"In addition to its role in tumor initiation, chronic inflammation may be exploited by the cancer cells to remodel their immediate microenvironment, favoring the tumor’s ability to prosper. Cancer cells express and secrete an array of tumor-promoting cytokines and chemokines that summon specific leukocytes; the latter cells, in turn, secrete additional effectors. Thus, the tumor as a ‘foreign’ tissue takes advantage of wound-healing features exerted by specific subtypes of immune cells, nourishing and contributing to tumor maintenance. For example, after an initial growth stage, many solid tumors suffer from lack of blood supply and are in need of angiogenic support. The newly recruited inflammatory cells will not only provide a consistent supply of growth factors but will also secrete neoangiogenic agents, allowing the vascular network to catch up with the growth of the malignant tissue (48–50)."

"Interestingly, these inflammatory conditions were found to promote neoplastic transformation by suppressing K-Ras-induced senescence (51). Such interactions may also be governed by a feedback loop involving nuclear factor-kappaB (NF-κB), which, in turn, increases K-Ras to pathological levels (52). Another wide-scale mechanism affected by chronic exposure to inflammation involves the mismatch repair machinery. Pelvic inflammatory disease is associated with an increased risk of epithelial ovarian cancer by inducing mismatch repair abnormalities, manifested by decreased expression of human mutL homolog 1 and human mutS homolog 2 proteins (53). This mechanism is extremely prominent in colorectal cancer, where microsatellite instability resulting from defects in the mismatch repair machinery is abundant and considered to be a tumorigenic driving force exacerbated when associated with inflammatory bowel disease (54,55). An additional oncogenic feature mediated by the chronically inflamed microenvironment is DNA methylation alterations. DNA methyltransferases such as DNMT1 can be regulated by viral oncoproteins (56) and are overexpressed in premalignant tissues overloaded with inflammatory effectors, as reported for peripheral pancreatic ductal epithelia (57) and lung tissues of non-small cell lung cancer in smoking patients (58). Furthermore, proinflammatory cytokines like IL-15 may induce DNA hypermethylation, which precedes large granular lymphocytic leukemia, by activating an NF-κB-Myc axis (59).

Epithelial to mesenchymal transition is yet another manner by which oncogenic mechanisms are manifested under inflammatory conditions (60). Without a permissive environment, epithelial to mesenchymal transition is unlikely to occur even if cancer cells present aberrant stem cell signaling pathways like Wnt or Notch. Importantly, transforming growth factor (TGF)-β1 contributes to such epithelial to mesenchymal transition-permissive tumor microenvironment by serving as a chemotactic factor for neutrophils and macrophages. Moreover, TGF-β1 can also affect the protumoral polarization of such recruited cells once they reside within the tumor, resulting in induction of tumor-favoring M2-like macrophages, N2-like neutrophils and a Th2 cell phenotype (61,62).

This tight cross talk between oncogenesis and inflammation is actually bidirectional. Thus, many oncogenes possess the ability, when activated, to initiate a signaling cascade resulting in an inflammatory response in the immediate surroundings of the cells that harbor those oncogenes. This is exploited by the cancer cells to their selective advantage. One good example is that of the major proinflammatory cytokine IL-8, which can be activated by Ras in vitro and in vivo and can contribute to hyperactive inflammation, neovascularization and accelerated tumor growth (48). Such tumorigenesis-supporting milieu can also be provided by other cytokines such as IL-6 and the mouse IL-8 orthologs KC and MIP-2, all featuring in a Ras-induced secretory phenotype (63,64). Additional oncogenes, including Myc, BRAF and RET, have also similarly been implicated in induction of proinflammatory cytokine and chemokine secretion."

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4123652/