Oral cancer is one of the major global threats to public health. The development of oral cancer is a tobacco-related multistep and multifocal process involving field cancerization and carcinogenesis. The rationale for molecular-targeted prevention of oral cancer is promising. Biomarkers of genomic instability, including aneuploidy and allelic imbalance, are possible to measure the cancer risk of oral premalignancies. Understanding of the biology of oral carcinogenesis will yield important advances for detecting high-risk patients, monitoring preventive interventions, and assessing cancer risk and pharmacogenomics. In addition, novel chemopreventive agents based on molecular mechanisms and targets against oral cancers will be derived from studies using appropriate animal carcinogenesis models. New approaches, such as molecular-targeted agents and agent combinations in high-risk oral individuals, are undoubtedly needed to reduce the devastating worldwide consequences of oral malignancy.

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Colorectal cancer (CRC) is the third most common epithelial malignancy in the world. Since CRC develops slowly from removable precancerous lesions, detection of the lesion at an early stage by regular health examinations can reduce the incidence and mortality of this malignancy. Colonoscopy significantly improves the detection rate of CRC, but the examination is expensive and inconvenient. Therefore, we need novel biomarkers that are non-invasive to enable us to detect CRC quite early. A number of validation studies have been conducted to evaluate genetic, epigenetic or protein markers for identification in the stool and/or serum. Currently, the fecal occult blood test is the most widely used method of screening for CRC. However, advances in genomics and proteomics will lead to the discovery of novel non-invasive biomarkers.

The inhibitory effects of novel prodrugs, inclusion complexes of 3-(4 0 -geranyloxy-3 0 -methoxyphenyl)-2-trans propenoic acid (GOFA) and auraptene (AUR) with b-cyclodextrin (CD), on colon carcinogenesis were investigated using an azoxymethane (AOM)/ dextran sodium sulfate (DSS) model. Male CD-1 (ICR) mice initiated with a single intraperitoneal injection of AOM (10 mg/kg body weight) were promoted by the addition of 1.5% (w/v) DSS to their drinking water for 7 days. They were then given a basal diet containing 2 dose levels (100 and 500 ppm) of GOFA/b-CD or AUR/b-CD for 15 weeks. At Week 18, the development of colonic adenocarcinoma was significantly inhibited by feeding with GOFA/b-CD at dose levels of 100 ppm (63% reduction in multiplicity, p < 0.05) and 500 ppm (83% reduction in the multiplicity, p < 0.001), when compared with the AOM/DSS group (multiplicity: 3.36 6 3.34). In addition, feeding with 100 and 500 ppm (p < 0.01) of AUR/b-CD suppressed the development of colonic adenocarcinomas. The dietary administration with GOFA/b-CD and AUR/b-CD inhibited colonic inflammation and also modulated proliferation, apoptosis and the expression of several proinflammatory cytokines, such as nuclear factor-kappaB, tumor necrosis factor-a, Stat3, NF-E2-related factor 2, interleukin (IL)-6 and IL-1b, which were induced in the adenocarcinomas. Our findings indicate that GOFA/b-CD and AUR/b-CD, especially GOFA/b-CD, are therefore able to inhibit colitis-related colon carcinogenesis by modulating inflammation, proliferation and the expression of proinflammatory cytokines in mice.There were $1 million new cases of colorectal cancer (CRC) in 2002 (9.4% of the total cancers). 1 Globally, the mortality of CRC was reported to be 655,000 deaths per year in 2005. 2 There is at least a 25-fold variation in the occurrence of CRC worldwide.1 The highest rates of incidence are in North America, Australia/New Zealand, Western Europe and Japan, especially in Japanese men.1 These large geographic differences for CRC are probably explained by differences in environmental exposures and lifestyles.There are several types of pathogenesis of CRC. 3 Among them, inflammation is linked with CRC development. 4 The risk of CRC in patients with inflammatory bowel disease inflammatory bowel disease; IL: interleukin; iNOS: inducible nitric oxide synthase; NF-jB: nuclear factor-kappaB; Nrf2: NF-E2-related factor 2; TdT: terminal deoxynucleotidyl transferase; Tnf: tumor necrosis factor;