Cancer Therapy-Induced Inflammation and Its Consequences

The inflammatory process often modifies the natural history of cancers. There is broad evidence that chronic inflammatory responses, associated with, e.g., persistent viral or bacterial infections, promote carcinogenesis. Cancer treatment is also associated with an inflammatory process that may either induce an antitumor immune response or, conversely, favor tumor recurrence. Here, we will revise the major aspects of therapy-induced inflammation and its consequences for tumor recurrence or repopulation, emphasizing how the mode of tumor cell death elicits an antitumor response, the key elements associated with the clearance of dead cells within the tumor microenvironment and the unleashing of an innate tissue regenerative response, dependent on lipid mediators such as prostaglandin E2 and the platelet activation factor (PAF), that favor tumor regrowth. Therapy-induced inflammation may offer a window of opportunity for combination therapies that increase the effectiveness of conventional cancer treatment modalities. Nanobiotechnology offers versatile platforms for anti-inflammatory interventions. Here we also discuss RNA-based approaches in the nanoscale, which would allow targeted interventions of pro-tumoral inflammatory milieu assembled in the course of therapeutic regimens in order to avoid the emergence of treatment-resistant cancer cells that ultimately repopulate the tumor mass.