The mini-catalogue of protein expression changes should serve as a good reference/guide for future basic and translational cancer research. For example, not all cases of DCIS progress to carcinoma and whether all patients with DCIS should receive adjuvant therapy after breast-conserving surgery remains a topic of active debate. Our diploid screen identified 376 gene deletions sensitive to the DNA damaging agent doxorubicin, many of which overlap with those that function in recombinational repair and were also identified in our previous diploid IR screens. However, when a similar screen was performed in the isogenic haploid deletion collection, far fewer haploid mutants were detected that mediated resistance to DOX. We can attribute our enhanced success at identifying DOX resistance genes to two factors. First, our diploid screen WZ4002 1213269-23-8 employed DOX doses that were greater than that used in the haploid screen. Secondly, DSB damage such as that induced by DOX or IR is repaired preferentially by recombinational repair mechanisms utilizing a homologous chromosome or sister chromatid. DNA damage resistance genes that confer resistance to DOX and function exclusively in G1 or at the G1/S boundary prior to DNA synthesis are undetectable as mutants in haploid cells which have no homolog capable of serving as a template for recombination repair prior to DNA replication. Extracellular MMP inducer, a membrane glycoprotein greatly enriched on the surface of tumor cells is known to stimulate tumor and neighbouring stromal cells, such as fibroblasts and endothelial cells, to increase their synthesis of several MMPs. We have shown that EMMPRIN is not only an MMP inducer but can also increase the urokinase plasminogen activating system in tumor and endothelial cells, further increasing its proteolytic potential. EMMPRIN is also implicated in lactate efflux, essential for tumor cell invasion, via its cotransporter MCT4. Indeed, the conversion of glucose to lactic acid in the presence of oxygen, generally known as aerobic glycolysis or Warburg effect, is uniquely observed in cancer and the excess generation of lactate that accompanies the Warburg effect needs to be exported from the cell. Elevated EMMPRIN levels have been correlated with invasion and tumor progression in numerous malignant tumor models including melanoma. However, conflicting results regarding the putative involvement of EMMPRIN in the progression of melanoma were reported showing that EMMPRIN expression was observed in non invasive malignant melanoma lesions while both the benign lesions and the most metastatic melanomas were negative. The fact that many of these DOX resistant genes also overlap with mutants within a BRCA1 suppressor pathway that regulates transcription elongation, RNA polymerase II stability as well as mRNA export and decay in G1.