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Molecular epidemiology of Burkitt's lymphoma from South America:
differences in breakpoint location and Epstein-Barr virus association from
tumors in other world regions
MI Gutierrez, K Bhatia, F Barriga, B Diez, FS Muriel, ML de Andreas, S Epelman, C Risueno and IT Magrath
Pediatric Branch, National Cancer Institute, NIH, Bethesda, MD 20892.
We have previously shown that the endemic (African) and sporadic (North
American) forms of Burkitt's lymphoma (BL) differ at a molecular level. We
have now extended our studies to the molecular epidemiology of BL in South
America, specifically to two climatic regions: temperate (Argentina and
Chile) and tropical (Brazil). We have examined the patterns of chromosomal
breakpoint locations in 39 tumors with respect to geography and
Epstein-Barr virus (EBV) association. The result of these analyses provide
further support for the existence of pathogenetically distinct subtypes of
BL in different world regions. The majority of breakpoints on chromosome 8
in South American BL (41%) occurred in the immediate flanking region of
c-myc, ie, further 5' of the "typical" sporadic breakpoints, in the first
exon/intron region, and further 3' of the "typical" endemic breakpoints,
which are usually distant from c-myc. However, the distribution of
breakpoints on chromosome 14 in tumors from the temperate and tropical
regions of South America is similar to that observed in sporadic and
endemic tumors. Interestingly, only one tumor with an unrearranged c-myc
gene joined to the S mu region of chromosome 14 was observed. This
combination was also rarely observed in our earlier series and presumably
is either less readily generated by the mechanism that mediates 8;14
translocation or requires other, infrequent genetic changes to provide the
necessary selective advantage for lymphomagenesis. The frequency of EBV
association in South American BL (51%) is also intermediate with respect to
tumors from the United States (30%) and Africa (100%). No correlation with
the breakpoint location on chromosome 8 was discernable. Surprisingly, only
54% of tumors with breakpoint outside c-myc were EBV positive. This is in
contrast to endemic tumors and suggests that any pathogenetic contribution
of EBV is not dependent on breakpoint location, but is more likely to
complement additional pathogenetic elements that differ in different world
regions.
Volume 79,
Issue 12,
pp. 3261-3266,
06/15/1992
Copyright © 1992 by The American Society of Hematology
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