Results 21 to 30 of about 117,497 (280)

Epigenetic dysregulation in chronic myeloid leukaemia: A myriad of mechanisms and therapeutic options [PDF]

open access: yes, 2018
The onset of global epigenetic changes in chromatin that drive tumor proliferation and heterogeneity is a hallmark of many forms cancer. Identifying the epigenetic mechanisms that govern these changes and developing therapeutic approaches to modulate ...
Koschmieder, Steffen, Vetrie, David
core   +1 more source

A Novel Inducible Mouse Model of MLL-ENL-driven Mixed-lineage Acute Leukemia

open access: yesHemaSphere, 2018
. Previous retroviral and knock-in approaches to model human t(11;19)+ acute mixed-lineage leukemia in mice resulted in myeloproliferation and acute myeloid leukemia not fully recapitulating the human disease.
Vaia Stavropoulou   +13 more
doaj   +1 more source

Downregulating Notch counteracts KrasG12D-induced ERK activation and oxidative phosphorylation in myeloproliferative neoplasm. [PDF]

open access: yes, 2019
The Notch signaling pathway contributes to the pathogenesis of a wide spectrum of human cancers, including hematopoietic malignancies. Its functions are highly dependent on the specific cellular context. Gain-of-function NOTCH1 mutations are prevalent in
Chang, Yuan-I   +20 more
core   +1 more source

BCL2A1a over-expression in murine hematopoietic stem and progenitor cells decreases apoptosis and results in hematopoietic transformation. [PDF]

open access: yesPLoS ONE, 2012
We previously reported the development of a lethal myeloid sarcoma in a non-human primate model utilizing retroviral vectors to genetically modify hematopoietic stem and progenitor cells.
Jean-Yves Métais   +6 more
doaj   +1 more source

Spicamycin and KRN5500 Induce Apoptosis in Myeloid and Lymphoid Cell Lines with Down‐regulation of Bcl‐2 Expression and Modulation of Promyelocytic Leukemia Protein

open access: yesJapanese journal of cancer research : Gann, 2000
Spicamycin is a potent inducer of differentiation of human myeloid leukemia cells (HL‐60) and murine myeloid leukemia cells (M1). One of the spicamycin derivatives, KRN5500, shows a broad spectrum of antitumor activity against human tumor xenografts in ...
W. Zhang   +13 more
semanticscholar   +1 more source

Cathepsin G Is Expressed by Acute Lymphoblastic Leukemia and Is a Potential Immunotherapeutic Target

open access: yesFrontiers in Immunology, 2018
Cathepsin G (CG) is a myeloid azurophil granule protease that is highly expressed by acute myeloid leukemia (AML) blasts and leukemia stem cells. We previously identified CG1 (FLLPTGAEA), a human leukocyte antigen-A2-restricted nonameric peptide derived ...
Maliha Khan   +20 more
doaj   +1 more source

BH3 mimetics in combination with nilotinib or ponatinib represent a promising therapeutic strategy in blast phase chronic myeloid leukemia

open access: yesCell Death Discovery, 2022
Dysregulation of the BCL-2 family is implicated in protecting chronic myeloid leukemia (CML) cells from intracellular damage and BCR::ABL1-inhibition with tyrosine kinase inhibitors (TKIs) and may be a viable therapeutic target in blast phase (BP-)CML ...
Narissa Parry   +7 more
doaj   +1 more source

Targeting BTK for the treatment of FLT3-ITD mutated acute myeloid leukemia [PDF]

open access: yes, 2015
Approximately 20% of patients with acute myeloid leukaemia (AML) have a mutation in FMS-like-tyrosine-kinase-3 (FLT3). FLT3 is a trans-membrane receptor with a tyrosine kinase domain which, when activated, initiates a cascade of phosphorylated proteins ...
A Puissant   +49 more
core   +2 more sources

Chronic myeloid leukemia with an e1a3 BCR-ABL fusion protein: transformation to lymphoid blast crisis

open access: yesBiomarker Research, 2014
Chronic myelogenous leukemia (CML) results from the neoplastic transformation of a hematopoietic stem cell. CML is cytogenetically characterized by the presence of the Philadelphia chromosome (Ph’).
J. Martinez-serra   +12 more
semanticscholar   +1 more source

Chlorpromazine eliminates acute myeloid leukemia cells by perturbing subcellular localization of FLT3-ITD and KIT-D816V

open access: yesNature Communications, 2020
Mutated receptor tyrosine kinases (MT-RTKs) such as internal tandem duplication of FMS-like tyrosine kinase 3 (FLT3 ITD) and a point mutation KIT D816V are driver mutations for acute myeloid leukemia (AML).
S. Rai   +10 more
semanticscholar   +1 more source

Home - About - Disclaimer - Privacy