Two previous cohort studies reported positive associations between tooth loss or periodontitis and pancreatic cancer risk. Data on periodontal disease were obtained at baseline and every other year thereafter in a cohort of 51 529 male health professionals aged 40-75 years. A total of 216 patients were diagnosed with incident pancreatic cancer during 16 years of follow-up. Multivariable relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models controlling for potential confounders, including detailed smoking history. All statistical tests were two-sided. Compared with no periodontal disease, history of periodontal disease was associated with increased pancreatic cancer risk (overall, multivariable RR = 1.64, 95% CI = 1.19 to 2.26; P = .002; crude incidence rates: 61 versus 25 per 100 000 person-years; among never smokers, multivariable RR = 2.09, 95% CI = 1.18 to 3.71; P = .01; crude incidence rates: 61 versus 19 per 100 000 person-years). In contrast, baseline number of natural teeth and cumulative tooth loss during follow-up were not strongly associated with pancreatic cancer. The association between periodontal disease and increased risk of pancreatic cancer may occur through plausible biologic mechanisms, but confirmation of this association is necessary.

Michaud DS, Joshipura K, et al. Journal of the National Cancer Institute 2007 99(2):171-175,
http://jnci.oxfordjournals.org/cgi/ content/abstract/99/2/171

Plasma CRP concentrations are elevated among persons who subsequently develop colon cancer. These data support the hypothesis that inflammation is a risk factor for the development of colon cancer in average-risk individuals.

Erlinger TP, Platz EA, et.al., JAMA vol.291 No.5, Feb 4,2004.
http://jama.ama-assn.org/cgi/content/abstract/291/5/585

The strong association of CRP with PSA, independent of tumor stage, suggests that inflammation might be fundamental in prostate cancer, and that chronic inflammation may be a legitimate target for prostate cancer chemoprevention and treatment.

Lehrer S, Diamond EJ, et.al. BJU Int. 2005 May;95(7):961-2.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi? cmd=Retrieve&db=PubMed&list_uids=15839913&dopt=Abstract

To assess the association between the history of chronic periodontitis and the risk of tongue cancer. .After adjusting for the effects of age at diagnosis, smoking status, and number of teeth, each millimeter of alveolar bone loss was associated with a 5.23-fold increase in the risk of tongue cancer (odds ratio, 5.23; 95% confidence interval, 2.64-10.35). Conclusions: This study suggests an association between chronic periodontitis and the risk of tongue cancer in men, independent of smoking status, age, race, ethnicity, and number of teeth. This association needs to be confirmed by larger studies using quantitative assessment of lifetime tobacco exposure. If this association is confirmed, it has a potential impact on understanding the etiology of oral cancer as well as on its prevention and control.

Tezal Mine, Sullivan MA, et al. Arch Otolaryngol Head Neck Surg. 2007;133:450-454.
http://archotol.amaassn. org/cgi/content/abstract/133/5/450 450.

Matrix metalloproteinases (MMPs) have been implicated in ovarian cancer progression. Among them, MMP-8 that degrades type I collagen may play a crucial role. The aim of our study was to determine MMP-8 expression and regulation in ovarian cancer and its association with other MMPs and tissue inhibitors of metalloproteinases (TIMPs). Tissue microarrays (TMAs) containing tissue cylinders from 302 patients were used for immunohistochemical studies. In addition, MMP-8 expression in vitro was analysed by a specific immunoassay and PCR-analysis. MMP-7 (81%), MMP-8 (95%), MT3-MMP (100%), TIMP- 2 (100%), and TIMP-3 (96%) were expressed in all the OVCAs, but the staining intensities varied. MMP-3 (6%), MMP-9 (57%) and TIMP-1 (43%) expressions were more rarely detected. Only MMP-8 expression levels correlated with tumour grade (P<0.01), tumour stage (P<0.01), and a poor prognosis (P<0.05). MMP-8 protein and gene expression in vitro was found to be significantly upregulated by interleukin-1beta (IL-1beta, P<0.01). The data indicate that MMP-8 overexpression in OVCAs is regulated by IL-1beta and that pro-inflammatory cytokines may promote the invasive potential of ovarian cancer

