Important note: Information in this article was accurate in 1990. The state of the art may have changed since the publication date.
THE MOLECULAR GENETICS OF B-CELL MALIGNANCIES CARRYING T(8;14) CHROMOSOMAL TRANSLOCATIONS
Diss Abstr Int [B]; 50(7):2766 1990. Unique Identifier : AIDSLINE ICDB/90662262 Haluska FG; Univ. of Pennsylvania
Abstract:
The reciprocal chromosome translocation t(8;14), involving the heavy chain locus on chromosome 14 and the c-myc oncogene on chromosome 8 is a characteristic of the B-cell malignancies Burkitt lymphoma, AIDS-associated non-Hodgkin lymphoma (NHL), and acute lymphoblastic leukemia (ALL). Previous molecular analyses of these tumors indicated that a dichotomy exists in the molecular structure of the translocated chromosomes in sporadic and endemic Burkitt lymphomas. The present work utilizes the techniques of molecular cloning and DNA nucleotide sequence analysis to examine the molecular structure of the t(8;14) translocation of one case of ALL, two endemic Burkitt lymphomas, a sporadic case of Burkitt lymphoma, and an AIDS-associated NHL. It is demonstrated that some ALLs and endemic Burkitt lymphomas carry t(8;14) translocations which strongly suggest that the immunoglobulin recombinase enzymes aberrantly function to translocate chromosomes. The translocation junctions were cloned and sequenced. The architecture of the translocations demonstrates (1) breakage of chromosome 8 far 5' of c-myc; (2) breakage of chromosome 14 at J(H) segments; (3) the presence of conserved heptamer-nonamer sequences at the translocation breakpoints; (4) N regions at the breakpoints. These features are consonant with the operation of the immunoglobulin recombinase enzymes. A t(8;14) from a sporadic Burkitt lymphoma with a breakpoint in the region involved in the endemic Burkitt lymphomas was also examined. Despite the location of the breakpoint, the mechanism of translocation in this case implicates the isotype switching process. Taken together with the data from the ALL and endemic Burkitt lymphoma cases, these data suggest that the translocation mechanism correlates with the endemic versus sporadic phenotype of the Burkitt lymphoma. Finally, the t(8;14) translocation from an Epstein-Barr virus-positive AIDS-associated undifferentiated NHL is cloned and sequenced. The features of the translocation junction are shown to be similar to those from endemic cases. Thus it is suggested that the pathogenesis of EBV-positive AIDS-associated Burkitt lymphomas shares essential features with the pathogenesis of endemic Burkitt lymphomas. (Full text available from University Microfilms International, Ann Arbor, MI, as Order No. AAD89-22512)
Keywords: Acquired Immunodeficiency Syndrome/COMPLICATIONS/*GENETICS Burkitt's Lymphoma/*GENETICS Chromosomes, Human, Pair 14 Chromosomes, Human, Pair 8 Genetic Markers Human Leukemia, B-Cell, Acute/*GENETICS Lymphoma, Non-Hodgkin's/COMPLICATIONS/*GENETICS Proto-Oncogenes *Translocation (Genetics) THESIS 900630
M9060636
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Important note: Information in this article was accurate in 1990. The state of the art may have changed since the publication date.
