Corpus ID: 127544

Cloning of the ALL-1 fusion partner, the AF-6 gene, involved in acute myeloid leukemias with the t(6;11) chromosome translocation.

@article{Prasad1993CloningOT,
  title={Cloning of the ALL-1 fusion partner, the AF-6 gene, involved in acute myeloid leukemias with the t(6;11) chromosome translocation.},
  author={R. Prasad and Y. Gu and H. Alder and T. Nakamura and O. Canaani and H. Saito and K. Huebner and R. Gale and P. Nowell and K. Kuriyama},
  journal={Cancer research},
  year={1993},
  volume={53 23},
  pages={
          5624-8
        }
}
Reciprocal chromosome translocations involving 11q23 are frequently associated with acute leukemias, with the t(4;11) translocation predominating among acute lymphoblastic leukemias, and the t(9;11), t(11;19) and t(6;11) translocations most common among acute myeloid leukemias. In each of these translocations the ALL-1 gene, located at 11q23 and constituting the human homologue of Drosophila trithorax, fuses to a specific gene on the partner chromosome to produce a chimeric protein. Here we… Expand
ENL, the gene fused with HRX in t(11;19) leukemias, encodes a nuclear protein with transcriptional activation potential in lymphoid and myeloid cells.
TLDR
The leukemogenic contribution and transcriptional activation potential of Enl colocalize to its highly conserved carboxy terminus, suggesting that Hrx-Enl chimeric proteins mediate alterations in the transcription program of t(11;19)-bearing cells. Expand
The t(10;11) translocation in acute myeloid leukemia (M5) consistently fuses the leucine zipper motif of AF10 onto the HRX gene.
TLDR
The published data suggest that a similar conclusion can be drawn about the t(11;17) translocation, implying a critical role for this motif in the chimaeric HRX protein. Expand
A specific deletion in the breakpoint cluster region of the ALL-1 gene is associated with acute lymphoblastic T-cell leukemias.
TLDR
Findings support the hypothesis that the ALL-1 protein may be converted to an oncogenic variant, not only by chimerization or self-fusion, but also by deletion of sequences coded by exon 8 and suggest that these three different types of structural alterations of the All-1protein may each cause a distinct disease phenotype. Expand
The FEL (AF-4) protein donates transcriptional activation sequences to Hrx-Fel fusion proteins in leukemias containing T(4;11)(Q21;Q23) chromosomal translocations.
TLDR
It is demonstrated that Fel is capable of activating transcription from a minimal adenoviral E1b promoter as a Gal4-Fel fusion protein in transient transcriptional assays, consistent with a potential role of Hrx-Fel as a chimeric transcription factor in which Fel contributes transcriptional effector properties and suggest the requirement for cell-specific accessory factors. Expand
Cloning and characterization of the t(X;II) breakpoint from a leukemic cell line identify a new member of the forkhead gene family
TLDR
Cl cloning and sequencing the t(X;II) breakpoint region from a cell line established from an infant with acute lymphocytic leukemia and sequence analysis indicates a high degree of homology between AFXI and the forkhead family of transcription factors. Expand
Analysis of the t(6;11)(q27;q23) in leukemia shows a consistent breakpoint in AF6 in three patients and in the ML‐2 cell line
TLDR
R reverse transcriptase‐polymerase chain reaction (RT‐PCR) using an MLL sense primer and an AF6 antisense primer detected the MLL/AF6 fusion cDNA from three leukemia patients with the t(6;11) and one cell line, which indicates that an intact MLL gene is not necessary for survival of leukemic cells. Expand
Leukemia-associated Protein with a CXXC Domain , Is Fused to MLL in Acute Myeloid Leukemia with Trilineage Dysplasia Having t ( 10 ; 11 ) ( q 22 ; q 23 ) 1
There are a limited number of reports of acute myeloid leukemia (AML) with t(10;11)(q22;q23). We showed that the MLL gene on 11q23 was fused to the LCX (leukemia-associated protein with a CXXCExpand
MSF (MLL septin-like fusion), a fusion partner gene of MLL, in a therapy-related acute myeloid leukemia with a t(11;17)(q23;q25).
TLDR
A fusion partner of MLL is identified in a 10-year-old female who developed therapy-related acute myeloid leukemia 17 months after treatment for Hodgkin's disease and is named MSF (MLL septin-like fusion). Expand
Molecular analysis of the rearranged genome and chimeric mRNAs caused by the t(6;11)(q27;q23) chromosome translocation involving MLL in an infant acute monocytic leukemia
TLDR
Findings indicate that exon 6 of MLL is spliced out in the process of transcription in a variant MLL/AF6, and the splicing of ex on 6 in either this chimeric MLL /AF6 or MLL transcripts from untranslocated chromosomes by reverse transcriptase‐polymerase chain reaction. Expand
Molecular Genetic Detection of Chromosomal Abnormalities at 11q23 in Patients with De Novo and Secondary Acute Leukemia
TLDR
Investigation of patients with ALL, AML, and secondary leukemia for the presence of a chimeric mRNA known to be the equivalent of the various chromosomal translocations involving 11q23 found eight different MLL fusion mRNAs, indicating that the RTPCR technique is suitable to identify such gene rearrangements and can be used in order to define patients with acute leukemia belonging to a higher risk group. Expand
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References

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TLDR
The t(4;11) chromosome translocation results in two reciprocal fusion products coding for chimeric proteins derived from ALL-1 and from a gene on chromosome 4, which suggests that each 11q23 abnormality gives rise to a specific oncogenic fusion protein. Expand
Genes on chromosomes 4, 9, and 19 involved in 11q23 abnormalities in acute leukemia share sequence homology and/or common motifs.
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TLDR
Cloned and sequenced cDNAs derived from transcripts of the AF-4 and AF-9 genes involved in the most common chromosome abnormalities suggest that the different proteins fused to ALL-1 polypeptide(s) provide similar functional domains. Expand
A serine/proline-rich protein is fused to HRX in t(4;11) acute leukemias.
TLDR
CDNAs representative of transcription products from the derivative 11 chromosome were shown to contain HRX sequences fused to sequences derived from chromosome band 4q21, suggesting that HRX consistently contributes a novel DNA-binding motif to at least two different chimeric proteins in acute leukemias. Expand
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TLDR
Altered topoisomerase II activity in the presence of an active V-D-J recombinase may be a pathogenetic mechanism of acute myeloid leukemia with rearrangements at 11q23. Expand
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TLDR
A novel role for a trithorax-homologous protein in multilineage human leukemias that may be mediated by DNA binding within the minor groove at AT-rich sites is suggested, implicated to play an important role in bacterial IHF, yeast datin-, and mammalian HMG-mediated gene activation. Expand
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TLDR
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TLDR
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