Translocations involving the Mixed Lineage Leukemia (MLL) gene at 11q23 are found in both acute lymphoblastic leukemia (ALL) and acute myeloblastic leukemia (AML), but have different prognostic implications depending on the phenotype of the leukemia in de novo pediatric cases.
Diverse pathways should be considered in this transformation process: although therapeutic induction of ALL is extremely rare and no MLL/11q23 rearrangement was detected by chromosome banding analyses and interphase fluorescence in situ hybridization (FISH), T-lineage ALL might have been caused by HU therapy for the CMPD.
We studied 86 newly diagnosed adults entered on an ALL clinical trial to investigate the incidence of MLL gene rearrangements and to determine clinical, morphologic, immunologic and cytogenetic characteristics of such patients.
Depletion of JMJD1C impairs expansion and colony formation of human leukemic cell lines, with the strongest effect observed in the MLL-rearranged ALL cell line SEM.
Although MLL gene rearrangements are generally associated with a dismal outcome in ALL, two distinct subsets with MLL-ENL fusions have an excellent prognosis.
We report the different presentation features and clinical outcome between two identical infant twins with acute lymphoblastic leukaemia with a shared clonal disease and MLL gene rearrangement.
To validate BLI for the detection of a therapeutic response, systemic treatment with an anti-luciferase-targeting siRNA (siLuc) complexed with cationic nanoparticles was administered to mice with MLL-AF4 acute lymphoblastic leukemia.
However, since this disease is highly represented in the infant and paediatric population, this review will focus on this demographic group and summarise the biological, clinical and epidemiological knowledge on B cell acute lymphoblastic leukaemia of four well characterised subtypes: t(4;11) MLL-AF4, t(12;21) ETV6-RUNX1, t(1;19) E2A-PBX1 and t(9;22) BCR-ABL1.
Therapy-related B lymphoblastic leukemia with t(4;11)(q21;q23)/AF4-MLL in a patient with mantle cell lymphoma after recent aggressive chemotherapy: a unique case report.
ALL related to prior cytotoxic therapy (t-ALL) appears to be a distinct entity when compared to the de novo ALL, with characteristics including older age at the time of onset, female predominance and leukemia genetics enriched with KMT2A (MLL) gene rearrangement and chromosomes 5/7 abnormalities.
Previous studies on concordant acute lymphoblastic leukemia (ALL) in identical twins have identified the leukemia as monoclonal with MLL or ETV6-RUNX1 gene fusion as early or initiating events in utero.
Fms-like tyrosine kinase 3 (FLT3) is highly expressed in acute lymphoblastic leukemia with the mixed-lineage leukemia (MLL) gene rearrangement refractory to chemotherapy.
The translocation t(9;11)(p22;q23), which results in the fusion of MLL to AF9, is the most common of the 11q23 chromosomal abnormalities observed in de novo acute myeloid leukemia (AML), in therapy related leukemia (t-AML), and rarely in acute lymphoblastic leukemia (ALL).
Our findings show how amlexanox degrades the resistance of <i>KMT2A/AFF1</i>-positive ALL to TNFα by downregulating S100A6 expression, with immediate potential implications for improving clinical management of <i>KMT2A/AFF1</i>-positive ALL.<i></i>.
Frozen/thawed CARCIK-CD19 remained fully functional both in vitro and in an established patient-derived xenograft (PDX) of MLL-ENL rearranged acute lymphoblastic leukemia (ALL).
These combined data demonstrate that panobinostat cross-inhibits multiple epigenetic pathways, ultimately contributing to its highly efficacious targeting of MLL-rearranged ALL.
The MLL gene, located at chromosome 11, band q23, is frequently disrupted by a variety of chromosomal rearrangements that occur in acute lymphoblastic leukemias and in a subset of de novo and secondary acute myeloid leukemias.
Detectable by fluorescence in situ hybridization (FISH), these losses of sequence include deletion of the 5' region of the ABL gene and the 3' region of BCR in chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL), as well as the 5' region of ETO in acute myeloid leukemia (AML) French-American-British type M2 associated with t(8;21), 3'MLL in AML and ALL, and 3' core-binding factor beta (CBFbeta) in AML associated with inv(16).