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Patterns of chromosomal breakpoint locations in Burkitt's lymphoma:
relevance to geography and Epstein-Barr virus association
B Shiramizu, F Barriga, J Neequaye, A Jafri, R Dalla-Favera, A Neri, M Guttierez, P Levine and I Magrath
Pediatric Branch, National Cancer Institute, Bethesda, MD 20892.
We have examined, by Southern blotting, the patterns of chromosomal
breakpoint locations in 55 cases of Burkitt's lymphoma (BL) with respect to
geography and Epstein-Barr virus (EBV) association. We have confirmed the
association between chromosome 8 breakpoint and geography: 74% of endemic
(eBL) but only 9% of sporadic BL (sBL) had breakpoints outside the HindIII
fragment encompassing the c-myc gene (P2 less than .00001). Conversely, not
only did 91% of sBL manifest a rearranged HindIII fragment, but at least
56% of these cases, in contrast to 17% of eBL cases, had a breakpoint
within the first exon or intron of c-myc (P2 less than .004). Breakpoints
outside the switch mu (S mu) region (ie, the HindIII fragment encompassing
S mu) on chromosome 14 were twice as common overall (73%) as those within S
mu (27%), but in the 15 tumors with S mu breakpoints, 13 (87%) had a
rearranged c-myc gene. Breakpoints outside the HindIII fragment
encompassing c-myc on chromosome 8 were predominantly associated with non-S
mu breakpoints on chromosome 14 (85%) and this was the combination most
frequently associated with eBL (65%; 6% of sBL, P2 less than .00001). In
sBL, the most frequent breakpoint combination was a rearranged c-myc gene
with a non-S mu breakpoint (63%; 13% of eBL). Twenty-eight percent of sBL
and 13% of eBL had breakpoints both within c-myc and within S mu. EBV DNA
was present in 19 of 20 tumors with breakpoints outside c-myc, in none of 7
with a breakpoint in the immediate 5' region of c-myc, in 4 of 5 tumors
with breakpoints in the first exon, and in 7 of 12 tumors with breakpoints
in the first intron. These data suggest that the pathogeneses of eBL and
sBL differ with regard to the mechanism of c-myc deregulation, and probably
also with regard to the state of differentiation of the target cell for
malignant transformation. We have formulated a testable hypothesis
regarding the potential role of EBV in pathogenesis: that it is required to
contribute to the deregulation of c-myc in the presence of some, but not
all, types of c-myc damage arising from the chromosomal translocations.
Volume 77,
Issue 7,
pp. 1516-1526,
04/01/1991
Copyright © 1991 by The American Society of Hematology
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