Stadlmann S, Pollheimer J, et al. Eur J Cancer 2003 Nov;39(17):2499-505. http://www.ncbi.nlm.nih.gov/pubmed/14602136

Immune activation and chronic inflammation as the cause of malignancy in oral lichen planus: is there any evidence? [The association of chronic inflammation with a variety of epithelial malignancies has been recognised for centuries. Well established examples include, among many others, oesophageal adenocarcinoma associated with chronic oesophagitis and bowel cancer associated with chronic inflammatory bowel diseases. By now no data, other than clinical observation, have been available in understanding the pathogenesis of these inflammation-related tumours. However, recent molecular studies on the relationship between solid malignancies and the surrounding stroma have given new insights. There is now enough evidence to accept that the chronic inflammatory process per se is able to provide a cytokine-based microenvironment which is able to influence cell survival, growth, proliferation, differentiation and movement, hence contributing to cancer initiation, progression, invasion and metastasis. Here it is discussed whether also oral lichen planus (OLP), being a chronic inflammatory autoimmune disease which has been clinically associated with development of oral squamous cell carcinoma, might be categorised among these disorders. With this aim, we critically reviewed and detailed the presence, in OLP subepithelial infiltrate, of inflammatory cells and cytokine networks that might act to promote squamous tumorigenesis.

Mignogna M., Oral Oncology , Volume 40 , Issue 2 , Pages 120 - 130,http://linkinghub.elsevier.com/retrieve/pii/S1368837503001726

Recent data have expanded the concept that inflammation is a critical component of tumour progression. Many cancers arise from sites of infection, chronic irritation and inflammation. It is now becoming clear that the tumour microenvironment, which is largely orchestrated by inflammatory cells, is an indispensable participant in the neoplastic process, fostering proliferation, survival and migration. In addition, tumour cells have co-opted some of the signalling molecules of the innate immune system, such as selectins, chemokines and their receptors for invasion, migration and metastasis. These insights are fostering new anti-inflammatory therapeutic approaches to cancer development.

Coussens LM, Werb Z. Nature, Vol 420, p 860-867, December 2002,
http://osteosarcomasupport.org/ immunology/inflammationcancer- nature-2002.pdf

It is well established that cancer arises in chronically inflamed tissue, and this is particularly notable in the gastrointestinal tract. Classic examples include Helicobacter pylori pylori-associated -gastric cancer, hepatocellular carcinoma, and inflammatory bowel disease-associated colorectal cancer. There is growing evidence to suggest that this association is not coincidental but may indeed be causal. In this review, we discuss the role of chronic inflammation and cytokine gene polymorphisms in the pathogenesis of gastrointestinal malignancy and outline some of the possible mechanisms involved.

Maccarthur M, Hold, GL, El-Omar EE. Am J Physiol Gastrointest Liver Physiol 286: G515-G520, 2004, http://ajpgi.physiology.org/cgi/content/abstract/286/4/G515

C-reactive protein, a marker of inflammation circulating in the blood already associated with increased risk of heart disease, can also be used to identify a person's risk of developing colon cancer, according to a Johns Hopkins study. People with higher levels of CRP in their blood were more likely to develop colorectal cancers than those with low levels of CRP. Higher levels of C-reactive protein are linked to an increased risk of several apparently distinct, chronic diseases: heart disease, stroke, diabetes, and now colon cancer. The odds of developing colorectal cancers increased progressively with higher concentrations of CRP.

Johns Hopkins Medicine Office of Communications and Public Affairs. Feb. 3, 2004 JAMA. http://www.hopkinsmedicine.org/Press_releases/2004/02_10_04.html

UB study links gum disease with oral cancer risk. Oral tumors were four times more prevalent and pre-cancerous lesions were twice as prevalent in people with periodontal disease (as assessed by clinical attachment loss) than in those without periodontal disease. These findings suggest strongly that infection is associated with oral cancer. Research shows an association between H. pylori and stomach cancer, human papillomavirus and cervical cancer, and cytomegalovirus and Kaposi's sarcoma.

Tezal Mine, Grossi SG.,
http://www. eurekalert.org/pub_releases/2003- 03/uab-usl031303.php