Two cases were classified by immunological phenotyping as acute null-AL(L), one case as pre B-cell ALL (CD10+) and two cases expressed both immature B-cell markers CD19 and CD24 and myelomonocytic markers CD15 and CD14, suggesting mixed lineage leukemia.
Two cases were classified by immunological phenotyping as acute null-AL(L), one case as pre B-cell ALL (CD10+) and two cases expressed both immature B-cell markers CD19 and CD24 and myelomonocytic markers CD15 and CD14, suggesting mixed lineage leukemia.
Two cases were classified by immunological phenotyping as acute null-AL(L), one case as pre B-cell ALL (CD10+) and two cases expressed both immature B-cell markers CD19 and CD24 and myelomonocytic markers CD15 and CD14, suggesting mixed lineage leukemia.
We speculate that the other MLL-related infant leukemias may also develop in utero, and that the rearrangements may occur consistently in stem cells or early precursor cells, accounting for the frequency of mixed-lineage leukemia in infants.
To map potential transcriptional activation or repression domains of the MLL protein, yeast GAL4 DNA-binding domain and MLL hybrid protein-expressing plasmids were cotransfected with chloramphenicol acetyltransferase reporter plasmids in a transient transfection system.
We analyzed B-CLL samples for loss of heterozygosity (LOH) using microsatellite markers located at the ATM (D11S2179), mixed-lineage leukemia (MLL; D11S1356), and BCL1 (D11S987) loci, all of which are located around 11q23.
We analyzed B-CLL samples for loss of heterozygosity (LOH) using microsatellite markers located at the ATM (D11S2179), mixed-lineage leukemia (MLL; D11S1356), and BCL1 (D11S987) loci, all of which are located around 11q23.
The resulting chimeric protein consists of AT-hooks, methyltransferase, and transcription repressor domains of MLL in addition to the AF3p21 proline-rich domain and NLS but not the AF3p21 SH3 domain.
However, 11 adults with AML, and one adult with moab 7.1-positive CD7+ CD56+ myeloid/natural killer cell precursor acute leukemia were negative forMLL rearrangements as proved by Southern blot analysis.
We cloned the MLL fusion partner gene from leukemic cells from a therapy-related leukemia patient with t(3;11)(p21;q23) and designated the gene AF3p21.
Some of the MLL fusion partner genes encode transcription factors; others encode small GTP binding protein interacting molecules or cytoplasmic proteins, the functions of which are presently unknown.
Some of the MLL fusion partner genes encode transcription factors; others encode small GTP binding protein interacting molecules or cytoplasmic proteins, the functions of which are presently unknown.
Some of the MLL fusion partner genes encode transcription factors; others encode small GTP binding protein interacting molecules or cytoplasmic proteins, the functions of which are presently unknown.
Some of the MLL fusion partner genes encode transcription factors; others encode small GTP binding protein interacting molecules or cytoplasmic proteins, the functions of which are presently unknown.
Some of the MLL fusion partner genes encode transcription factors; others encode small GTP binding protein interacting molecules or cytoplasmic proteins, the functions of which are presently unknown.