Leukocyte Migration Inhibition and Lymphocyte Blastogenesis Responses in Breast Carcinoma Patients to Mouse Mammary Tumor Virus and to Virion gp52 Antigen and Rauscher Murine Leukemia Virus-Kirsten Sarcoma Virus gp69/71 Antigen

Publisher Website
Google Scholar
Abstract
Direct leukocyte migration inhibition (LMI) and lymphocyte proliferation (LP) assays were conducted with leukocytes from patients with breast cancer, benign breast disease, and other types of cancer and from normal donors with the use of mouse mammary tumor virus (MuMTV), its major glycoprotein (gp52), murine leukemia virus (MuLV) glycoproteins (gp69/71), and normal nonvirion glycoproteins. With the use of LMI, leukocytes from 13 of 15 (83%) breast carcinoma patients and 3 of 5 benign breast disease patients reacted with MuMTV, whereas leukocytes from 1 of 16 (6%) normal donors and 0 of 9 patients with other cancers reacted. LMI with gp52 was positive in 39 of 60 (65%) patients with breast cancer, 8 of 15 (53%) with fibrocystic disease, 2 of 11 (18%) with fibroadenoma, 1 of 15 (7%) normal donors, and 3 of 15 (29%) patients with other cancers. Specificity studies with gp69/71 preparations of Rauscher MuLV and Kirsten murine sarcoma virus gave approximately 40% incidence of reactivity in patients with breast cancer, 20% in patients with benign breast disease, 10% in normal donors, and 0% in patients with other cancers. However, significant reactivity of breast cancer patients was also observed with the nonvirion glycoproteins: fetuin from fetal bovine serum and human transferrin. Kinetic experiments with different harvest days and population studies with LP assays were unable to discriminate reactivity from that of normal donors against MuMTV, gp52, or gp69/71. Results suggested that many leukocytes from patients with breast carcinoma and benign breast disease have reactivity in LMI assays against glycoproteins of MuMTV, MuLV, and nonvirion fetuin and transferrin. Due to lack of restriction of LMI and LP specificity to antigens of MuMTV in both patients with malignant and benign breast disease, one must be cautious in interpreting the etiologic significance of these findings.

This publication has 0 references indexed in Scilit: