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The overall purpose of this project is to investigate the role of HOXC10 in breast cancer tumorigenicity and drug resistance. Since it was previously shown to be involved in proliferation and cell cycle, we investigated at the molecular level the role of HOXC10 and found that by affecting the RB/E2F1 pathway, it controls proliferation, G1/S transition and new origin firing. On the other hand, HOXC10 activates NF-kb, G2/M checkpoint and DNA repair through NER pathway, protecting cells from apoptosis and DNA damage, especially DNA crosslinks. Interestingly, HOXC10 functions at later stage of DNA damage response, mainly at maintenance of the checkpoint until repair is complete. This eventually leads the cells to become less sensitive to chemotherapy treatment. Most importantly, cells selected to become resistant to drug treatment over long time drug exposure show a significant increase in HOXC10 expression. In conclusion, in this report we show for the first time that HOXC10 upregulation in breast cancer may have some clinical implications since it affects tumor growth, genomic instability and response to some chemotherapy drugs.