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Bacterial Infection As a Cause of Cancer

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Bacterial Infection As a Cause of Cancer CORE Metadata, citation and similar papers at core.ac.uk Provided by PubMed Central Bacterial Infection as a Cause of Cancer Julie Parsonnet Departments of Medicine and Health Research and Policy, Stanford University School of Medicine, Stanford, California Bacterial infections traditionally have not been considered major causes of cancer. Recently, however, bacteria have been linked to cancer by two mechanisms: induction of chronic inflammation and production of carcinogenic bacterial metabolites. The most specific example of the inflammatory mechanism of carcinogenesis is Helicobacter pylori infection. H. pylori has been epidemiologically linked to adenocarcinoma of the distal stomach by its propensity to cause lifelong inflammation. This inflammation is in turn thought to cause cancer by inducing cell proliferation and production of mutagenic free radicals and N-nitroso compounds. H. pylori is the first bacterium to be termed a definite cause of cancer in humans by the International Agency for Research on Cancer. Mutagenic bacterial metabolites are also suspected to increase risk for cancer. This model is best exemplified in colon cancer. Bile salt metabolites increase colonic cell proliferation. Exogenous compounds such as rutin may be metabolized into mutagens by resident colonic flora. Moreover, Bacteroides species can produce fecapentaenes, potent in vitro mutagens, in relatively high concentrations. In vivo data on human carcinogenesis by bacterial metabolites, however, are inconsistent. Local bacterial infections may also predispose to nonnodal lymphomas, although the mechanisms for this are unknown. Gastric lymphomas and immunoproliferative small intestinal disease have been most strongly linked to underlying bacterial infection. Because bacterial infections can be cured with antibiotics, identification of bacterial causes of malignancy could have important implications for cancer prevention. - Environ Health Perspect 1 03(Suppl 8):263-268 (1995) Key words: bacteria, neoplasm, gastric cancer, colorectal cancer, Helicobacterpylori, epidemiology, carcinogenesis, normal flora Introduction link between active tuberculosis and chronic osteomyelitis was the first to be A substantial number of bacterial pathogens malignancy is currently ascribed to reacti- convincingly associated with cancer in have been putatively linked to cancer. As vation of infection in immunocompro- humans. Constant irritation of a draining early as 1772, Mycobacterium tuberculosis mised cancer patients rather than to a sinus tract by inflammatory exudates of the was thought to cause malignancy (1). It cause-and-effect relationship between underlying bone predisposes the host to was observed that bronchogenic carcinomas infection and neoplasm (2-4). carcinoma of the skin, regardless of the frequently appeared in areas of pulmonary Despite this early misstep, bacterial specific bacterial pathogen involved (9). scarring, presumably from tuberculosis. theories for carcinogenesis continue to be Fortunately, in the era of antibiotics Persons with lung cancer also were noted promulgated (5). Now, however, rather chronic osteomyelitis contributes a vanish- to have active tuberculosis more frequently than directly attributing cancer to specific ingly small number of cases to the cancer than the general population. Like many organisms, attention has focused on non- registry. A similar mechanism has been hypotheses attributing cancer to specific specific mechanisms of carcinogenesis. proposed for bladder cancer in persons infectious agents, however, the tuber- Two such mechanisms are induction of with recurrent or persistent cystitis (10,11). culosis-cancer theory did not stand the test inflammation, and production of muta- Currently, a popular model for bacterial of time. Most bronchogenic carcinomas in genic compounds by bacterial metabolism. carcinogenesis is that of Helicobacter pylori persons with tuberculosis do not occur at The first mechanism is best exemplified by infection and gastric adenocarcinoma. H. scar sites but elsewhere in the lung. Helicobacter pylori infection and gastric pylori is a Gram-negative rod that lives in a Furthermore, observed scars at tumor cancer. Colon cancer provides a model for neutral pH niche between the mucus layer sites now appear to be the result of the the second of these mechanisms. Yet a of the stomach and the gastric epithelium. malignancy rather than the cause. Any third mechanism, that for lymphomas, has Although H. pylori can be found lining the yet to be credibly modeled. mucus layer adjacent to ectopic gastric tis- Bacteria, Inflammation, and sue (e.g., in Meckel's diverticula), it is never This paper was presented at the