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Gene ontology analysis using the DAVID tool, focusing on the genes upregulated by pefloxacin and whose upregulation was suppressed by dexamethasone co-administration, revealed that several pathways related to oxidative stress, such as response to hydrogen peroxide and hydrogen peroxide catabolic process, were enriched (Figure 5A)
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(2) dissociation of tumor cells from the primary tumor mass, (3) invasion of the neighboring tissue, (4) intravasation into pre-existing and newly formed blood and lymph vessels, (5) transport through the vessels, (6) extravasation from the vessels, (7) establishment of circulating tumor cells (CTCs) and the disseminated cells at a secondary anatomical site, where they can stay dormant for a prolonged period of time, (8) metastatic outgrowth of micrometastases and macrometastases creating clinically detectable secondary tumors and neoplastic process [13]
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