Effect of estradiol and degree of cell differentiation on human melanoma susceptibility to killing by monoclonal antibodies.

An estradiol non-responsive melanotic (E-M+ShA) was derived from an estradiol-responsive melanotic (E+M+ShA), and an estradiol-responsive amelanotic (E+M-SR) was derived from estradiol non-responsive amelanotic (E-M-SR) cell lines by deprivation and supplementation of the culture medium with estradiol, respectively. E+M+ShA cells became E-M+ShA after 5 weeks, i.e. 2 subcultures, of culture in the absence of estrogen, and E-M-SR cells became E+M-SR after 7 weeks, i.e. 2 subcultures, of culture in the presence of 10(-7) M 17 beta-estradiol. Spleen lymphocytes from mice pre-immunized with E+M+ShA, E-M+ShA, E-M-SR and E+M-SR have been fused with murine non-producer myeloma cells to obtain mouse-mouse hybridoma cultures that synthesize monoclonal antibodies against human malignant melanoma. The complement-dependent cytotoxin activities of these antibodies linked responsiveness to estradiol with melanotropin biosynthesis.