MKI67 and breast carcinoma: While these data don't exclude the possibility of a paracrine regulation of cell proliferation by ERα in these cells, the colocalization of ERα and Ki-67 does support the hypothesis that ERα may mediate cell proliferation in an autocrine mode in these ERα-positive breast cancer cell lines, a mechanism absent in normal mammary cells and most primary breast tumors [1-3,16-18,23,24].