Infectious agents and cancer
10.29.09 by Sharmila Pejawar-Gaddy
Several cancers have been attributed to infectious agents. It is estimated that approximately 18% of all cancers worldwide are caused by infectious agents. 26% of these are in developing countries and 8% in developed countries. These figures and discrepancies between the developed and developing worlds point to differences in disease prevalence, either due to sanitary conditions or shortage of vaccines. Infectious agents can be classified as indirect or direct carcinogens. Indirect carcinogenic agents are those that cause chronic infection and thus chronic inflammation, which then leads to the advent of cancer. Examples of these include, Helicobacter pylori infection that is the an attributing factor to a majority of stomach/gastric cancers, as well as chronic hepatitis B and C infections that are causally linked to a majority of liver cancers. On the other hand, direct carcinogenic agents are those that can incorporate oncogenes into the cell’s genome. Examples of these are human papillomavirus that causes a majority of cervical cancers, as well as in some cases, penile cancer, vaginal cancer and genital warts; Epstein-Barr virus linked to a majority of Naso-pharengeal carcinomas and human herpes virus-8 linked to Kaposi’s sarcoma. This list grows every day. The good news is this: most of these infections, and thus the advent of several cancers, can be prevented by vaccination.
Adapted from Parkin, DM. 2006. Int J Cancer. 118:3030 and Dr. Douglas Lowy
Related articles
- Parkin, DM. 2006. The global health burden of infection-associated cancers in the year 2002. Int J Cancer. 118:3030.
- Campbell, K. 2006. The infectious causes of cancer. Nurs Times. 102(33):28.
- FDA approves Gardasil to prevent genital warts in boys (ctv.ca)
- FDA Approves Merck’s Gardasil for Boys (abcnews.go.com)
The Future of Brain Tumor Therapy
06.14.09 by Daniel Gaddy
A little over a year ago, the announcement that Senator Ted Kennedy was diagnosed with a malignant brain tumor brought a lot of attention to brain cancer research. Brain cancers are among the most perplexing types of cancers. Indeed, until now, it was not even known how brain cancers form. It was believed for many years that brain tumor metastasis, or the process whereby cancerous cells move from the location where a tumor has initially grown and spreads to other parts of the body, was the product of “brain-specific homing” of metastatic cancer cells from other areas of the body, followed by direct interactions of the cancer cells with neural tissues. However, recent research from Oxford University, published in the journal PLOS One, demonstrated that metastatic cancer cells in mouse and human tissue utilized “vascular cooption” for seeding brain tumors rather than invading and growing within the neural tissue. What this means is that cancer cells enter blood vessels, where they can then be transported throughout the body. This information is not new. What the Oxford researchers, led by Professor Ruth Muschel, showed is that once in the blood vessels, cancer cells can establish residence and begin to grow along the blood vessel walls. By thus co-opting blood vessels in the brain, tumors can utilize readily available nutrients and oxygen from the blood without having to grow their own blood vessels, which occurs via processes known as neovascularization and angiogenesis.
Cancer vaccines: a brief introduction
05.8.09 by Sharmila Pejawar-Gaddy
From the time of the first documented vaccine against smallpox by Edward Jenner, developing an effective vaccine to prevent deadly disease caused by existing or newly emerging pathogens has been the goal of many microbiologists and immunologists. With a single exception, that of the rabies vaccine, all vaccines developed previously have been prophylactic, meaning that they are administered in order to prevent the onset of disease. The concept of a vaccine has slowly evolved to currently include a therapeutic vaccine, meant to ameliorate an existing disease state by potentially strengthening an ongoing but not fully effective immune response against a pathogen. Further broadening of the concept of a vaccine has come about with the realization that in addition to eliciting an immune response where there was none, a vaccine could also be designed to change an existing immune response from one type to another. Most recently, vaccines are being considered not only for elicitation of immunity but also potentially for induction of tolerance [1, 2]. This concept has also increased potential targets of vaccines from diseases caused by pathogens to any disease that involves the immune system, such as cancer, autoimmunity and graft rejection. [3-6].
Challenges facing cancer vaccines
Choosing the right antigen and adjuvant are the sine qua non of an effective vaccine.
The “right” antigen: Antigens used in cancer vaccines should preferably be molecules that are different between normal cells and tumor cells ensuring that the immune response generated by vaccination will target for destruction antigen-bearing tumor cells and not normal cells [7, 8]. This requirement is satisfied more easily in the case of vaccines against pathogens because their antigens are all foreign to the host and thus immunity generated against them, in most instances, does not cross-react with normal host tissues. In cancer, most antigens are derived from mutated or modified self-proteins against which there is often a certain level of immune tolerance. This creates particular challenges for the appropriate design of vaccines that have to overcome this tolerance in order to elicit anti-tumor immunity without autoimmunity [9].
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