Results 41 to 50 of about 16,106 (168)

Identification of genes transcriptionally responsive to the loss of MLL fusions in MLL-rearranged acute lymphoblastic leukemia. [PDF]

PLoS ONE, 2015
MLL-rearranged acute lymphoblastic leukemia (ALL) in infants (
Marieke H van der Linden, Lidija Seslija, Pauline Schneider, Emma M C Driessen, Patricia Garrido Castro, Dominique J P M Stumpel, Eddy van Roon, Jasper de Boer, Owen Williams, Rob Pieters, Ronald W Stam   +10 more
doaj   +1 more source

Bone marrow mesenchymal stem cells from infants with MLL-AF4+ acute leukemia harbor and express the MLL-AF4 fusion gene [PDF]

Journal of Experimental Medicine, 2009
MLL-AF4 fusion is a hallmark genetic abnormality in infant B-acute lymphoblastic leukemia (B-ALL) known to arise in utero. The cellular origin of leukemic fusion genes during human development is difficult to ascertain. The bone marrow (BM) microenvironment plays an important role in the pathogenesis of several hematological malignances. BM mesenchymal
Menendez, Pablo, Catalina, Purificacion, Rodriguez, Rene, Melen, Gustavo, Bueno, Clara, Arriero, Mar, García-Sanchez, Felix, Lassaletta, Alvaro, García Sanz, Ramón, García-Castro, Javier   +9 more
openaire   +4 more sources

Harnessing the hidden antitumor power of the MLL-AF4 oncogene to fight leukemia. [PDF]

Cancer Cell, 2014
It is unclear whether the antiproliferative/proapoptotic activity of oncogenes can be pharmacologically reactivated in cancer cells. In this issue of Cancer Cell, Liu and colleagues report that a proteasome inhibitor reactivates an MLL-AF4 controlled antitumor program to kill leukemia cells in an oncogene dose- and cell type-dependent manner.
Matkar S, Katona BW, Hua X.
europepmc   +4 more sources

MiR-130b and miR-128a are essential lineage-specific co-drivers of t(4;11) MLL-AF4 acute leukemia.

Blood, 2021
t(4;11) MLL-AF4 acute leukemia is one of the most aggressive malignancies in the infant and pediatric population, yet we have little information on the molecular mechanisms responsible for disease progression.
C. Malouf, E. Antunes, M. O'Dwyer, H. Jakobczyk, F. Sahm, Sophie-Luise Landua, Richard A. Anderson, A. Soufi, C. Halsey, K. Ottersbach   +9 more
semanticscholar   +1 more source

Reconstructing the Disease Model and Epigenetic Networks for MLL-AF4 Leukemia [PDF]

Cancer Cell, 2008
The lack of a proper animal model has impeded understanding of the molecular mechanism of leukemia associated with the MLL-AF4 fusion. In this issue of Cancer Cell, Krivtsov et al. report a much-improved murine Mll-AF4 model and propose a molecular link with H3K79 methylation mediated by the histone methyltransferase DOT1L.
Zeisig, B B, Chueng, N, Yeung, J, So, C W   +3 more
openaire   +2 more sources

MLL-AF4 driven leukemogenesis: what are we missing? [PDF]

Cell Res, 2012
Infant pro-B acute lymphoblastic leukemia (ALL) harboring MLL-AF4 fusion proteins instigated by chromosomal translocation t(4;11), represents an aggressive, high-risk type of childhood leukemia, characterized by a very brief disease latency and undisputedly originates in utero.
Stam RW.
europepmc   +4 more sources

Overexpression of the catalytically impaired Taspase1 T234V or Taspase1 D233A variants does not have a dominant negative effect in T(4;11) leukemia cells. [PDF]

PLoS ONE, 2012
BACKGROUND: The chromosomal translocation t(4;11)(q21;q23) is associated with high-risk acute lymphoblastic leukemia of infants. The resulting AF4•MLL oncoprotein becomes activated by Taspase1 hydrolysis and is considered to promote oncogenic ...
Carolin Bier, Rouven Hecht, Lena Kunst, Sabine Scheiding, Désirée Wünsch, Dorothée Goesswein, Günter Schneider, Oliver H Krämer, Shirley K Knauer, Roland H Stauber   +9 more
doaj   +1 more source

HBO1-MLL interaction promotes AF4/ENL/P-TEFb-mediated leukemogenesis

eLife, 2021
Leukemic oncoproteins cause uncontrolled self-renewal of hematopoietic progenitors by aberrant gene activation, eventually causing leukemia. However, the molecular mechanism underlying aberrant gene activation remains elusive.
Satoshi Takahashi, Akinori Kanai, Hiroshi Okuda, Ryo Miyamoto, Yosuke Komata, Takeshi Kawamura, Hirotaka Matsui, Toshiya Inaba, Akifumi Takaori-Kondo, Akihiko Yokoyama   +9 more
doaj   +1 more source

Targeting IGF2BP3 Enhances Anti-Leukemic Effects of Menin-MLL Inhibition in MLL-AF4 Leukemia

Blood, 2023
Background: MLL-rearranged leukemias are a clinically challenging and biologically unique subtype of leukemias associated with poor prognosis.
Tasha L. Lin, Alexander J Ritter, A. K. Jaiswal, Jenna Reppas, T. Tran, Zachary T Neeb, Sol Katzman, Michelle L. Thaxton, Amanda Cohen, Jeremy R. Sanford, Dinesh S. Rao   +10 more
semanticscholar   +1 more source

Epigenetic regulator genes direct lineage switching in MLL-AF4 leukaemia

bioRxiv, 2021
The fusion gene MLL-AF4 defines a high-risk subtype of pro-B acute lymphoblastic leukaemia. However, relapse can be associated with a switch from acute lymphoblastic to acute myeloid leukaemia.
R. Tirtakusuma, K. Szoltysek, P. Milne, V. Grinev, A. Ptasinska, C. Meyer, S. Nakjang, J. Hehir-Kwa, D. Williamson, P. Cauchy, Salam A. Assi, M. Imperato, F. Vogiatzi, Shan Lin, M. Wunderlich, J. Stutterheim, A. Komkov, E. Zerkalenkova, Paul Evans, H. McNeill, A. Elder, N. Martinez-Soria, S. Fordham, Yuzhe Shi, L. Russell, D. Pal, Alex Smith, Z. Kingsbury, J. Becq, C. Eckert, O. Haas, P. Carey, S. Bailey, R. Skinner, N. Miakova, M. Collin, V. Bigley, M. Haniffa, R. Marschalek, C. Harrison, C. Cargo, D. Schewe, Y. Olshanskaya, M. Thirman, P. Cockerill, J. Mulloy, H. Blair, J. Vormoor, J. Allan, C. Bonifer, O. Heidenreich, S. Bomken   +51 more
semanticscholar   +1 more source