Two cases of acute promyelocytic leukemia with variant translocations: The importance of chromosome No. 17 abnormality

Yamada, Kiyomi; Sugimoto, Eisuke; Amano, Masamichi; Imamura, Yukio; Kubota, Tatsumi; Matsumoto, M

doi:10.1016/0165-4608(83)90029-8

Cited by 40 publications

(10 citation statements)

References 21 publications

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“…These include t(14;17)(q22;q21), 20 t(8;17)(p21;q21), 21 t(1;17)(p36;q21), 22,23 and t(7;17)(q36;q22). 23 Since the fusion partners have not been cloned it is possible that some or all may represent cryptic rearrangements of PML-RAR or the other APL variants. There are thus insufficient data to determine if these represent novel variants.…”

Section: Leukemiamentioning

confidence: 99%

Variations on a theme: the alternate translocations in APL

2002

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The t(15;17)(q22;q21) translocation is tightly linked to the APL phenotype, and the resultant PML-RAR fusion can be demonstrated in 98% of APL cases. Rare variant translocations have been reported, the majority of which on detailed analysis represent cryptic PML-RAR fusions. However, a handful of APL cases have been described with different genotypes. These include the t(11;17)(q23;q21) that produces the PLZF-RAR fusion, t(5;17)(q35;q21) that forms NPM-RAR, t(11;17)(q13;q21) that generates NUMA-RAR, and der(17) that creates STAT5b-RAR. In this review we will discuss these variant translocations, and discuss the insights that we have gained from their study.

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Section: Leukemiamentioning

confidence: 99%

Variations on a theme: the alternate translocations in APL

2002

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“…The polymorphic nature and increased heterozygosity of these repeats compared with current markers make them ideal candidates for physical and genetic mapping of the human genome and for disease diagnosis (62). Such repetitive elements are thought to contribute to chromosomal translocations and deletions (29) and are possible sites for translocation known to occur within the 1p36 locus (15)(16)(17)(18)(19). Additionally, polypurine-polypyrimidine sequences have been shown to form DNA triplexes (H-DNA) (31).…”

Section: Tnf-r P75/80 Gene Structurementioning

confidence: 99%

“…Mapping of TNF-R p75 to chromosome 1p36 (13,14) revealed that nonrandom translocations occur near this locus in some hematopoietic malignancies. Specifically, a (1;3)(p36;q21) translocation has been observed in myelodysplastic syndromes (15)(16)(17) and acute nonlymphocytic leukemias (18), while a (1;17)(p36;q21) translocation has been reported in acute promyelocytic leukemia (19). The 1p36 locus has also been shown to be abnormal in malignant lymphoma, neuroblastoma, glioma (13), and non-Burkitt lymphoma (20).…”

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confidence: 99%

Human Tumor Necrosis Factor Receptor p75/80 (CD120b) Gene Structure and Promoter Characterization

Santee

Owen‐Schaub

1996

Journal of Biological Chemistry

139

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Tumor necrosis factor receptor p75 (TNF-R p75) is a 75-kDa type I transmembrane protein expressed predominantly on cells of hematopoietic lineage. TNF-R p75 belongs to the TNF receptor superfamily characterized by cysteine-rich extracellular regions composed of three to six disulfide-linked domains. In the present report we have characterized, for the first time, the complete gene structure for human TNF-R p75, which spans approximately 43 kbp. The gene consists of 10 exons (ranging from 34 base pairs to 2.5 kilobase pairs) and nine introns (343 base pairs to 19 kilobase pairs). Consensus elements for transcription factors involved in T cell development and activation were noted in the 5-flanking region including T cell factor-1, Ikaros, AP-1, CK-2, interleukin-6 receptor E (IL-

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“…Such variant translocations have been reported (Table I); two cases of simple t(1;17)(p36;q21) (Yamada et al, 1983;Schwartz et al, 1986) and other cases with more complex translocations (Osella et al, 1991;Ohyashiki et al, 1985). In all cases but one, breakpoint on chromosome 1 was located in 1p36.…”

Section: Discussionmentioning

confidence: 96%

PML/RARα rearrangement in acute promyelocytic leukaemia with t(1;17) elucidated using fluorescence in situ hybridization

Éclache¹,

Benzacken²,

Roux³

et al. 1997

Br J Haematol

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Summary. Acute promyelocytic leukaemia (APL) is characterized by t(15;17)(q22;q21) which results in the formation of two chimaeric genes, PML/RARa and RARa/PML, thought to play a role in leukaemogenesis. We report a case of a patient with APL apparently lacking the t(15;17) but with t(1;17) translocation identified by fluorescence in situ hybridization (FISH). Chromosome 15 seemed intact but PML/RARa fusion transcript was detected by molecular analysis. The patient achieved complete remission with alltrans retinoic acid treatment associated with chemotherapy. This case illustrates the usefulness of combined cytogenetics, FISH and molecular biology in cases with no evident t(15;17) to predict response to treatment.

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Two cases of acute promyelocytic leukemia with variant translocations: The importance of chromosome No. 17 abnormality

Cited by 40 publications

References 21 publications

Variations on a theme: the alternate translocations in APL

Variations on a theme: the alternate translocations in APL

Human Tumor Necrosis Factor Receptor p75/80 (CD120b) Gene Structure and Promoter Characterization

PML/RARα rearrangement in acute promyelocytic leukaemia with t(1;17) elucidated using fluorescence in situ hybridization

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