Results 51 to 60 of about 68,946 (284)

DNA vaccination against bcr-abl-positive cells in mice

open access: yesInternational Journal of Oncology, 2009
A series of DNA vaccines based on the bcr-abl fusion gene were developed and tested in mice. Two mouse (BALB/c) bcr-abl-transformed cell lines, B210 and 12B1, which both expressed p210bcr-abl and were oncogenic for syngeneic animals but differed in some other respects, were used as a model system.
Vincent Lucansky   +4 more
openaire   +4 more sources

Imatinib and leptomycin B are effective in overcoming imatinib-resistance due to Bcr-Abl amplification and clonal evolution but not due to Bcr-Abl kinase domain mutation

open access: yesHaematologica, 2008
Treatment with imatinib is very effective in Bcr-Abl positive leukemia. However, development of resistance to this drug is a common phenomenon in late stage disease.
Rama Krishna Kancha   +5 more
doaj   +1 more source

Elucidation of mechanism of disease resistance and persistence in chronic myeloid leukemia. [PDF]

open access: yes, 2011
Chronic myeloid leukemia (CML) is a clonal disorder of the hematopoietic stem cell caused by the BCR-ABL receptor tyrosine kinase. Imatinib mesylate (IM) is an inhibitor of BCR-ABL and has been approved for the treatment of CML.
Kumari, Ashu
core   +1 more source

Multi-Lineage BCR-ABL Expression in Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia Is Associated With Improved Prognosis but No Specific Molecular Features

open access: yesFrontiers in Oncology, 2020
BackgroundRecently, various blood cell lineages expressing the BCR-ABL fusion gene in Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL) have been reported. However, the biological and clinical significance of these BCR-ABL lineages
Satoshi Nishiwaki   +14 more
doaj   +1 more source

MTSS1 is a critical epigenetically regulated tumor suppressor in CML [PDF]

open access: yes, 2015
Chronic myeloid leukemia (CML) is driven by malignant stem cells that can persist despite therapy. We have identified Metastasis suppressor 1 (Mtss1/MIM) to be downregulated in hematopoietic stem and progenitor cells from leukemic transgenic SCLtTA/Bcr ...
Braunschweig, T.   +18 more
core   +1 more source

A dual origin for Bcr-Abl gene translocation/fusion as dynamics of synergism of the hematopoietic stem cell and hemangioblast in chronic myeloid leukemia [PDF]

open access: yes, 2015
Contextual BCR-ABL tyrosine kinase over-activity determines in formulated fashion the emergence of proliferation and anti-apoptosis that arise largely as derived phenomena of otherwise homeostatic mechanisms of the c-ABL gene within hematopoietic ...
Agius, Lawrence M.
core   +1 more source

Silencing of suppressor of cytokine signaling-3 due to methylation results in phosphorylation of STAT3 in imatinib resistant BCR-ABL positive chronic myeloid leukemia cells.

open access: yesAsian Pacific Journal of Cancer Prevention, 2014
BACKGROUND Silencing due to methylation of suppressor of cytokine signaling-3 (SOCS-3), a negative regulator gene for the JAK/STAT signaling pathway has been reported to play important roles in leukemogenesis.
H. A. Al-Jamal   +5 more
semanticscholar   +1 more source

The Bcr-Abl kinase inhibitor INNO-406 induces autophagy and different modes of cell death execution in Bcr-Abl-positive leukemias [PDF]

open access: yesCell Death & Differentiation, 2008
Bcr-Abl tyrosine kinase (TK) inhibitors are promising therapeutic agents for Bcr-Abl-positive (Bcr-Abl(+)) leukemias. Although they are known to promote caspase-mediated apoptosis, it remains unclear whether caspase-independent cell death-inducing mechanisms are also triggered.
Y. Kamitsuji   +18 more
semanticscholar   +3 more sources

The chronic myeloid leukemia stem cell: stemming the tide of persistence [PDF]

open access: yes, 2017
Chronic myeloid leukaemia (CML) is caused by the acquisition of the tyrosine kinase BCR-ABL1 in a haemopoietic stem cell (HSC), transforming it into a leukaemic stem cell (LSC) that self-renews, proliferates and differentiates to give rise to a ...
Holyoake, Tessa L., Vetrie, David
core   +1 more source

Hypoxia-Like Signatures Induced by BCR-ABL Potentially Alter the Glutamine Uptake for Maintaining Oxidative Phosphorylation. [PDF]

open access: yesPLoS ONE, 2016
The Warburg effect is probably the most prominent metabolic feature of cancer cells, although little is known about the underlying mechanisms and consequences. Here, we set out to study these features in detail in a number of leukemia backgrounds.
Pallavi Sontakke   +8 more
doaj   +1 more source

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