scholarly journals BURKITT’S LYMPHOMA IN KIDNEY: A RARE ENTITY.

2021 ◽  
Vol 5 (4) ◽  
Author(s):  
Muhammad Mohsin Riaz ◽  
Arous Khaqan ◽  
Omer Sabir

Burkitt’s Lymphoma is an aggressive form of Non-Hodgkin’s Lymphoma, with higher incidence in children comprising 30% of pediatric lymphoma. The hallmark of which is a translocation involving c-MYC gene on chromosome 8. Burkitt’s Lymphoma comprises of 6.35% of all lymphoma cases in Pakistan, with male predominance. Lymphoma rarely presents as a primary pathology of acute kidney injury. Burkitt’s lymphoma in adult population is uncommon and few cases have been reported where Burkitt’s lymphoma presents as a cause of acute kidney injury. There are three epidemiological subtypes Endemic (African), sporadic (non-endemic) and immunodeficiency related. Sporadic cases dominate amongst others in Pakistan.

1987 ◽  
Vol 7 (6) ◽  
pp. 2037-2045
Author(s):  
P Hartl ◽  
M Lipp

We analyzed the Burkitt's lymphoma line BL64 in which a reciprocal translocation joins the immunoglobulin kappa light-chain locus on chromosome 2 to the c-myc gene on chromosome 8. The breakpoints on the two marker chromosomes 8+ and 2p- occurred 5' of the Js segment within the conserved nonamer and heptamer recombination sequences. Both signals were detected directly adjacent to the breakpoints in sequences of chromosome 8 suggesting that the translocation in BL64 was catalyzed by enzymes normally involved in V-J recombination. The distance between the c-myc gene and the breakpoint in J kappa amounts to at least 90 kilobases on the DNA level. In one allele of the c-myc gene somatic mutations were found in the promoter-leader region. This allele is transcribed and is supposed to be involved in the translocation. The half-life of the c-myc-specific mRNA in BL64 cells is not prolonged in comparison to the normal c-myc message. These results suggest that in Burkitt's lymphoma the translocation occurs during an early stage of B-cell differentiation and that in the variant translocations mechanisms other than a prolonged half-life, such as changes in transcriptional rates, or other posttranscriptional RNA processing contribute to the high steady-state level of c-myc RNA in the cytoplasm.


2016 ◽  
pp. bcr2016214780 ◽  
Author(s):  
Eva ter Haar ◽  
Veerle Labarque ◽  
Thomas Tousseyn ◽  
Djalila Mekahli

Blood ◽  
1991 ◽  
Vol 77 (7) ◽  
pp. 1516-1526 ◽  
Author(s):  
B Shiramizu ◽  
F Barriga ◽  
J Neequaye ◽  
A Jafri ◽  
R Dalla-Favera ◽  
...  

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.


1987 ◽  
Vol 7 (6) ◽  
pp. 2037-2045 ◽  
Author(s):  
P Hartl ◽  
M Lipp

We analyzed the Burkitt's lymphoma line BL64 in which a reciprocal translocation joins the immunoglobulin kappa light-chain locus on chromosome 2 to the c-myc gene on chromosome 8. The breakpoints on the two marker chromosomes 8+ and 2p- occurred 5' of the Js segment within the conserved nonamer and heptamer recombination sequences. Both signals were detected directly adjacent to the breakpoints in sequences of chromosome 8 suggesting that the translocation in BL64 was catalyzed by enzymes normally involved in V-J recombination. The distance between the c-myc gene and the breakpoint in J kappa amounts to at least 90 kilobases on the DNA level. In one allele of the c-myc gene somatic mutations were found in the promoter-leader region. This allele is transcribed and is supposed to be involved in the translocation. The half-life of the c-myc-specific mRNA in BL64 cells is not prolonged in comparison to the normal c-myc message. These results suggest that in Burkitt's lymphoma the translocation occurs during an early stage of B-cell differentiation and that in the variant translocations mechanisms other than a prolonged half-life, such as changes in transcriptional rates, or other posttranscriptional RNA processing contribute to the high steady-state level of c-myc RNA in the cytoplasm.


