EBAG9 and breast carcinoma: Nakashima et al (1999) recently reported that activated CD3+ T lymphocytes express a putative receptor for EBAG9/RCAS1. This receptor expression was enhanced by activation of the lymphocytes, and when these receptor-positive cells were cultured with EBAG9/RCAS1 peptides, their growth was strongly suppressed, and they were eventually led to cell death by apoptosis (Nakashima et al, 1999). In breast carcinoma, EBAG9 immunoreactivity was inversely associated with the degree of intratumoral infiltration of mononuclear cells or CD3+ T lymphocytes (Suzuki et al, 2001).