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Inflammation and Cancer: a Comparative View

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Inflammation and Cancer: a Comparative View Review J Vet Intern Med 2012;26:18–31 Inflammation and Cancer: A Comparative View Wallace B. Morrison Rudolph Virchow first speculated on a relationship between inflammation and cancer more than 150 years ago. Subse- quently, chronic inflammation and associated reactive free radical overload and some types of bacterial, viral, and parasite infections that cause inflammation were recognized as important risk factors for cancer development and account for one in four of all human cancers worldwide. Even viruses that do not directly cause inflammation can cause cancer when they act in conjunction with proinflammatory cofactors or when they initiate or promote cancer via the same signaling path- ways utilized in inflammation. Whatever its origin, inflammation in the tumor microenvironment has many cancer-promot- ing effects and aids in the proliferation and survival of malignant cells and promotes angiogenesis and metastasis. Mediators of inflammation such as cytokines, free radicals, prostaglandins, and growth factors can induce DNA damage in tumor suppressor genes and post-translational modifications of proteins involved in essential cellular processes including apoptosis, DNA repair, and cell cycle checkpoints that can lead to initiation and progression of cancer. Key words: Cancer; Comparative; Infection; Inflammation; Tumor. pidemiologic evidence suggests that approximately that has documented similar or identical genetic E25% of all human cancer worldwide is associated expression, inflammatory cell infiltrates, cytokine and with chronic inflammation, chronic infection, or both chemokine expression, and other biomarkers in (Tables 1 and 2).1–5 Local inflammation as an anteced- humans and many domestic mammals with morpho- ent event to cancer development has long been recog- logically equivalent cancers.65–78 The author is una- nized in cancer patients. Over 150 years ago, Rudolph ware of reliable estimates of the total percentage of Virchow speculated on a link between inflammation cancer in domestic species that are the result of inflam- and cancer based on his observations of finding leuko- mation, but the economic impact of cancer resulting cytes in human breast carcinomas.1,4,6,7 He suggested from infections causing cancer in some domestic ani- that the “lymphoreticular infiltrate” reflected the origin mals has been documented.79 There are numerous of cancer at sites of chronic inflammation. Since examples of inflammation and infection in veterinary Virchow’s observation, a large and growing body of patients that can culminate in malignant transforma- factual, epidemiologic, and circumstantial evidence tion of susceptible cells (Tables 3 and 4).80–131 How- defining the wide array of inflammatory and infectious ever, many are individual case reports and anecdotal conditions that predispose susceptible cells to carcino- reports, but taken together they reflect a spectrum of genic changes has developed. Chronic inflammation disorders that are linked to cancer. alone is sufficient to cause oncogenesis.3,6,7 Frequently however, infection is the primary event and chronic Basic Concepts of Carcinogenesis inflammation is the result. Numerous reviews have explored the relationship of The process of carcinogenesis can conceptually be inflammation to cancer and the known or postulated represented in a number of ways. One way is with the mechanisms of malignant transformation in humans classic stepwise evolution of a malignancy in 3 phases and in laboratory animals.1–64 Although none of the that begins with initiation of susceptible normal cells, literature to date in domesticated mammals has sum- promotion of accumulated genetic damage, and pro- marized the evidence for a similar and broad relation- gression of disorders we collectively refer to as can- ship, such a relationship does exist. It is likely that the cer.7,10 Initiation is characterized by the accumulation mechanisms of chronic, local inflammation with or of genetic change in a cell such as point mutations, without infection that induces cancer in humans and deletions and amplification, methylation of DNA, and laboratory animals and those that induce cancer in rearrangements of genes and chromosomes that fail to veterinary patients are similar. This hypothesis is based be repaired and lead to irreversible changes in cells on a large and rapidly growing library of literature that survive a critical transforming level of genetic damage. Mediators of inflammation such as cytokines, reactive oxygen and nitrogen species, prostaglandins, and growth factors are capable of initiating these types From the Diplomate ACVIM (Small Animal Internal of DNA mutations within cells that then can experi- Medicine), Department