Author pages are created from data sourced from our academic publisher partnerships and public sources.
Share This Author
LCX, leukemia-associated protein with a CXXC domain, is fused to MLL in acute myeloid leukemia with trilineage dysplasia having t(10;11)(q22;q23).
- R. Ono, T. Taki, T. Taketani, M. Taniwaki, Hajime Kobayashi, Y. Hayashi
- BiologyCancer research
- 15 July 2002
The MLL gene on 11q23 was fused to the LCX (leukemia-associated protein with a CXXC domain) gene on 10q22 in a de novoadult AML-M2 with trilineage dysplasia having t(10;11)(q22;q23), which suggests that these fusion proteins are involved in the pathogenesis of 11Q23-associated leukemia through similar mechanisms.
FLT3 mutations in the activation loop of tyrosine kinase domain are frequently found in infant ALL with MLL rearrangements and pediatric ALL with hyperdiploidy.
Results suggested that FLT3-D835/I836 mutations are one of the second genetic events in infant ALL with MLL rearrangements or pediatric ALL with hyperdiploidy.
AF5q31, a newly identified AF4-related gene, is fused to MLL in infant acute lymphoblastic leukemia with ins(5;11)(q31;q13q23).
- T. Taki, H. Kano, M. Taniwaki, M. Sako, M. Yanagisawa, Y. Hayashi
- Biology, MedicineProceedings of the National Academy of Sciences…
- 7 December 1999
AF5q31 and AF4 might define a new family particularly involved in the pathogenesis of 11q23-associated-ALL, which is associated with extremely poor prognosis as compared with other 11Q23 translocations.
Dimerization of MLL fusion proteins and FLT3 activation synergize to induce multiple-lineage leukemogenesis.
It is demonstrated that the fusion partner-mediated homo-oligomerization of MLL-SEPT6 is essential to immortalize hematopoietic progenitors in vitro and direct evidence for a multistep leukemogenesis mediated by MLL fusion proteins is shown.
SEPTIN6, a human homologue to mouse Septin6, is fused to MLL in infant acute myeloid leukemia with complex chromosomal abnormalities involving 11q23 and Xq24.
AML with the MLL-SEPTIN6 fusion gene is a subset of infant AML, which differentiate into the myeloid lineage, although AML with other MLL fusion genes is capable of differentiating into theMyelomonocytic or monocytic lineage.
Adenoviral E1A-associated protein p300 is involved in acute myeloid leukemia with t(11;22)(q23;q13).
It is identified here that the p300 gene is fused to the MLL gene and that in-frame MLL-p300 fusion protein is generated in acute myeloid leukemia (AML) with t(11; 22)(q23; q13).
Tandem duplication of the FLT3 gene is found in acute lymphoblastic leukaemia as well as acute myeloid leukaemia but not in myelodysplastic syndrome or juvenile chronic myelogenous leukaemia in…
The results suggest that tandem duplication is involved in ALL in addition to AML, but not in childhood MDS or JCML, and that childhood AML patients with the tandem duplication have a poor prognosis.
AF17q25, a putative septin family gene, fuses the MLL gene in acute myeloid leukemia with t(11;17)(q23;q25).
The results suggest that AF17q25 and hCDCrel might define a new septin family particularly involved in the pathogenesis of 11q23-associated leukemia.
FBXW7 and NOTCH1 mutations in childhood T cell acute lymphoblastic leukaemia and T cell non‐Hodgkin lymphoma
Five‐year event‐free survival and overall survival for patients with FBXW7 and/or NOTCH1 mutations were 95·5% (95% CI, 71·9–99·4%) and 100% respectively, suggesting that T‐ALL patients withFBXW8 and/ or NOTCH2 mutation represent a good prognosis compared to those without.
Mutations of the PTPN11 and RAS genes in rhabdomyosarcoma and pediatric hematological malignancies
The data suggest that mutations of PTPN11 as well as RAS play a role in the pathogenesis of not only myeloid hematological malignancies but also a subset of RMSmalignancies.