Seventy-eight patients with Burkitt's lymphoma and seventy controls from Ghana were typed for HLA-A, B, C and DR antigens, to determine whether there is an association between the HLA system and Burkitt's lymphoma.
A pilot study is reported of HLA-A, B, and C antigens in 141 East African Blacks comprising patients with Burkitt's lymphoma or nasopharyngeal carcinoma, either with active disease or in long-term remission, together with comparable controls.
It is possible that the expression of malignancy in Burkitt lymphoma is caused by immunoglobulin V region gene translocation resulting in activation of a gene on the long arm of human chromosome 8.
We have determined the sequence of the normal human c-myc gene and compared it to portions of a c-myc gene that has been translocated into the immunoglobulin heavy chain locus in a Burkitt lymphoma cell.
The breakpoint on human chromosome 8 may therefore also differ in different Burkitt lymphoma cell lines, because we have observed DNA rearrangement of the c-myc gene with the C(mu) gene in only some of the Burkitt lymphoma cell lines studied elsewhere.
Recombinant DNA clones have been used to directly demonstrate that the Burkitt lymphoma cell line Raji, t(8;14) (q24;q32), has a rearranged copy of the c-myc gene adjacent to the gamma 1 constant region gene of the human immunoglobulin heavy-chain locus; the genes are arranged in the opposite direction for transcription.
These results support a model in which c-myc oncogene activation in Burkitt's lymphoma occurs by disruption of a normal transcriptional control mechanism in which the c-myc protein is itself involved.
Our present data fit into the concept that in all Burkitt lymphoma lines investigated so far, including cases with t(8;14) and the variant translocations t(2;8) and t(8;22), the c-myc gene becomes situated at the 5' side of an immunoglobulin constant gene.
The translocated c-myc gene in AW-Ramos, a Burkitt lymphoma cell line carrying the 8;14 translocation, is expressed at 2- to 5-fold higher levels than c-myc in lymphoblastoid cell lines.
If similar enhancers exist in humans they may lead to increased transcription of the translocated c-myc gene and thus contribute to oncogenesis in Burkitt lymphoma.
In particular, the c-myc gene is translocated in Burkitt's lymphoma and is amplified in the human promyelocytic leukaemia cell line, HL-60, which contains double minute chromosomes (DMs).
We have characterized a variant Burkitt lymphoma in which translocation joins the immunoglobulin kappa locus on chromosome 2 to the c-myc gene on chromosome 8.
We have cloned and sequenced the translocated c-myc gene from the Burkitt's lymphoma CA46 cell line that carries a reciprocal translocation between chromosomes 8 and 14.
BL67 and BL18 are Burkitt's lymphoma cell lines with t(8;14) translocations (the breakpoint is in the first exon and first intron, respectively) in which the mu-heavy chain switch region is fused to the c-myc gene in head to head orientation.