| Grant number: | 09/11002-9 |
| Support Opportunities: | Scholarships in Brazil - Scientific Initiation |
| Start date: | October 01, 2009 |
| End date: | September 30, 2011 |
| Field of knowledge: | Biological Sciences - Immunology |
| Principal Investigator: | Gabriela Silva Bisson |
| Grantee: | Patricia Modiano |
| Host Institution: | Escola de Enfermagem de Ribeirão Preto (EERP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil |
Abstract Colon cancer is the second leading cause of cancer-related death in the Western World. Nowadays, only a few cases of colorectal cancer (CRC) are diagnosed in early stages and the available treatments are often not able to completely eradicate the tumor. The development of colon cancer is a slow process that has a natural history of transition from normal crypts through adenoma to overt adenocarcinoma occurring over an average of 10 to 20 years, thereby providing a great opportunity for prevention and intervention strategies. Evidence shows a reduction of morbidity and mortality associated with early detection of invasive lesions and precursor adenomatous polyps. Currently, most attention has focused on screening for chemopreventive agents to reduce the number of CRC patients. Contributing or preventing tumor growth, inflammation is an integral part of cancer biology. The most convincing examples of chronic inflammation-induced carcinogenesis are seen within the gastrointestinal tract, such as colon cancer arising in individuals with inflammatory diseases of the bowel. Currently, the human colorectal cancer represents a paradigm for the well-established connections between inflammation and cancer. Altered cellular glycosylations are common phenotypic changes observed in human malignancies. Similar changes in glycosylation occur in the colonic epithelium in colorectal cancer, in precancerous adenomatous polyps and in inflammatory conditions such as ulcerative colitis. They include, for example, increased expression of oncofetal carbohydrate antigens such as sialil-Tn, and the TF antigen. Lectins can interact with aberrant glycans expressed in tumor cells and thus can interfere with the biology of transformed cells, modifying cell proliferation, promoting cell death, as well as interfering with the process of invasion and metastatization. These molecules have been adopted in alternative therapies of tumors in several European countries. Jacalin is a non-cytotoxic lectin present in the seeds of Artocarpus integrifolia that specifically recognizes TF antigens and has anti-proliferative effects on human colon cancer cells. In the present work, using an animal model of colon carcinogenesis, we will study the effects of jacalin on the carcinogenic process, in order to evaluate its potential use as a colon cancer chemopreventive agent. (AU) | |
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