scholarly journals Deletion of Pten in CD45-expressing cells leads to development of T-cell lymphoblastic lymphoma but not myeloid malignancies

Blood ◽  
2016 ◽  
Vol 127 (15) ◽  
pp. 1907-1911 ◽  
Author(s):  
Cristina Mirantes ◽  
Maria Alba Dosil ◽  
David Hills ◽  
Jian Yang ◽  
Núria Eritja ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Mouse Model ◽  
Lymphoblastic Leukemia ◽  
Hematopoietic Cells ◽  
Hematologic Malignancies ◽  
Lymphoblastic Lymphoma ◽  
Key Points ◽  
Pten Deletion ◽  
Cell Acute Lymphoblastic Leukemia

Key Points CD45-driven expression of Cre generates the first mouse model that allows specific and exclusive deletion of Pten in hematopoietic cells. Pten deletion in CD45-expressing cells causes T-cell acute lymphoblastic leukemia, but no other hematologic malignancies.

scholarly journals RUNX1 is required for oncogenic Myb and Myc enhancer activity in T-cell acute lymphoblastic leukemia

Blood ◽  
2017 ◽  
Vol 130 (15) ◽  
pp. 1722-1733 ◽  
Author(s):  
AHyun Choi ◽  
Anuradha Illendula ◽  
John A. Pulikkan ◽  
Justine E. Roderick ◽  
Jessica Tesell ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Hematopoietic Cells ◽  
Enhancer Activity ◽  
Key Points ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Normal Human

Key Points RUNX1 maintains Myb and Myc enhancer activity and is required for leukemogenesis in vivo. RUNX1 inhibition impairs the growth of primary T-ALL patient cells without an effect on normal human hematopoietic cells.

PTEN microdeletions in T-cell acute lymphoblastic leukemia are caused by illegitimate RAG-mediated recombination events

Blood ◽  
2014 ◽  
Vol 124 (4) ◽  
pp. 567-578 ◽  
Author(s):  
Rui D. Mendes ◽  
Leonor M. Sarmento ◽  
Kirsten Canté-Barrett ◽  
Linda Zuurbier ◽  
Jessica G. C. A. M. Buijs-Gladdines ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Human T Cell ◽  
Key Points ◽  
Inactivation Mechanism ◽  
Cell Acute Lymphoblastic Leukemia

Key Points Microdeletions represent an additional inactivation mechanism for PTEN in human T-cell acute lymphoblastic leukemia. PTEN microdeletions are RAG-mediated aberrations.

scholarly journals Homeobox protein TLX3 activates miR-125b expression to promote T-cell acute lymphoblastic leukemia

2017 ◽  
Vol 1 (12) ◽  
pp. 733-747 ◽  
Author(s):  
Laurent Renou ◽  
Pierre-Yves Boelle ◽  
Caroline Deswarte ◽  
Salvatore Spicuglia ◽  
Aissa Benyoucef ◽  
...  
Keyword(s):  
T Cells ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Host Gene ◽  
Key Points ◽  
Homeobox Protein ◽  
Cell Acute Lymphoblastic Leukemia

Key Points TLX3 transactivates LINC00478, the host gene of oncogenic miR-125b-2 in T-ALL. TLX3 and miR-125b contribute to the differentiation arrest and the expansion of transformed T cells.

scholarly journals JAK3 mutants transform hematopoietic cells through JAK1 activation, causing T-cell acute lymphoblastic leukemia in a mouse model

Blood ◽  
2014 ◽  
Vol 124 (20) ◽  
pp. 3092-3100 ◽  
Author(s):  
Sandrine Degryse ◽  
Charles E. de Bock ◽  
Luk Cox ◽  
Sofie Demeyer ◽  
Olga Gielen ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Lymphoblastic Leukemia ◽  
Mouse Model ◽  
Lymphoblastic Leukemia ◽  
Marrow Transplant ◽  
Selective Inhibitor ◽  
Mouse Bone Marrow ◽  
Key Points ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Transplant Model

Key Points JAK3 pseudokinase mutants require JAK1 for their transforming potential. JAK3 mutants cause T-ALL in a mouse bone marrow transplant model and respond to tofacitinib, a JAK3-selective inhibitor.

scholarly journals Bone marrow sites differently imprint dormancy and chemoresistance to T-cell acute lymphoblastic leukemia

2017 ◽  
Vol 1 (20) ◽  
pp. 1760-1772 ◽  
Author(s):  
Xavier Cahu ◽  
Julien Calvo ◽  
Sandrine Poglio ◽  
Nais Prade ◽  
Benoit Colsch ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Lymphoblastic Leukemia ◽  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Key Points ◽  
Cell Acute Lymphoblastic Leukemia

Key Points BM niches differentially support T-ALL. BM niches differentially protect T-ALL cells from chemotherapy.

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