A complex, four-way variant t(15;17) in acute promyelocytic leukemia

Yoo, Soo Jin; Seo, Eul‐Ju; Lee, Jae Hoon; Seo, Yiel-Hea; Park, Pil-Whan; Ahn, Jeong Yeal

doi:10.1016/j.cancergencyto.2005.12.006

Cited by 28 publications

(14 citation statements)

References 26 publications

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“…Our case is the first report of new three-way variant translocation to our knowledge. Yoo [21,25,31]. These findings may indicate that the involvement of 22q11 have no significant role in leukemogenesis and treatment response although we did not verify the implication on any oncogene located in 22q11.…”

Section: Discussioncontrasting

confidence: 75%

A new three-way variant t(15;22;17)(q22;q11.2;q21) in acute promyelocytic leukemia

et al. 2009

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Acute promyelocytic leukemia (APL) is characterized by the t(15;17)(q22;q21), which results in the fusion of the promyelocytic leukemia (PML) gene at 15q22 with the retinoic acid alpha-receptor (RARA) at 17q21. We report the case of a 44-year-old man with APL carrying a new complex variant translocation (15;22;17). Karyotypic analysis with G-banding of bone marrow cells revealed t(15;22;17) (q22;q11.2;q21). Fluorescence in situ hybridization with a PML/RARA dual-color DNA probe showed the fusion signals. RT-PCR analysis showed long-form PML/RARA fusion transcripts. A complete remission was attained with a course of conventional chemotherapy with all-trans retinoic acid (ATRA). This is the first report of a new three-way translocation of 22q11 involvement with APL.

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Section: Discussioncontrasting

confidence: 75%

A new three-way variant t(15;22;17)(q22;q11.2;q21) in acute promyelocytic leukemia

et al. 2009

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“…Several complex variant translocations have been reported in APL with three-way or more complex translocations [5][6][7][8][9][10][11]. To our knowledge, our case is the first report of a new four-way variant translocation of 5q33 and 20q11 involvement in APL.…”

Section: Discussionmentioning

confidence: 59%

“…This fusion transcript is known to play a pivotal role in the pathogenesis of APL and the sensitivity to alltrans retinoic acid (ATRA) [3]. APL patients with alternative translocations, such as t(11;17)(q23;q21) [4] have been reported, and more complex variant (15;17) translocations are increasingly recognized in APL [5][6][7][8][9][10][11]. Molecular and cytogenetic characterization of variant translocations is important for a better understanding of the pathogenesis of the disease and to predict the response to ATRA.…”

Section: Introductionmentioning

confidence: 99%

A new four-way variant t(5;17;15;20)(q33;q12;q22;q11.2) in acute promyelocytic leukemia

et al. 2011

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Acute promyelocytic leukemia (APL) is characterized by t(15;17)(q22;q21), which results in the fusion of the promyelocytic leukemia (PML) gene at 15q22 with the retinoic acid alpha-receptor (RARA) at 17q21. We report a patient with APL carrying a new complex variant translocation (5;17;15;20). Spectral karyotyping analysis of bone marrow cells revealed t(5;17;15;20)(q33;q12;q22;q11.2). Fluorescence in situ hybridization with a PML/RARA dual-color DNA probe showed a single fusion signal, and RT-PCR analysis showed PML/RARA fusion transcripts. Complete remission was attained with a course of conventional chemotherapy with all-trans retinoic acid (ATRA). To our knowledge, this is the first report of a four-way translocation of 5q33 and 20q11 involvement in APL.

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“…Promyelocytic leukemia (PML), which is encoded by a PML gene mapped on chromosome 15q22 in humans, contains a nuclear localization signal (NLS), an α-helical coiled-coil region and B-Boxes (5). In 1991, it was discovered that the consistent chromosomal translocation of APL, t (15:17), fused the RARα gene to the PML gene on chromosome 15 (6), yielding the fusion protein PML-RARα (7), which represents the etiologic agent of APL. This translocation has become the definitive marker for the disease and is detected in 95% of patients with APL (8).…”

Section: Introductionmentioning

confidence: 99%

Location of NLS-RARα protein in NB4 cell and nude mice

et al. 2017

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In the majority of acute promyelocytic leukemia (APL) cases, translocons produce a promyelocytic leukemia protein-retinoic acid receptor α (PML-RARα) fusion gene. Studies have reported that neutrophil elastase (NE) cleaves bcr-1-derived PML-RAα in early myeloid cells, leaving only the nuclear localization signal (NLS) of PML attached to RARα. NLS-RARα promotes cell growth and inhibits differentiation in response to ATRA. However, the mechanisms by which NLS-RARα affects cell biological characteristics are yet to be fully elucidated. The present study found that the location of RARαwas altered after it was cleaved by NE. Firstly, NE was overexpressed during the preparation of recombinant plasmid NB-4/pCMV6-NE-Myc to cleave PML-RARα. The total protein expression levels of myc and NE and expression levels of NLS-RARα in nucleoprotein were detected by western blotting. Location of NLS-RARα protein was detected by immunofluorescence and confocal laser scanning. Secondly, a nude mice model was constructed and NE protein, NLS-RARα and RARα protein assays, and the location of NLS-RARα and RARα proteins were assessed as described. The present results showed that, compared with the control groups, the location of NLS-RARα protein was predominantly detected in the nucleus, whereas RARα was mainly distributed in the cytoplasm. These findings were consistent with those of the nude mice model, and these may be used as a foundation to explain the occurrence mechanism of APL.

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A complex, four-way variant t(15;17) in acute promyelocytic leukemia

Cited by 28 publications

References 26 publications

A new three-way variant t(15;22;17)(q22;q11.2;q21) in acute promyelocytic leukemia

A new three-way variant t(15;22;17)(q22;q11.2;q21) in acute promyelocytic leukemia

A new four-way variant t(5;17;15;20)(q33;q12;q22;q11.2) in acute promyelocytic leukemia

Location of NLS-RARα protein in NB4 cell and nude mice

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