Retrovirally induced murine B‐cell tumors rarely show proviral integration in sites common in T‐cell tumors

Matthews, E. A.; Vasmel, W. L. E.; Schoenmakers, H. J.; Melief, Cornelis J.M.

doi:10.1002/ijc.2910430627

Cited by 8 publications

(2 citation statements)

References 41 publications

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“…21,22) In mouse spontaneous lymphomas, however, a provirus insertion into cmyc is frequently found in T-cell lymphomas 23,24) but relatively rarely in B-cell lymphomas 25) except for those in some AKXD recombinant inbred strains, 26) Cdkn2a-targeted C57BL mice injected with Moloney MuLV 27) and athymic mice infected with MuLV. 28) The prevalence of pre-B lymphomas in SL/Kh mice may be explained by their host genetic predisposition. The SL/Kh mice show transient expansion of pre-B cells in bone marrow at 3-6 weeks of age in advance of lymphoma development.…”

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confidence: 99%

Svi3: A provirus common integration site in c‐myc in SL/Kh pre‐B lymphomas

et al. 2003

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t has been shown that retroviral insertions in host DNA may cause hematopoietic malignancies by enhancing the expression of a proto-oncogene or by disrupting tumor suppressor genes at the integration sites.1) Recent progress in the technique of retrotransposon tagging has greatly facilitated the identification of cancer-related genes.2) SL/Kh, a pre-B lymphoma-prone inbred mouse strain, provides a unique model to investigate the host genetic and epigenetic factors determining susceptibility and types of disease. 3)Mice of this strain develop spontaneous pre-B lymphomas at >90% incidence by 6 months of age. 4) Several lines of evidence indicate that the endogenous murine leukemia virus (MuLV) plays an etiologic role in the genesis of SL/Kh lymphoma. 5-7)Somatically acquired proviruses are frequently observed in the genomic DNAs of lymphomas. 6) By applying inverse polymerase chain reaction (IPCR), we have identified a number of virus integration hot spots in SL/Kh lymphoma DNA; we have named them SL/Kh virus integration sites (Svi) and numbered them serially in the order of discovery. 7) Svi3 is one of them, in which 3 out of 60 SL/Kh lymphomas had clonal integration of a provirus of the ecotropic MuLV within the promoter region and the first exon of the c-myc. The c-myc encodes a transcription factor that is a cellular homologue of the viral transforming gene encoded by the avian myelocytomatosis virus MC29. 8)Leukemias and lymphomas induced by retroviruses frequently have integration in or near the c-myc gene, 9,10) suggesting that these tumors are clonal or semi-clonal outgrowths of cells that acquired a selective growth advantage in vivo as a consequence of c-myc insertions. In this report, we will describe the provirus integrations at Svi3 and their biological effects in SL/Kh mouse lymphomagenesis. Materials and MethodsMouse strain. SL/Kh is an inbred mouse strain maintained in

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Section: Discussionmentioning

confidence: 99%

Svi3: A provirus common integration site in c‐myc in SL/Kh pre‐B lymphomas

et al. 2003

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“…No consistent chromosomal anomaly was detected in the murine B-cell lymphomas, although some structural aberrations were found more than once. Molecular analyses of a large series of B-cell lymphomas, including the karyotyped lymphomas described here, are documented in the companion paper (Matthews et al, 1989).…”

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Distinct chromosomal abnormalities in murine leukemia virus‐induced T‐ and B‐cell lymphomas

Vasmel

Matthews

Gillis

et al. 1989

Intl Journal of Cancer

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We performed a cytogenetic study on 16 murine mature B-cell lymphomas and 10 T-cell lymphomas, using G-banding techniques. All tumors, with the exception of 3 spontaneous B-cell tumors, were induced by various slowly transforming murine leukemia viruses (MuLV). Metaphases were obtained from primary (10 B-cell tumors) and first or second transplant generation lymphomas (6 B-cell and 10 T-cell tumors), all of which were well characterized with respect to phenotypic, histologic and genotypic features. In the T-cell tumors we found relatively simple karyotypic abnormalities, including various numerical aberrations, such as trisomy 15, in line with many earlier reports. However, the majority of B-cell tumors showed a great variety of both structural and numerical chromosomal anomalies. Three B-cell lymphomas had an apparently normal karyotype. No single cytogenetic abnormality occurred commonly in the B-cell lymphomas, but some structural abnormalities were found in more than one stemline, in particular, ins (II) (A1; A2) in 3 tumors, and deletions involving the D-region of chromosome 14 in 3 other lymphomas. These cytogenetic results clearly indicate that the pathogenic mechanisms involved in MuLV-induced (long latency) B-cell lymphomagenesis and (short latency) T-cell lymphomagenesis differ considerably.

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