Taken together, these data imply that cell-cell contact between nontransformed G2B-10A cells and malignant R2-T1AS cells promotes secretion of IL-6 by R2-T1AS breast cancer cells, and that IL-6 is a good candidate to mediate enhanced tumorigenicity of R2-T1AS cells, possibly by inducing tumor stem cell survival. This evidence concerns the gene IL6 and breast carcinoma.