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.
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.
21171 Background: Background: Axillary lymph node metastasis is the most significant marker for the pathologic staging of breast cancer. However a proportion of lymph node-negative breast cancer will develop metastatic disease. Therefore, molecular markers of invasion in these patients are needed Methods: We selected 10 primary breast cancer cases, 5 lymph node-negative (T1N0) and 4 lymph node-positive (T1N1). In these cases we searched for gene expression of 8 genes (bbc3, cegp1, fgf18, flt1, cffm4, gstm3, hec, tgfb3) selected from previous studies as a good candidates for metastasis prediction. A quantitative Real-Time PCR was performed using beta-2- microglobulin gene expression to normalized gene expression of each gene. The expression average of beta-2-microglobulin was 303,291 among T1N0 and 342,533 among T1N1 cases (ratio 0.88). The expression average of these 8 genes was 2.11 and 0.002 at T1N0 and T1N1 respectively (ratio 1,055). At least 3 genes were significantly down-regulated in T1N1 (bbc3, flt1, gstm3) in comparison with T1N1 breast carcinomas Results: Computational analysis reveals that these 3 genes (bbc3, flt1, gstm3) contain CpG islands in their promoter regions. Although preliminary data, we found group of genes that are down-regulated in T1N1 tumor Conclusions: The finding that these genes are epigenetically regulated, suggest that could be a good candidates for metastasis prediction, by methylation approach (MethyLight System). Since this down-regulation occurs in primary tumor, the analysis of these genes might be useful to predict metastasis in lymph node-negative breast cancer. No significant financial relationships to disclose.
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