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Cryptic MLL-AF10 fusion caused by insertion of duplicated 5' part of MLL into 10p12 in acute leukemia: a case report

Jarosova M, Takacova S, Holzerova M, Priwitzerova M, Divoka M, Lakoma I, Mihal V, Indrak K, Divoky V.

. 2005 ; 162 (2) : 179-182.

Jazyk angličtina Země Spojené státy americké

Typ dokumentu abstrakty

Perzistentní odkaz   https://www.medvik.cz/link/bmc07506627

Grantová podpora
NR7849 MZ0 CEP - Centrální evidence projektů

Digitální knihovna NLK
Plný text - Část
Zdroj

E-zdroje Online

NLK ScienceDirect (archiv) od 1993-01-01 do 2009-12-31

Odkazy

Knihovny.cz E-zdroje

Chromosomal translocations involving the mixed lineage leukemia gene (MLL) located at 11q23 belong to common chromosomal abnormalities in both acute lymphoblastic (ALL) and acute myeloid leukemias (AML). It has been suggested that the mechanism of MLL leukemogenesis might be a result of a gain-of-function effect of the MLL fusion gene and simultaneous loss of function of one of the MLL alleles (haploinsufficiency). One of the recurrent translocations in AML-M5 involves chromosomal locus 10p12 and results in the MLL-AF10 fusion gene. Several mechanisms leading to MLL-AF10 fusion have been reported, and they have involved rearrangement of the 11q23 region. We present a detailed structural analysis of an AML case with an extra copy of the 5' part of MLL region and its insertion into the short arm of chromosome 10, resulting in an MLL-AF10 fusion without rearrangement of the MLL alleles on both chromosomes 11. Our observation supports a role for a simple MLL gain-of-function in leukemogenesis.

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$a Chromosomal translocations involving the mixed lineage leukemia gene (MLL) located at 11q23 belong to common chromosomal abnormalities in both acute lymphoblastic (ALL) and acute myeloid leukemias (AML). It has been suggested that the mechanism of MLL leukemogenesis might be a result of a gain-of-function effect of the MLL fusion gene and simultaneous loss of function of one of the MLL alleles (haploinsufficiency). One of the recurrent translocations in AML-M5 involves chromosomal locus 10p12 and results in the MLL-AF10 fusion gene. Several mechanisms leading to MLL-AF10 fusion have been reported, and they have involved rearrangement of the 11q23 region. We present a detailed structural analysis of an AML case with an extra copy of the 5' part of MLL region and its insertion into the short arm of chromosome 10, resulting in an MLL-AF10 fusion without rearrangement of the MLL alleles on both chromosomes 11. Our observation supports a role for a simple MLL gain-of-function in leukemogenesis.
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