Translocation (13;17)(q14;q25) as a novel chromosomal abnormality in acute myeloid leukemia-M4

Turhan, Nihan Sölpük; Yurur-Kutlay, Nüket; Topçuoğlu, Pervin; Sayki, Müyesser; Yüksel, Meltem Kurt; Gürman, Günhan; Tükün, Ajlan

doi:10.1016/j.leukres.2005.12.011

Cited by 5 publications

(5 citation statements)

References 18 publications

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“…The t(13;17)(q14;q25), which caused the loss of RB1 sequences in the present patient has not been previously described in ALL [ 1 ]. This translocation has only been detected in an AML-M4 patient who did not show deletion of the RB1 gene [ 8 ], and in a case of Sézary syndrome in which the status of RB1 gene was not tested [ 9 ]. Although we did not know the extent of present 13q deletion, some features of the patient such as genome instability, poor prognosis, and shortened survival suggest that she had a large deletion inclusive of the RB1 gene.…”

mentioning

confidence: 99%

B-cell Acute Lymphoblastic Leukemia With t(9;22)(q34;q11) Translocation and Clonal Divergence Through ider(22) Chromosome and t(13;17)(q14;q25) Translocation

et al. 2016

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mentioning

confidence: 99%

B-cell Acute Lymphoblastic Leukemia With t(9;22)(q34;q11) Translocation and Clonal Divergence Through ider(22) Chromosome and t(13;17)(q14;q25) Translocation

et al. 2016

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“…In human acute myeloid leukemia M4, region 17q25 is involved in translocations, t(13;17) (q14;q25), which are associated with poor prognosis. 37 A fusion gene in acute myeloid leukemia (AML) also involves the chromosomal region in question (17q25), such that AF17q25 is fused with the MLL gene in AML with t(11;17) (q23;q25) translocations. 38 In chronic myeloid leukemia, breakpoint clusters have been reported around 17q25.…”

Section: E2 Subband Is Always Trisomic In V-abl/myc Pct Genesismentioning

confidence: 99%

Duplication of Subcytoband 11E2 of Chromosome 11 Is Regularly Associated with Accelerated Tumor Development in v-abl/myc-Induced Mouse Plasmacytomas

Wiener

Schmälter²,

Mowat³

et al. 2010

Genes & Cancer

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Chromosome 11 aberrations constitute the second most frequent chromosomal aberration in mouse plasmacytomas (PCTs) in which both the myc and abl oncogenes are constitutively expressed. In these tumors, previous G-banding studies had revealed numerical aberrations including duplication of the entire chromosome 11 or segments of telomeric bands D and E. The trisomy of chromosome 11 was always associated with accelerated pristane + v-abl/myc-induced PCT development. In the present study, PCT development was studied in a unique BALB/c congenic mouse strain, (T38HxBALB/c) F1, carrying a reciprocal translocation between chromosomes X and 11. After v-abl/myc induction, PCTs in this strain had acquired a nonrandom duplication of subcytoband 11E2. This duplication was always associated with accelerated PCT development. Corresponding synteny regions in the human and rat are changed in many tumors and involved in duplication, amplification, or translocation events. Thus, together with these synteny data, our findings strongly suggest a causal involvement of 11E2 in the acceleration of v-abl/myc-induced PCTs.

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“…Cytoband 11E2 is syntenic to human chromosome 17q25 and rat 10q32 [22] . It is frequently altered in tumors of lymphoid and nonlymphoid origin [23] , [24] , [25] . The mean latency of fast-onset PCTs is only 45 days [19] , [21] .…”

Section: Introductionmentioning

confidence: 99%

Changes in Nuclear Orientation Patterns of Chromosome 11 during Mouse Plasmacytoma Development

Schmälter

Righolt

Kuzyk

et al. 2015

Translational Oncology

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Studying changes in nuclear architecture is a unique approach toward the understanding of nuclear remodeling during tumor development. One aspect of nuclear architecture is the orientation of chromosomes in the three-dimensional nuclear space. We studied mouse chromosome 11 in lymphocytes of [T38HxBALB/c]N mice with a reciprocal translocation between chromosome X and 11 (T38HT(X;11)) exhibiting a long chromosome T(11;X) and a short chromosome T(X;11) and in fast-onset plasmacytomas (PCTs) induced in the same strain. We determined the three-dimensional orientation of chromosome 11 using a mouse chromosome 11 specific multicolor banding probe. We also examined the nuclear position of the small translocation chromosome T(X;11) which contains cytoband 11E2 and parts of E1. Chromosomes can point either with their centromeric or with their telomeric end toward the nuclear center or periphery, or their position is found in parallel to the nuclear border. In T38HT(X;11) nuclei, the most frequently observed orientation pattern was with both chromosomes 11 in parallel to the nuclear border (“PP”). PCT cells showed nuclei with two or more copies of chromosome 11. In PCTs, the most frequent orientation pattern was with one chromosome in parallel and the other pointing with its centromeric end toward the nuclear periphery (“CP”). There is a significant difference between the orientation patterns observed in T38HT(X;11) and in PCT nuclei (P < .0001).

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Translocation (13;17)(q14;q25) as a novel chromosomal abnormality in acute myeloid leukemia-M4

Cited by 5 publications

References 18 publications

B-cell Acute Lymphoblastic Leukemia With t(9;22)(q34;q11) Translocation and Clonal Divergence Through ider(22) Chromosome and t(13;17)(q14;q25) Translocation

B-cell Acute Lymphoblastic Leukemia With t(9;22)(q34;q11) Translocation and Clonal Divergence Through ider(22) Chromosome and t(13;17)(q14;q25) Translocation

Duplication of Subcytoband 11E2 of Chromosome 11 Is Regularly Associated with Accelerated Tumor Development in v-abl/myc-Induced Mouse Plasmacytomas

Changes in Nuclear Orientation Patterns of Chromosome 11 during Mouse Plasmacytoma Development

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