scholarly journals Multiple proto-oncogene activations in avian leukosis virus-induced lymphomas: evidence for stage-specific events.

1989 ◽  
Vol 9 (6) ◽  
pp. 2657-2664 ◽  
Author(s):  
B E Clurman ◽  
W S Hayward
Keyword(s):  
B Cell ◽  
Tumor Progression ◽  
Avian Leukosis Virus ◽  
Viral Integration ◽  
B Cell Lymphomas ◽  
Late Stages

We have examined avian leukosis virus-induced B-cell lymphomas for multiple, stage-specific oncogene activations. Three targets for viral integration were identified: c-myb, c-myc, and a newly identified locus termed c-bic. The c-myb and c-myc genes were associated with different lymphoma phenotypes. The c-bic locus was a target for integration in one class of lymphomas, usually in conjunction with c-myc activation. The data indicate that c-myc and c-bic may act synergistically during lymphomagenesis and that c-bic is involved in late stages of tumor progression.

Multiple proto-oncogene activations in avian leukosis virus-induced lymphomas: evidence for stage-specific events

1989 ◽  
Vol 9 (6) ◽  
pp. 2657-2664 ◽  
Author(s):  
B E Clurman ◽  
W S Hayward
Keyword(s):  
B Cell ◽  
Tumor Progression ◽  
Avian Leukosis Virus ◽  
Viral Integration ◽  
B Cell Lymphomas ◽  
Late Stages

We have examined avian leukosis virus-induced B-cell lymphomas for multiple, stage-specific oncogene activations. Three targets for viral integration were identified: c-myb, c-myc, and a newly identified locus termed c-bic. The c-myb and c-myc genes were associated with different lymphoma phenotypes. The c-bic locus was a target for integration in one class of lymphomas, usually in conjunction with c-myc activation. The data indicate that c-myc and c-bic may act synergistically during lymphomagenesis and that c-bic is involved in late stages of tumor progression.

scholarly journals Selection for avian leukosis virus integration sites determines the clonal progression of B-cell lymphomas

2017 ◽  
Vol 13 (11) ◽  
pp. e1006708 ◽  
Author(s):  
Sanandan Malhotra ◽  
Shelby Winans ◽  
Gary Lam ◽  
James Justice ◽  
Robin Morgan ◽  
...  
Keyword(s):  
B Cell ◽  
Avian Leukosis Virus ◽  
B Cell Lymphomas ◽  
Integration Sites ◽  
Selection For ◽  
Virus Integration ◽  
Clonal Progression

scholarly journals Absence of missense mutations in activated c-myc genes in avian leukosis virus-induced B-cell lymphomas.

1988 ◽  
Vol 8 (6) ◽  
pp. 2659-2663 ◽  
Author(s):  
M Hahn ◽  
W S Hayward
Keyword(s):  
B Cell ◽  
Gene Product ◽  
Primary Structure ◽  
Avian Leukosis Virus ◽  
Nucleotide Sequences ◽  
Missense Mutations ◽  
B Cell Lymphomas ◽  
Altered Expression

We have determined the nucleotide sequences of two independent DNA clones which contained the activated c-myc genes from avian leukosis virus-induced B-cell lymphomas. Neither of these c-myc genes contained missense mutations. This strongly supports the notion that the c-myc proto-oncogene in avian leukosis virus-induced B-cell lymphomas can be oncogenically activated by altered expression of the gene without a change in the primary structure of the gene product.

scholarly journals Common Viral Integration Sites Identified in Avian Leukosis Virus-Induced B-Cell Lymphomas

mBio ◽  
2015 ◽  
Vol 6 (6) ◽  
Author(s):  
James F. Justice ◽  
Robin W. Morgan ◽  
Karen L. Beemon
Keyword(s):  
B Cell ◽  
High Throughput ◽  
High Throughput Sequencing ◽  
Consensus Sequence ◽  
B Cell Lymphoma ◽  
Avian Leukosis Virus ◽  
B Cell Lymphomas ◽  
Genome Wide ◽  
Integration Sites

