Results 31 to 40 of about 81,803 (228)

Abcg2 overexpression represents a novel mechanism for acquired resistance to the multi-kinase inhibitor Danusertib in BCR-ABL-positive cells in vitro. [PDF]

open access: yes, 2011
The success of Imatinib (IM) therapy in chronic myeloid leukemia (CML) is compromised by the development of IM resistance and by a limited IM effect on hematopoietic stem cells.
Carsten Bokemeyer   +40 more
core   +2 more sources

A novel imatinib-upregulated long noncoding RNA plays a critical role in inhibition of tumor growth induced by Abl oncogenes

open access: yesMolecular Cancer, 2022
Background Dysregulation of long noncoding RNAs (lncRNAs) has been linked to various human cancers. Bcr-Abl oncogene that results from a reciprocal translocation between human chromosome 9 and 22, is associated with several hematological malignancies ...
Yun Ma   +7 more
doaj   +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

Out Foxing Bcr-Abl [PDF]

open access: yesCancer Biology & Therapy, 2011
Commentary to:Bortezomib treatment causes remission in a Ph+ ALL patient and reveals FoxO as a theranostic markerRajan Dewar, Sing-Tsung Chen, Heather Yeckes-Rodin, Kenneth Miller and Roya Khosravi ...
openaire   +2 more sources

The effect of the dual Src/Abl kinase inhibitor AZD0530 on Philadelphia positive leukaemia cell lines [PDF]

open access: yes, 2009
Background Imatinib mesylate, a selective inhibitor of Abl tyrosine kinase, is efficacious in treating chronic myeloid leukaemia (CML) and Ph+ acute lymphoblastic leukaemia (ALL).
Schwarz, Kerstin   +12 more
core   +1 more source

Induction of autophagy by Imatinib sequesters Bcr‐Abl in autophagosomes and down‐regulates Bcr‐Abl protein [PDF]

open access: yesAmerican Journal of Hematology, 2013
Chronic Myeloid Leukemia (CML) is a disease of hematopoietic stem cells which harbor the chimeric gene Bcr‐Abl. Expression levels of this constitutively active tyrosine kinase are critical for response to tyrosine kinase inhibitor treatment and also disease progression, yet the regulation of protein stability is poorly understood.
Elzinga, Baukje M.   +5 more
openaire   +5 more sources

Management of imatinib-resistant CML patients [PDF]

open access: yes, 2007
Imatinib has had marked impact on outcomes in chronic myelogenous leukemia (CML) patients for all stages of the disease and is endorsed by international treatment guidelines as the first line option.
Dempke, Wolfram, Linke, Rolf
core   +1 more source

A certified plasmid reference material for the standardisation of BCR-ABL1 mRNA quantification by real time quantitative PCR [PDF]

open access: yes, 2015
Serial quantification of BCR–ABL1 mRNA is an important therapeutic indicator in chronic myeloid leukaemia, but there is a substantial variation in results reported by different laboratories.
Mitterbauer, G.   +316 more
core   +3 more sources

Protein Kinase CK2: A Targetable BCR-ABL Partner in Philadelphia Positive Leukemias

open access: yesAdvances in Hematology, 2015
BCR-ABL-mediated leukemias, either Chronic Myeloid Leukemia (CML) or Philadelphia positive Acute Lymphoblastic Leukemia (ALL), are the paradigm of targeted molecular therapy of cancer due to the impressive clinical responses obtained with BCR-ABL ...
Alessandro Morotti   +6 more
doaj   +1 more source

Differential effects of selective inhibitors targeting the PI3K/AKT/mTOR pathway in acute lymphoblastic leukemia [PDF]

open access: yes, 2013
Purpose: Aberrant PI3K/AKT/mTOR signaling has been linked to oncogenesis and therapy resistance in various malignancies including leukemias. In Philadelphia chromosome (Ph) positive leukemias, activation of PI3K by dysregulated BCR-ABL tyrosine kinase ...
Oliver G Ottmann   +38 more
core   +1 more source

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