How Infections Can Trigger Cancer in the Body

According to a recent article published in the Proceedings of the National Academy of Sciences of the United States of America, some infections and bacteria can implicate, transform, and even trigger cancers in the human body.

This article, published in December of 2018, provides evidence that a strain of mycoplasma (called DnaK, which we’ll dive into more in a moment) triggered and promoted the growth and development of a lymphoma in a vivo mouse model. The researchers and scientist behind this study introduced a bacterial chaperone protein known as DnaK into a vivo mouse model and observed a transformation process that grew resistant to anticancer drugs.

The theory behind this resistance?

The DnaK transformed and interfering with vital pathways that controlled both DNA-damage control and repair as well as apoptosis (the death of cells that occurs as a normal part of an organism’s development).

The idea within this study is that bacteria and infection can become so involved in the cellular transformation process that it can actually become resistant to anti-cancer drugs. The method by which researchers believe this is possible can be compared to a hit-and-hide or a hit-and-run process.

Overall, within this study, researchers believe they found significant evidence to support the idea that DnaK was taken up by the uninfected cells and was impaired to the point of affecting critical cellular functions. This resulted in a significant effect on the control of cell growth as well as the control of uninfected cells.

How Exactly Do Infections Trigger Cancer?

According to this study, about 20 percent of human cancers are caused by recognized, known infection agents. Some of these cancers will transform cells directly, like leukemia virus-1 or HPV, however, others will encode genes that will transform and interfere with cellular regulation mechanisms, while others still will affect the cell’s microenvironment in order to affect and alter the cell.

In this study, researchers found supporting evidence to back the concept that bacteria and infections can translocate proteins into cells by attaching to the outside of the membrane or invade the cell directly.

Acknowledging this experiment and published study, and basing findings off the recorded data, it’s hypothesized that the bacterial DnaK protein presence works in two ways. For starters, it interacts with the function of cellular proteins in a negative way, interfering with the critical proteins that are necessary for an effective DNA repair, ultimately leading (in theory) to an accumulation of DNA damage. Additionally, it’s hypothesized that at the same time, the bacterial DnaK protein’s presence is reducing the activity of anti-cancer medications, thereby preventing anti-cancer effectiveness.

Why Is this Study (and the Results) Relevant?

These hypotheses are relevant for several clinical reasons. For starters, it’s vital to recognize that a plethora of human cancers will arise due to certain events or happenings that lead to a flaw in DNA repair process, and, according to this study, this was prevalent with the presence of specific infections like DnaK proteins. Secondly, this could imply that the basics of cancer are more heavily revolved around bacteria and infections that initially considered – this would result in a change in approach to how we deal with cancers.