Therefore, our data suggests that cancer-associated inflammation, as assessed by serum ferritin and CRP, is either 1) inducing resistance to cancer therapies (trastuzumab alone, chemotherapy alone, or the combination of both) either directly through activation of molecular pathways or indirectly through affecting the structure and density of tumor vasculature and thus decreasing drug distribution, or 2) enhancing tumorigenesis through various mechanisms that counteract and compensate for the anti-tumorigenic effects of this therapy. The gene discussed is CRP; the disease is neoplasm.