Acute myeloblastic leukemia (AML) with t(6;9) (p23;q34): A specific subgroup of AML?

Sandberg, Avery A.; Morgan, Rodman; McCallister, John A.; Kaiser-McCaw, B; Hecht, Frederick

doi:10.1016/0165-4608(83)90117-6

Cited by 43 publications

(10 citation statements)

References 6 publications

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“…Nakano/Shimamoto/Suga/Kobayashi dek-can Fusion Gene in Leukemia D iscussio n A t(6;9) (p23;q34) can be found in 0.5-4% of patients with AML [1,2,16]. Our patient had a preceding myelo dysplasia and developed AML M2, similar to previous reports.…”

supporting

confidence: 75%

Detection of Minimal Residual Disease in a Patient with Acute Myeloid Leukemia and t(6;9) at the Time of Peripheral Blood Stem Cell Transplantation

et al. 1995

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A 16-year-old Japanese woman with acute myelogenous leukemia (AML) and t(6;9) received peripheral blood stem cell transplantation (PBSCT). Although chromosomal studies just prior to and following PBSCT showed a normal karyotype, reverse transcription-polymerase chain reaction (RT-PCR) detected the mRNA derived from the dekcan fusion gene of t(6;9) following PBSCT and in the harvested stem cells. Following PBSCT, she relapsed. To our knowledge, this case is the first report from Japan in which minimal residual disease was detected with RT-PCR in AML with t(6;9). These methods should improve the use and outcome of PBSCT.

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supporting

confidence: 75%

Detection of Minimal Residual Disease in a Patient with Acute Myeloid Leukemia and t(6;9) at the Time of Peripheral Blood Stem Cell Transplantation

et al. 1995

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“…Hughes [59] speculated that the congress of the six genes did not happen by chance but was driven by natural selection favouring grouping in a single region of genes with a very broad pattern of expression and encoding long polypeptide chains. (Interestingly, translocations between human chromosomes 6 and 9 are known to occur repeatedly; they are characteristic of a specific subtype of acute myeloid leukaemia [60,61].) The breakpoints on both chromosomes are always located in the same introns of specific genes: CAN on chromosome 9 and DEK on chromosome 6.…”

Section: Origin Of Non-class I/ii Genesmentioning

confidence: 99%

Birth of the Major Histocompatibility Complex

Klein

Sato

1998

Scand J Immunol

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“…In chronic myeloid leukemia this is a BCR-ABL protein that has an enhanced tyrosine kinase activity (34, 49) directly responsible for its in vivo tumorigenic potential (14,25). In acute promyelocytic leukemia a PMLRARa fusion protein that represents an altered transcription factor (16, 33) is found.The third translocation is the t(6;9) (p23;q34), found in a specific subtype of acute myeloid leukemia (AML) (1,39,41). This leukemia is characterized by a poor prognosis, affects young adults, and is classified mostly as M2 or M4 and rarely as Ml (according to the French-American-British classification of AML).…”

mentioning

confidence: 99%

“…The third translocation is the t(6;9) (p23;q34), found in a specific subtype of acute myeloid leukemia (AML) (1,39,41). This leukemia is characterized by a poor prognosis, affects young adults, and is classified mostly as M2 or M4 and rarely as Ml (according to the French-American-British classification of AML).…”

mentioning

confidence: 99%

The translocation (6;9), associated with a specific subtype of acute myeloid leukemia, results in the fusion of two genes, dek and can, and the expression of a chimeric, leukemia-specific dek-can mRNA.

et al. 1992

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The translocation (6;9) is associated with a specific subtype of acute myeloid leukemia (AML). Previously, it was found that breakpoints on chromosome 9 are clustered in one of the introns of a large gene named Cain (can). cDNA probes derived from the 3' part of can detect an aberrant, leukemia-specific 5.5-kb transcript in bone marrow cells from t(6;9) AML patients. cDNA cloning of this mRNA revealed that it is a fusion of sequences encoded on chromosome 6 and 3' can. A novel gene on chromosome 6 which was named dek was isolated. In dek the t(6;9) breakpoints also occur in one intron. As a result the dek-can fusion gene, present Defined karyotypic aberrations are associated with specific subtypes of leukemia. Detailed molecular characterization of these aberrations may identify genes involved in leukemogenesis and in the precise regulation of proliferation and differentiation in the hematopoietic system. Translocations are the best-studied chromosomal abnormalities. As the result of a translocation, the function or activity of oncogenes located at or near the translocation breakpoint is altered. In myeloid leukemia three translocation breakpoints have been cloned and analyzed at the molecular level.The two best studied, t(9;22) in chronic myeloid leukemia (27, 43) and t(15;17) in acute promyelocytic leukemia (2,8,12), result in the formation of chimeric genes that encode fusion proteins. In chronic myeloid leukemia this is a BCR-ABL protein that has an enhanced tyrosine kinase activity (34, 49) directly responsible for its in vivo tumorigenic potential (14,25). In acute promyelocytic leukemia a PMLRARa fusion protein that represents an altered transcription factor (16, 33) is found.The third translocation is the t(6;9) (p23;q34), found in a specific subtype of acute myeloid leukemia (AML) (1,39,41). This leukemia is characterized by a poor prognosis, affects young adults, and is classified mostly as M2 or M4 and rarely as Ml (according to the French-American-British classification of AML). A region on chromosome 9 situated 360 kb downstream of the c-abl gene was cloned and analyzed. It was found that breakpoints were clustered in a region of 8 kb in five patients, four with t(6;9) AML and one with acute undifferentiated leukemia (AUL) (47). Through cDNA cloning this region could be identified as one of the introns of a large gene (>100 kb) encoding a 7-kb transcript. This intron was named icb-9; the intron containing the breakpoints on chromosome 9 and situated in the middle of * Corresponding author. a gene named Cain (can). The 3' part of can is translocated to the 6p-chromosome, and only 3' can probes detect an additional, leukemia-specific 5.5-kb transcript in bone marrow cells from t(6;9) AML patients. No additional transcripts were detected with 5' can probes. The breakpoint region on chromosome 6p23 was isolated from a genomic XEMBL3 library constructed of bone marrow DNA from one of the t(6;9) patients. An area of 40 kb of chromosome 6 DNA was cloned in overlapping phages. Southern blot analysis sh...

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Acute myeloblastic leukemia (AML) with t(6;9) (p23;q34): A specific subgroup of AML?

Cited by 43 publications

References 6 publications

Detection of Minimal Residual Disease in a Patient with Acute Myeloid Leukemia and t(6;9) at the Time of Peripheral Blood Stem Cell Transplantation

Detection of Minimal Residual Disease in a Patient with Acute Myeloid Leukemia and t(6;9) at the Time of Peripheral Blood Stem Cell Transplantation

Birth of the Major Histocompatibility Complex

The translocation (6;9), associated with a specific subtype of acute myeloid leukemia, results in the fusion of two genes, dek and can, and the expression of a chimeric, leukemia-specific dek-can mRNA.

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