Scientists have uncovered how infection with a malaria-causing parasite can increase the chances of immune cells developing into cancer cells.

The way that malaria increases the risk of a type of blood cancer is called Burkitt’s lymphoma. It has remained a mystery for more than 50 years.

Researchers found that the DNA of a type of immune cell known as B lymphocyte became vulnerable to cancer-causing faults when exposed to long-term infection with the malaria-causing parasite.

The research was carried out in mice. Therefore the findings don’t necessarily mean the same thing occurs when malaria infects humans. However, the mice experiments closely mimic some of the key features of Burkitt’s lymphoma, so the results are informative.

The B lymphocytes multiplied extensively and continued to produce a protein called AID during prolonged immune responses to malaria.

AID generally changes the DNA code of antibody genes to promote shuffling of DNA. This is a crucial process that helps in the production of a variety of antibodies which are necessary to fight the infection.

Researchers found that in the case of malaria-infected B cells cause DNA rearrangements in other genes including those involved in the development of cancer.

However, researchers found that Burkitt’s lymphoma only developed in the mice’s immune cells when they lacked a second protein, called p53. The mice were chosen specifically because they lacked the key gene called p53. 

Cases of Burkitt’s lymphoma are also linked to infection with a virus called the Epstein-Barr virus.

Although chronic malaria and Epstein-Barr virus infections together increase the likelihood of developing Burkitt’s lymphoma, there are a variety of other factors involved.

Researchers stress that these findings should be viewed alongside other studies to get a clearer picture of how the disease develops.

More research is necessary in order to determine the sequence of events in humans is the disease develops.

Read the source article here.


Gerry Oginski
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