Effects of chronic exposure to norepinephrine and tobacco-derived carcinogen NNK o...
| Grant number: | 09/12046-0 |
| Support Opportunities: | Regular Research Grants |
| Start date: | December 01, 2009 |
| End date: | May 31, 2012 |
| Field of knowledge: | Biological Sciences - Immunology |
| Principal Investigator: | Gabriela Silva Bisson |
| Grantee: | Gabriela Silva Bisson |
| 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. Tumors are composed, besides the tumoral cells, of a wide population of leukocytes and other types of immune cells infiltrate to the developing tumor site and establish the tumor inflammatory microenvironment. Reciprocal interactions between neoplastic cells and their surrounding microenvironment are determining factors in tumor progression. The presence of a well defined inflammatory infiltrate is evident even in pre-neoplastic conditions. Inflammation can foster or inhibit cancer growth, depending on the composition of infiltrating cell populations, the context and the stage of tumor development. CRC represents a paradigm for the well-established connections between inflammation and cancer. Altered cellular glycosylations are common phenotypic changes observed in human malignant neoplasias. 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 carbohydrate antigens such as 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 in colon cancer chemoprevention and treatment. (AU)
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