Abstract
The genesis of Burkitt's lymphoma is visualized as proceeding in three steps: I. Primary EBV infection affects the young child, probably at a relatively high multiplicity. It immortalizes a certain number of B-lymphocytes in vivo. II. This is followed by the impact of an environmental promoting agent, perhaps chronic holoendemic malaria, providing a chronic stimulus to the proliferation of the EBV-carrying preneoplastic cells. III. Chromosomally abnormal variants appear in the stimulated tissue by chance. After certain types of changes, particularly the 8 to 14 translocation that leads to the 14q + marker, the affected B lymphocyte would no longer obey the negative feedback controls that would otherwise restrict its proliferation in vivo.
Original language | English |
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Pages (from-to) | 25-36 |
Number of pages | 12 |
Journal | Haematologia |
Volume | 12 |
Issue number | 1-4 |
State | Published - 1978 |
Externally published | Yes |