Chromosome Changes (Trisomies #15 and 17) Associated With Tumor Progression in Leukemias Induced by Radiation Leukemia Virus2

Wiener, Francis; Ohno, Shinsuke; Spira, Jack; Haran-Ghera, Nechama; Klein, George

doi:10.1093/jnci/61.1.227

Cited by 106 publications

(28 citation statements)

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“…It has been found in spontaneous thymic lymphomas and in T cell lymphomas induced by diverse agents such as x-rays, the chemical carcinogen dimethylbenz [a]anthracene, radiation leukemia virus, and Moloney virus (1)(2)(3)(4)(5). In CBAT6T6 mice that carry a 14;15 translocation we have shown that the active region of chromosome 15 is in the distal (translocated) part of chromosome 15 (5).…”

mentioning

confidence: 74%

Is trisomy cause or consequence of murine T cell leukemia development? Studies on Robertsonian translocation mice.

Spira¹,

Wiener²,

Ohno³

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

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mentioning

confidence: 74%

Is trisomy cause or consequence of murine T cell leukemia development? Studies on Robertsonian translocation mice.

Spira¹,

Wiener²,

Ohno³

et al. 1979

Proc. Natl. Acad. Sci. U.S.A.

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“…Other frequently observed CNAs included whole copy gains of chromosomes 10 and 15. It has been noted, however, that these chromosomes are also frequently involved in several other studies of mouse leukemias, 36 as well as in some solid tumors. 37 Given the shorter tumor latency period in the third and fourth transplants, it is very unlikely that the multiple CNAs seen in the LNs develop de novo each time, in exactly the same way in each passage.…”

Section: Discussionmentioning

confidence: 99%

Genetic fingerprinting of the development and progression of T-cell lymphoma in a murine model of atypical myeloproliferative disorder initiated by the ZNF198–fibroblast growth factor receptor-1 chimeric tyrosine kinase

Ren

Cowell

2009

Blood

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A mouse model of human ZNF198-fibroblast growth factor receptor-1 (FGFR1) stem cell leukemia lymphoma has been developed to investigate mechanisms of oncogenesis and progression. Using array-based comparative genomic hybridization, we followed disease progression after serial transplantation of ZNF198-FGFR1-transformed stem cells that give rise to a distinct myeloproliferative disorder and T-lymphoblastic leukemia. A consistent, frequently homozygous, chr14:53880459-55011545 deletion, containing the T-cell receptor ␣ and ␦ genes, was identified in the bone marrow, spleen, and lymph nodes in all cases. The absence of cell-surface T-cell receptor ␣ in tumor cells precludes CD3 recruitment, resulting in loss of a functional T-cell receptor complex, supporting the idea that prevention of maturation of CD4 ؉ / CD8 ؉ double-positive immature T cells is important in ZNF198-FGFR1 disease development. Up-regulation of the B-cell line 2, interleukin 7 receptor ␣ and interleuking 2 receptor ␣ prosurvival genes in these undifferentiated tumor precursor cells suggests one mechanism that allows them to escape apoptosis in the thymus. Thus, we have defined an important event in the process of ZNF198- IntroductionHuman stem cell leukemia-lymphoma syndrome (SCLL), also known as 8p11 myeloproliferative syndrome, is a rare atypical myeloproliferative disorder. SCLL constitutes a clinical phenotype with features of both lymphoma and eosinophilic myeloproliferative disorders and is characterized by a reciprocal chromosome translocation, resulting in a chimeric protein that activates the kinase domain of the fibroblast growth factor receptor-1 (FGFR1). 1 To date, at least 8 gene partners have been shown to fuse to FGFR1, including ZNF198 on 13q12, 2,3 CEP110 on 9q33, 4 and FOP on 6q27 5 (see Tefferi and Gilliland 1 for review). The most commonly observed translocation is the t(8;13) (p11;q12), in which the zinc finger domain of ZNF198 is fused to the intracellular kinase domain of FGFR1. 2,3,6 Hepatosplenomegaly is characteristic of these myeloproliferative disorder patients, and almost all show T-lymphoblastic lymphoma, except for one case with B-cell acute lymphoblastic lymphoma. 7 The clinical course of SCLL is aggressive, with rapid transformation to acute myeloid leukemia and lymphoblastic lymphoma of common T-cell origin. [7][8][9][10][11] Treatment with conventional chemotherapy is often not effective, 12,13 and allogeneic bone marrow (BM) transplantation seems to be the only potentially curative therapeutic option. 7 In SCLL, both myeloid and lymphoid lineage cells exhibited the 8p11 translocation, suggesting a stem cell origin. The FGFR1 fusion protein in SCLL results in the constitutive and ligandindependent activitation of the FGFR1 signal transduction pathway, and is believed to be essential for disease pathogenesis, as evidenced in the clinical cases and murine models. 14,15 How the ZNF198-FGFR1 fusion kinase results in disease progression, however, remains unclear, as does its relationship with the development of concu...