President's found remote from gastric epithelium and Cancer Panel Conference on Avoidable Causes of Cancer: the Helicobacterpylori does not invade tissue; it neither enters Cancer held 7-8 April 1994 in Bethesda, Maryland. Model epithelial cells nor penetrates the basement Manuscript received 9 March 1995; manuscript accepted 24 March 1995. Infections have been nonspecifically tied to membrane. Despite this lack of invasion, This work is supported in part by a Junior Faculty malignancy through their ability to cause H. pylori infection is invariably associated Research Award from the American Cancer Society chronic inflammation. Among the chronic with inflammation (12,13). Once estab- and by a Clinical Epidemiology Fellowship from Merck and the Society for Epidemiologic Research. inflammatory processes linked to cancer are lished, H. pylori infection and its associated Address correspondence to Dr. Julie Parsonnet, parasitic infections [e.g., Schistosoma inflammation are thought to last for Departments of Medicine and Health Research and haematobium and Opisthorchis viverrini decades if not a lifetime (14). At least 50% Policy, HRP Building, Room 225, Stanford University and viruses B In gen- of the world's harbors the School of Medicine, Stanford, CA 94305. Telephone: (6,7)] [hepatitis (8)]. population (415) 723-7274. Fax: (415) 725-6951. E-mail: eral, these infections cause cancer in direct organism (14). [email protected] proportion to their chronicity; the longer Recently, H. pylori was declared by the Abbreviations used: IPSID, immunoproliferative the inflammatory process persists, the more International Agency for Research on small intestinal disease; MALT, mucosal-associated lymphoid tissue; IARC, International Agency for likely malignancy is to develop (7,8). Cancer (IARC) to be a Group 1 carcino- Research on Cancer. Among bacterial inflammatory processes, gen, a definite cause of human cancer (7). Environmental Health Perspectives 263 J. PARSONNET Support for this decision came principally case-control studies of H. pylori in gastric damage to the epithelium by the inflamma- from pathologic studies of the natural his- cancer have shown significant associations tory response (49,53-57). Cell proliferation tory of gastric adenocarcinoma and epi- between infection and malignancy (32-35), in turn increases risk for DNA replication demiologic studies statistically linking H. others have not (36-40). error and predisposes mucosal cells to pylori to malignancy. The most convincing data implicating transformation by dietary or endogenous Chronic superficial gastritis has long H. pylori as a cause of cancer are four mutagens (58,59). been thought to be a precursor lesion to nested case-control studies from Hawaii, Other elements of inflammation also gastric adenocarcinoma (15,16). Even in California, Great Britain, and Taiwan can be seen as tumor-promoting processes the absence of more advanced preneoplas- (41-44). In the first three studies (mean (48,58). Inflammatory cells increase con- tic lesions, superficial gastritis increases follow-up 13, 14, and 6 years, respec- version of nitrates to nitrites, enhancing the cancer risk 2-fold (17). In approximately 3 tively), serologic evidence of H. pylori likelihood of N-nitrosamine formation (6). to 5% of persons per year, superficial gas- infection increased risk of later developing This may explain the epidemiologic obser- tritis progresses to chronic atrophic gastri- gastric cancer between 2.8- and 6-fold vation that in some populations high tis, a more advanced cancer precursor (41-43). The fourth nested case-control dietary nitrates increase gastric cancer risk lesion (18-20). With extensive atrophy, study also identified an elevated risk of (60). Moreover, activated macrophages cancer risk increases up to 9-fold (17). As cancer (odds ratio = 1.6), but the finding produce nitrite, nitrate, and nitrosating atrophy worsens, patches of intestinal was not statistically significant (44). This agents (61). When macrophages are cul- metaplasia arise and the gastric epithelium last study was hampered, however, by a tured with appropriate amines, N-nitroso transforms to either small or large bowel small number of cases (n = 29) and short compounds are formed. Free radicals pro- morphology. Cancer ensues thereafter. follow-up period (mean = 3 years). Overall, duced by the inflammatory response, e.g., Since H. pylori causes the vast majority the association between H. pylori and 0- and superoxide, alter the structure and of superficial gastritis, it can be deduced cancer appeared to be restricted to tumors function oflipids, proteins, and DNA caus- from the data above that H. pylori is a distal to the gastric cardia (41,43). ing changes in cell metabolism and gene likely risk factor for malignancy and A combined analysis of three nested
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