ABSTRACTAvian leukosis virus (ALV) induces B-cell lymphoma and other neoplasms in chickens by integrating within or near cancer genes and perturbing their expression. Four genes—MYC,MYB,Mir-155, andTERT—have previously been identified as common integration sites in these virus-induced lymphomas and are thought to play a causal role in tumorigenesis. In this study, we employ high-throughput sequencing to identify additional genes driving tumorigenesis in ALV-induced B-cell lymphomas. In addition to the four genes implicated previously, we identify other genes as common integration sites, includingTNFRSF1A,MEF2C,CTDSPL,TAB2,RUNX1,MLL5,CXorf57, andBACH2. We also analyze the genome-wide ALV integration landscapein vivoand find increased frequency of ALV integration near transcriptional start sites and within transcripts. Previous work has shown ALV prefers a weak consensus sequence for integration in cultured human cells. We confirm this consensus sequence for ALV integrationin vivoin the chicken genome.IMPORTANCEAvian leukosis virus induces B-cell lymphomas in chickens. Earlier studies showed that ALV can induce tumors through insertional mutagenesis, and several genes have been implicated in the development of these tumors. In this study, we use high-throughput sequencing to reveal the genome-wide ALV integration landscape in ALV-induced B-cell lymphomas. We find elevated levels of ALV integration near transcription start sites and use common integration site analysis to greatly expand the number of genes implicated in the development of these tumors. Interestingly, we identify several genes targeted by viral insertions that have not been previously shown to be involved in cancer.

Molecular Genetics in the Diagnosis and Biology of Lymphoid Neoplasms

2019 ◽  
Vol 152 (3) ◽  
pp. 277-301 ◽  
Author(s):  
Megan S Lim ◽  
Nathanael G Bailey ◽  
Rebecca L King ◽  
Miguel Piris
Keyword(s):  
B Cell ◽  
Tumor Progression ◽  
Molecular Genetics ◽  
Cell Lymphoma ◽  
Clonal Evolution ◽  
Acquired Resistance ◽  
B Cell Lymphoma ◽  
B Cell Lymphomas ◽  
Transcriptional Reprogramming ◽  
Lymphoid Neoplasms

AbstractObjectivesThe 2017 Workshop of the Society for Hematopathology/European Association for Haematopathology reviewed the role of molecular genetics in the diagnosis and biology of lymphoid neoplasms.MethodsThe Workshop Panel reviewed 82 cases.ResultsMolecular genetic testing reveals alterations that expand the spectrum of diseases such as DUSP22 rearrangement in ALK-negative anaplastic large cell lymphoma, large B-cell lymphoma with IRF4 rearrangement, MYD88 mutations in B-cell lymphomas, Burkitt-like lymphoma with 11q aberrations, and diagnostic criteria for high-grade B-cell lymphomas. Therapeutic agents and natural tumor progression may be associated with transcriptional reprogramming that lead to transdifferentiation and lineage switch.ConclusionsApplication of emerging technical advances has revealed the complexity of genetic events in lymphomagenesis, progression, and acquired resistance to therapies. They also contribute to enhanced understanding of the biology of indolent vs aggressive behavior, clonal evolution, tumor progression, and transcriptional reprogramming associated with transdifferentiation events that may occur subsequent to therapy.

Absence of missense mutations in activated c-myc genes in avian leukosis virus-induced B-cell lymphomas

1988 ◽  
Vol 8 (6) ◽  
pp. 2659-2663
Author(s):  
M Hahn ◽  
W S Hayward
Keyword(s):  
B Cell ◽  
Gene Product ◽  
Primary Structure ◽  
Avian Leukosis Virus ◽  
Nucleotide Sequences ◽  
Missense Mutations ◽  
B Cell Lymphomas ◽  
Altered Expression

We have determined the nucleotide sequences of two independent DNA clones which contained the activated c-myc genes from avian leukosis virus-induced B-cell lymphomas. Neither of these c-myc genes contained missense mutations. This strongly supports the notion that the c-myc proto-oncogene in avian leukosis virus-induced B-cell lymphomas can be oncogenically activated by altered expression of the gene without a change in the primary structure of the gene product.

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