumor burden itself may not be an important factor in determining the onset of cancer cachexia symptoms. These findings are consistent with the human literature [41, 26, 33, 20], and with previous experiments in the Yoshida sarcoma and other animal models [16, 48, 46, 29, 13, 9, 1, 36, 24]. …”

“…Insulin function is often impaired in individuals with and animal models of cancer cachexia [21, 14, 47, 41, 26, 33, 20, 45, 5, 6, 16, 48, 46, 29, 11, 9, 1, 36, 24, 13]. Given the ability of insulin dysfunction to result in altered body composition in other animal models of disease [31], there is interest in determining the role that insulin resistance may play in cachexia development [23].…”