Further studies on chromosome 15 trisomy in murine T‐cell lymphomas: Mapping of the relevant chromosome segment

Silva, Santiago; Babonits, Magda; Wiener, Francis; Klein, George

doi:10.1002/ijc.2910410517

Cited by 17 publications

(10 citation statements)

References 32 publications

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“…Mouse chromosome 15 is syntenic with human chromosome 8. Silva et al [1988] have demonstrated that trisomy of bands 15D2-3 contributes to the development or progression of T-cell lymphomas. Mouse chromosome 15 contains the Myc gene at the 15D2-3 region which has been extensively studied in mouse model systems involving experimental plasmacytomas [Potter, 2003].…”

Section: Discussionmentioning

confidence: 98%

Multicolor spectral karyotyping of the L5178YTk+/−-3.7.2C mouse lymphoma cell line

Sawyer

Binz

Wang

et al. 2006

Environ. Mol. Mutagen.

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The L5178Y/Tk+/- -3.7.2C mouse lymphoma cell line is characterized, at the cytogenetic level, by a karyotype involving both numerical and complex structural aberrations. While the karyotype is remarkably normal for a transformed cell line that has been in culture for almost half a century, there are a number of chromosomal alterations that because of their complexity cannot be fully characterized by routine or even high-resolution G-banding studies. Multicolor spectral karyotyping (SKY) was performed on the cell line in anticipation of identifying the previously unresolved chromosome aberrations and confirming interpretations previously identified by banding studies. New chromosome aberrations detected by SKY include numerical aberrations of chromosome 15, duplications of regions of chromosomes 4, 5, 12, and 18, and deletion of chromosome 14. Complex unbalanced translocations involved segments of chromosomes 6, 14, and 15. In total, the SKY technique was able to provide new refined designations on segments of eight different chromosome pairs (4, 5, 6, 9, 12, 14, 15, 18) and identified all three previously unidentified marker chromosomes. This analysis provides an updated standard reference for the karyotype of the L5178Y/Tk+/- -3.7.2C cell line used in the in vitro mouse lymphoma mutation assay.

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Section: Discussionmentioning

confidence: 98%

Multicolor spectral karyotyping of the L5178YTk+/−-3.7.2C mouse lymphoma cell line

Sawyer

Binz

Wang

et al. 2006

Environ. Mol. Mutagen.

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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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“…Trisomy 15 is the most common abnormality in murine T-cell lymphomas and in murine B-cell leukemias arising in irradiated E-BCL2 transgenic mice. 30,31 Moreover, we have detected trisomy 15 in myeloid neoplasms arising in a number of murine models that recapitulate the genetic mutations in human myeloid leukemias. 32 To determine whether other MPDs arising in Egr1 Ϫ/Ϫ and Egr1 Ϫ/Ϫ mice were characterized by trisomy 15, we performed interphase FISH analysis using a PAC clone containing the mouse Myc gene on chromosome 15 (Table S2).…”

Section: Secondary Mutations Are Required For Disease Progressionmentioning

confidence: 99%

Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders

Joslin

Fernald

Tennant

et al. 2007

Blood

195

145

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Further studies on chromosome 15 trisomy in murine T‐cell lymphomas: Mapping of the relevant chromosome segment

Cited by 17 publications

References 32 publications

Multicolor spectral karyotyping of the L5178YTk+/−-3.7.2C mouse lymphoma cell line

Multicolor spectral karyotyping of the L5178YTk+/−-3.7.2C mouse lymphoma cell line

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

Haploinsufficiency of EGR1, a candidate gene in the del(5q), leads to the development of myeloid disorders

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