In equatorial Africa, a region of the globe is known as the “lymphoma belt”. Here the children are 10 times more likely than in other parts of the world to develop Burkitt’s lymphoma, a highly aggressive blood cancer that can be fatal if left untreated.
That area is also plagued by high rates of malaria.
And now after more than 5 decades of research, scientists in New York have uncovered children infected with malaria might experience DNA damage that can lead to Burkitt’s lymphoma, a highly aggressive blood cancer.
"The body needs this enzyme in order to produce potent antibodies to fight malaria. But in the process, the enzyme can cause substantial collateral damage to the cells that produce it, and that can lead to lymphoma."Davide Robbiani, Co-author, Rockefeller University, New York
In the study, the researchers infected mice with a form of the parasite that causes malaria. They immediately noticed that the mice experienced a huge increase in white blood cells that can give rise to Burkitt’s lymphoma.
As these cells rapidly proliferate, they also express high levels of an enzyme known as activation-induced cytidine deaminase (AID), which damages the DNA.
As a result, these cells can diversify to generate a wide range of antibodies.
But in addition to beneficial mutations in antibody genes, said Robbiani, AID can cause “off-target” damage and shuffling of cancer-causing genes.
Next, the researchers bred mice lacking the p53 gene, which is known to protect cells from many types of cancer, including Burkitt’s lymphoma.
This finding sheds new light on a long-standing mystery of why two seemingly different diseases are associated with each other. Scientists are now working on limiting the collateral damage to cancer-causing genes without reducing the infection-fighting powers of cells.
The research has been published in medical journal Cell.
(With inputs from PTI)