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“…[28][29][30][31][32] By analyzing T-cell lymphomas arising in mice with constitutional translocations involving chromosome 15, Silva et al 33 demonstrated that trisomy for bands 15D2-3 (syntenic to human 8q23-24) contributes to the development or progression (or both) of these T-cell lymphomas. This region contains the Myc and Pvt1 genes.…”

Section: Discussionmentioning

confidence: 99%

Recurring chromosomal abnormalities in leukemia inPML-RARA transgenic mice parallel human acute promyelocytic leukemia

Beau

Bitts

Davis

et al. 2002

Blood

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Acute promyelocytic leukemia (APL) is characterized by the t(15;17)(q22;q11.2), which results in the PML-RARA fusion gene. In previous studies, we demonstrated that expression of a human PML-RARA complementary DNA in murine granulocyte precursor cells initiated the development of leukemia. However, leukemogenesis by PML-RARA required additional genetic alterations. To identify genetic changes that cooperate with PML-RARA in leukemogenesis, we performed spectral karyotyping analysis of myeloid leukemias from hMRP8-PML-RARA mice (11 cases) and from mice coexpressing PML-RARA and BCL2 (8 cases). Clonal abnormalities were detected in 18 of 19 cases (95%). Recurring numerical abnormalities identified in these murine leukemias included ؉15 (15 cases, 79%); loss of a sex chromosome (12 cases, 63%); ؉8 (10 cases, 53%); ؉10 (9 cases, 47%); ؉4, ؉7, or ؉14 (8 cases each, 42%); ؉16 (7 cases, 37%); and ؉6 (5 cases, 26%). In a series of 965 patients with APL, we identified secondary abnormalities in 368 (38%). The most common recurring abnormalities were ؉8 or partial trisomy of 8q (120 patients, 12.4%) and ider(17) t(15;17) (42 patients, 4.4%). The critical consequence of ؉8 in human leukemias appears to be the gain of 8q24, which is syntenic to mouse 15. Thus, our results suggest that PML-RARA-initiated murine leukemia is associated with a defined spectrum of genetic changes, and that these secondary mutations recapitulate, in part, the cytogenetic abnormalities found in human APL. (Blood. 2002;99:2985-2991

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Chromosome Changes (Trisomies #15 and 17) Associated With Tumor Progression in Leukemias Induced by Radiation Leukemia Virus2

Cited by 106 publications

References 0 publications

Is trisomy cause or consequence of murine T cell leukemia development? Studies on Robertsonian translocation mice.

Is trisomy cause or consequence of murine T cell leukemia development? Studies on Robertsonian translocation mice.

Genetic fingerprinting of the development and progression of T-cell lymphoma in a murine model of atypical myeloproliferative disorder initiated by the ZNF198–fibroblast growth factor receptor-1 chimeric tyrosine kinase

Recurring chromosomal abnormalities in leukemia inPML-RARA transgenic mice parallel human acute promyelocytic leukemia

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