According to a recent JAMA Study (1) exam...
Virus, Bacteria and Cancer Oh My!
Jan 31, 2019
Many people ask: “what causes cancer”? Is it genetic, is it environmental, is it something I did? The answer to this question is that “getting cancer” can be for any of these reasons. Some cancers may arise because of a genetic mutation as you age, or because you inherited a gene that causes it. Others may occur because of smoking, lack of exercise, obesity, hormones, chronic inflammation, or being exposed to cancer causing chemicals. A percentage of cancer comes to rise because of viruses and bacteria that you can be exposed to in the environment.
Currently people are more aware of cancers caused by certain types of viruses such as papillomavirus that causes cervical cancer, and hepatitis virus that causes liver cancer, and Epstein-Barr virus that causes Burkitt’s lymphoma. For years scientist thought that viruses played a role in the development of maybe 10 to 20 percent of cancers. Findings published in the Journal of Virology in August of 2013 challenges this previous thought, suggesting this percentage may actually be as high at 40 percent of cancers are caused by viruses. Once virus-cancer correlations are made, scientist lead campaigns to making vaccines against such viruses to reduce the cancer burden. These types of campaigns have led to new available vaccines such at the HPV vaccine for the human-papillomavirus which will hopeful add in reducing the incidence of cervical cancer.
Bacteria have also been linked and are thought to be more significant in causing cancer by two mechanisms: induction of chronic inflammation and production of carcinogenic bacterial metabolites. A fifth of all cancers are caused by microbial infections such as: Helicobacter pylori can cause stomach cancer, Salmonella typhi has been associated with the development of gallbladder cancer, and Chlamydia trachomatis can cause cervical cancer. Even more interesting is that bacterial proteins can encourage cancer development by potentially inducing carcinogenesis, chronic infection, immune evasion and immune suppression. For example, in a mouse model it was shown that in mice infected with mycoplasma, DnaK, a chaperone protein for other proteins protecting them from damage or helping them to fold- reduces the activity of important cellular proteins involved in DNA repair and anticancer activities, such as p53. Thus, cells infected with mycoplasma would not be able to properly repair damaged DNA, theoretically increasing the risk for cancer development.
There are so many factors that affect the propensity of developing cancer. Finding a single “off-switch” is not as easy as we would all hope. As new information is learned about the interactions of cells in their microenvironment and the effects of viruses and bacteria are further understood, scientist can learn new ways to aid the immune system, and other cell types in combating cancer.