of Veterinary Clinical Sciences, School of ence disruptions of critical signaling pathways respon- Veterinary Medicine, Purdue University, West Lafayette, IN. Corresponding author: Wallace B. Morrison, DVM, MS, sible for maintaining normal cellular homeostasis. The Department of Veterinary Clinical Sciences, 625 Harrison Street, initiated cell with its permanent DNA mutations is a Purdue University, West Lafayette, IN 47907, e-mail: wbm@pur- sine qua non for cancer development. Most cells with due.edu minor DNA mutations survive because the damaged Submitted October 7, 2010; Revised September 22, 2011; DNA is repaired, or if the level of damage is incom- Accepted October 5, 2011. patible with survival are signaled to die via apoptosis. © Copyright 2011 by the American College of Veterinary Internal For cancer to develop, the damage to DNA must per- Medicine 10.1111/j.1939-1676.2011.00836.x sist and resist the many DNA-repair processes and be Inflammation and Cancer 19 Table 1. Cancers linked to inflammation in humans. Table 2. Cancers linked to chronic infection in humans. Associated Increased Risk of Predisposing Condition Cancer Human Papilloma Virus Ulcerative colitis Colon carcinoma (HPV)–Especially High Cervical, Vulvar, Penile, Anal, and Crohn’s disease Colon carcinoma Risk Types Oral (Head and Neck) Cancers Chronic pancreatitis Pancreatic carcinoma Herpes family of viruses Chronic acid reflux Esophageal carcinoma Epstein-Barr virus Burkitts lymphoma, Hodgkin’s Solar exposure and sun burn Melanoma, basal cell carcinoma lymphoma, nasopharyngeal Foreign material carcinoma, AIDS associated Implanted medical devices Breast carcinoma lymphoma Metallic implants Primary bone tumors Sinonasal angiocentric T-cell Asbestosis Mesothelioma lymphoma Silica Various pulmonary cancers Immunnosuppression-related Talc Various pulmonary cancers lymphoma (post-transplantation, Carbon nanotubes Various pulmonary cancers AIDS, X-linked Particulate carcinogens Various pulmonary cancers lymphoproliferative disorders) Shrapnel and bullet trauma Various carcinomas and Hodgkin’s lymphoma in sarcomas immunocompetent individuals Surgical sponge Angiosarcoma Undifferentiated nasopharyngeal Chronic prostatitis Prostate carcinoma carcinoma Thermal burns Skin carcinoma Lymphoepithelioma-like gastric carcinomaa Gastric adenocarcinomaa Breast cancera readable by DNA polymerase, which creates and Leiomyosarcoma in maintains the mutation. As genetic changes accumulate immunocompromised individuals in cells, some growth advantage over unaffected cells is Lymphoepithelioma lung cancer conferred and a precancerous lesion can form.10 Com- Human herpes virus-8 Kaposi’s sarcoma, primary effusion mon preneoplastic DNA mutations are those that (HHV-8) lymphoma Castleman’s disease (angiofollicular result in increased expression of oncogenes like myc, hyperplasia) ras, abl, and bcl-2 or decreased activity of tumor sup- 4 Human cytomegalovirus Not regarded as independently pressor genes like Rb and p53. A locked DNA muta- (HCMV) oncogenic but has been tion continuously contributes to the propagation of implicated as a cofactor in colon cells with mutated genetic material with each subse- cancer, malignant glioma, quent cell division. Activation of oncogenes, inactiva- prostate carcinoma, breast cancer tion of tumor suppressor genes, and the influences of Hepatitis B, C or B + C Hepatic carcinoma other key regulators of cellular proliferation, such as Human T-lymphotrophic T-cell leukemia, T-cell lymphoma IL-2 and IFN-c, during initiation lead to changes in Virus-1 and 2 (HTLV-1 the cellular microenvironment that promote tumor cell and HTLV-2) Helicobacter pylori Gastric carcinoma, MALT survival and clonal expansion of “initiated cells” in the 10 colonization lymphoma, pancreatic carcinoma phase known as promotion. During tumor promo- Mycobacterium Lung cancer tion, initiated cells interact via secreted factors from tuberculosis colonization normal leukocytes/immunocytes and are further trans- Human JC polyoma virus Merkel cell carcinoma 4 formed into cancer cells. This process is very complex Shistosoma hematobium Bladder cancer, prostate and less well defined than the process of initiation. carcinoma,b squamous cell Progression involves substantial growth and/or metas- carcinoma of cervixb tasis of the established cancer. Shistosoma mansoni Hepatocellular carcinoma, colorectal carcinomab Shistosoma japonicum Hepatocellular carcinoma,b The Relationship of Inflammation to colorectal carcinomab Carcinogenesis Opisthorchis viverrini Cholangiocarcinoma Clonorchis sinensis Cholangiocarcinoma Inflammation is a rapid, multistep, and normal response to acute tissue damage resulting from physi- aAlthough EBV is frequently present in these tumors it is cal injury, ischemic injury, toxins, or other types of unclear if EBV plays a pathogenic role in their
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