Burkitt lymphoma (BL) is a rare aggressive form of B-cell non-Hodgkin lymphoma that accounts for 30-50% of lymphomas in children and 1-2% of lymphomas in adults. BL incidence peak occurs once throughout childhood/adolescence and once following the age of 40 years. A Male preponderance is observed in BL cases. HIV patients with a history of ineffective antiviral treatment are also known to have high susceptibility of contracting BL. It exists in two forms: the endemic form that is linked to the Epstein Barr virus (EBV) occurring in the form of maxillary tumor and sporadic form that mostly develops in the abdomen. The disorder can develop in the ear, nose, and throat and rarely in other locations including orbit, kidney, or bone. The main clinical features include abdominal pain, nausea, tumors and modification of general and/or the presentation of lymph nodes. BL is diagnosed through biopsy of a mass, an effusion puncture or bone marrow which uncovers the occurrence of tumor cells. Meanwhile, the size of the tumor can be revealed through employing images including ultrasound and scanning. BL can be managed through professional oncology/hematology centres, while treatment includes few months of intensive chemotherapy.
Burkitt lymphoma originates from chromosomal translocations which involve the MYC gene and either the lambda or kappa light chain immunoglobulin genes. MYC gene consists of 439 amino acids and has a molecular weight of 48,804 kDa. BL is also linked to the Epstein-Barr virus (EBV) as it influences the genesis of the endemic form of BL, although the responsible pathogenetic mechanisms are still vague. Nearly in all cases, BL is correlated with a particular translocation t(8;14)(q24;q32) that juxtaposes the MYC gene (8q24) next to the heavy chain immunoglobulin gene (14q32). In rare cases, the translocation influences either kappa chain in immunoglobulins (chromosome 2) or lambda chain in immunoglobulins (chromosome 22). The tumors' proliferation index is tremendously high (Ki67 > 95%).