This study has revealed a regulatory loop in which genotoxic stress created by chemotherapeutic drugs limited the survival of breast tumor cells, but the expression of tumor necrosis factor α (TNFα) was also increased and has led to elevated production of CXCL1/2 by the tumor cells; these chemokines recruited CXCR2-expressing CD11b+ Gr1+ myeloid cells which in turn acted via S100A8/9 factors to promote the viability of tumor cells that expressed CXCR2. This evidence concerns the gene CXCR2 and breast neoplasm.