Colonorectal cancer is a major health problem across the globe. Its occurrence is highest in the developed countries in North America and Europe. It is considered as the second most common cause of death from neoplasma. Only in 2008 1.23 million new cases were reported and 608 000 deaths due to the disease. At the end of August a new study suggesting an association Fusobacterium of the oral cavity and the occurence of colorectal cancer was published. Intestinal bacteria inhabiting in the oral cavity may have an impact on the immune response and activation of supresor genes. The research team hopes to further research in order to establish quicker and simpler methods of diagnosis, prevention and treatment of colorectal cancer.
Our body hosts trillions of bacteria, mostly in the digestive system. Symbiotic bacteria such as Escherichia coli ensure the health and equilibrium of the body, competing with pathogenic bacteria. As it turns out, not only a disturbed the balance between symbiotic and pathogenic intestinal bacteria may promote the occurrence of colon cancer, but also a single type of bacteria may be a trouble-making trigger.
Research published in JournalCell Host & Microbe pay particular attention to the bacterium called Fusobacterium nucleatum, described by periodontists as a member of the so-called ‘orange group’ of bacteria often detected in the oral cavity accompanying periodontal diseases.
Colorectal cancer causes 655 000 deaths per year. In America it is known to be the second most common cause of death from cancer. Researchers have found that Fusobacterium nucleatum abundant in the oral cavity is also present in tissues of people who suffer from colon cancer. The link between the presence of micro-organisms and the occurrence of intestinal tumors has become more apparent, but the manner in which the bacteria would be involved in this process remained unclear.
There have been numerous studies on the topic – the researchers found the presence of Fusobacterium in benign lesions, that may develop into cancer over time. This suggests that they may contribute to tumor formation in the early stage of the disease. Studies conducted on laboratory rodents with induced colon cancer proved an accelerated development of cancer in the presence of bacteria. They induced taxis on myeloid cells penetrating deep into the lesions causing inflammation, leading to a rapid formation of cancer. Another study identified Fusobacterium adhesin ( FadA ), which bacteria use to increase adhesion and facilitate tumor cell invasion. This leads to inflammation and tumor formation. In healthy tissues the FadA content contain is considerably lower, than in patients suffering from colorectal cancer.
Fortunatelly a compound that can stop the action FadA against tumor cells has been identified as well. FadA binds to E-cadherin, activates β-catenin signaling, and regulates the inflammatory and oncogenic responses. The FadA-binding site on E-cadherin is mapped to an 11-amino-acid region. A synthetic peptide derived from this region of E-cadherin abolishes FadA-induced colonorectal cancer cell growth and oncogenic and inflammatory responses.
The studies suggest that FadA may be a marker useful in detecting colorectal cancer, allowing early treatment and prevention of this severe disease.
Written by: Maria Bilińska
Source:
1.http://en.wikipedia.org/wiki/Colorectal_cancer
2.”Fusobacterium nucleatum Potentiates Intestinal Tumorigenesis and Modulates the Tumor-Immune Microenvironment”; Aleksandar D. Kostic, Eunyoung Chun, Lauren Robertson, Jonathan N. Glickman, Carey Ann Gallini, Monia Michaud, Thomas E. Clancy, Daniel C. Chung, Paul Lochhead, Georgina L. Hold, and others; Cell Host & Microbe 14(2) pp. 207 – 215 published online 14 August 2013; DOI: 10.1016/j.chom.2013.07.007
3.”Fusobacterium nucleatum Promotes Colorectal Carcinogenesis by Modulating E-Cadherin/β-Catenin Signaling via its FadA Adhesin”; Mara Roxana Rubinstein, Xiaowei Wang, Wendy Liu, Yujun Hao, Guifang Cai, Yiping W. Han; Cell Host & Microbe 14(2) pp. 195 – 206 published online 14 August 2013; DOI: 10.1016/j.chom.2013.07.012;
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