Views and Suppositions About Malarial Infections in Cancer Development and Progression

Burkitt lymphoma (BL) is an aggressive non-Hodgkin lymphoma. The prevalence of BL is ten-fold higher in areas with stable transmission of Plasmodium falciparum malaria, where it is the most common childhood cancer, and is referred to as endemic BL (eBL). In addition to its association with exposure to P. falciparum infection, eBL is strongly associated with Epstein-Barr virus (EBV) infection (>90%). This is in contrast to BL as it occurs outside P. falciparum-endemic areas (sporadic BL), where only a minority of the tumors are EBV-positive. Although the striking geographical overlap in the distribution of eBL and P. falciparum was noted shortly after the first detailed description of eBL in 1958, the molecular details of the interaction between malaria and eBL remain unresolved. It is furthermore unexplained why exposure to P. falciparum appears to be essentially a prerequisite to the development of eBL, whereas other types of malaria parasites that infect humans have no impact. 1 Researchers have found that the damage to DNA caused by malaria parasite in cells increases the risk of those cells turning into cancerous cells. Burkitt's lymphoma – a B cell cancer – has previously been epidemiologically linked with malaria endemic areas. Burkitt lymphoma (BL) was first described by Denis Burkitt in the 1950s. While working in Uganda, he observed numerous children with large jaw tumors (usually observed in endemic BL), subsequently noting that the geographical distribution of these tumors tended to correspond to that of malaria. BL has been associated with Epstein-Barr virus (EBV) infection; however, given that EBV is found ubiquitously, EBV infection alone does not explain the burden of BL in Africa but rather, is hypothesized to act as a co-factor for BL along with malaria infection. 2   In our article we try to find the correlation between plasmodium falciparum infection and rising rate of endemic Burkitt lymphoma in African countries from the point of view of karyogamic theory.

 On the basis of experimental data and information in the literature, one possible basis for the initial tumor cell is a hybrid originated by means of the fusion of two normal somatic cells, there can be created perforations of the plasma membrane. Pores of some definite sizes can lead to the fusion of cells. In the first stage of carcinogenesis(initiation), as a result of a fusion of nuclei, a so-called precancerous sinkaryons with a tetraploid set of chromosomes may be created. Such types of cells can exist in the tissue for a long time. At the stage of promotion they can be transformed into full tumor cells under any perfect carcinogens or promoters. 3