1990 ◽  
Vol 10 (4) ◽  
pp. 1835-1839 ◽  
Author(s):  
E Shtivelman ◽  
J M Bishop

We have previously described a transcription unit on human chromosome 8, designated as PVT, that is consistently disrupted by the minority forms of translocations [t(2;8) and t(8;22)] in Burkitt's lymphoma. PVT begins 57 kilobase pairs downstream of the proto-oncogene MYC and is more than 200 kilobase pairs in length. In order to explore the pathogenic impact of translocations affecting PVT, we have characterized further the structure and transcription of the locus. In normal cells, PVT is transcribed into a variety of RNAs, the diversity of which remains unexplained. Alleles of PVT affected by translocations give rise to additional RNAs. These RNAs arise from a fusion of the first exon of PVT on chromosome 8 to the constant region of an immunoglobulin light chain on either chromosome 2 or chromosome 22. We have found no evidence that any of the normal or abnormal transcripts of PVT give rise to a protein. Our results suggest that the pathogenic effects of the variant translocations in Burkitt's lymphoma are not executed by a gene situated in a vicinity of the chromosomal breakpoints. Instead, our data leave open the possibility that the effects of the translocations may be mediated by activation of the relatively distant MYC gene.


Blood ◽  
1991 ◽  
Vol 77 (7) ◽  
pp. 1516-1526 ◽  
Author(s):  
B Shiramizu ◽  
F Barriga ◽  
J Neequaye ◽  
A Jafri ◽  
R Dalla-Favera ◽  
...  

Abstract 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.


1990 ◽  
Vol 10 (4) ◽  
pp. 1835-1839
Author(s):  
E Shtivelman ◽  
J M Bishop

We have previously described a transcription unit on human chromosome 8, designated as PVT, that is consistently disrupted by the minority forms of translocations [t(2;8) and t(8;22)] in Burkitt's lymphoma. PVT begins 57 kilobase pairs downstream of the proto-oncogene MYC and is more than 200 kilobase pairs in length. In order to explore the pathogenic impact of translocations affecting PVT, we have characterized further the structure and transcription of the locus. In normal cells, PVT is transcribed into a variety of RNAs, the diversity of which remains unexplained. Alleles of PVT affected by translocations give rise to additional RNAs. These RNAs arise from a fusion of the first exon of PVT on chromosome 8 to the constant region of an immunoglobulin light chain on either chromosome 2 or chromosome 22. We have found no evidence that any of the normal or abnormal transcripts of PVT give rise to a protein. Our results suggest that the pathogenic effects of the variant translocations in Burkitt's lymphoma are not executed by a gene situated in a vicinity of the chromosomal breakpoints. Instead, our data leave open the possibility that the effects of the translocations may be mediated by activation of the relatively distant MYC gene.


Blood ◽  
1990 ◽  
Vol 75 (9) ◽  
pp. 1848-1852 ◽  
Author(s):  
B Shiramizu ◽  
I Magrath

Abstract Translocations involving chromosomes 8 and 14 in Burkitt's lymphoma (BL) often involve the switch mu (Smu) region on chromosome 14, which contains multiple repeats. This has enabled us to use the polymerase chain reaction (PCR) to detect breakpoints that involve this region on chromosome 14 and the c-myc gene on chromosome 8. Using pairs of flanking primers, each pair including one annealing to repeat sequences within the switch region and one of three primers from the c-myc region (first intron, 3′, or 5′ flanking sequence of the first exon of c-myc), we have been able to amplify DNA fragments containing the corresponding breakpoint regions from chromosome 14 in both cell lines and biopsied tumor samples. The definitive demonstration of sequences from both chromosomes in these fragments permitted the confirmation of the presence of a translocation. Because of the sensitivity of PCR, we were able to localize breakpoints in samples containing as few as 1 neoplastic cell in 10(8) cells. PCR provides a valuable tool for the detection of 8;14 chromosomal translocations, which should prove to be of value in diagnosis and molecular epidemiologic studies, as well as providing a means of detecting minimal disease.


Blood ◽  
1990 ◽  
Vol 75 (9) ◽  
pp. 1848-1852 ◽  
Author(s):  
B Shiramizu ◽  
I Magrath

Translocations involving chromosomes 8 and 14 in Burkitt's lymphoma (BL) often involve the switch mu (Smu) region on chromosome 14, which contains multiple repeats. This has enabled us to use the polymerase chain reaction (PCR) to detect breakpoints that involve this region on chromosome 14 and the c-myc gene on chromosome 8. Using pairs of flanking primers, each pair including one annealing to repeat sequences within the switch region and one of three primers from the c-myc region (first intron, 3′, or 5′ flanking sequence of the first exon of c-myc), we have been able to amplify DNA fragments containing the corresponding breakpoint regions from chromosome 14 in both cell lines and biopsied tumor samples. The definitive demonstration of sequences from both chromosomes in these fragments permitted the confirmation of the presence of a translocation. Because of the sensitivity of PCR, we were able to localize breakpoints in samples containing as few as 1 neoplastic cell in 10(8) cells. PCR provides a valuable tool for the detection of 8;14 chromosomal translocations, which should prove to be of value in diagnosis and molecular epidemiologic studies, as well as providing a means of detecting minimal disease.


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