Results 21 to 30 of about 81,803 (228)

BCR and its mutants, the reciprocal t(9;22)-associated ABL/BCR fusion proteins, differentially regulate the cytoskeleton and cell motility [PDF]

open access: yes, 2006
Background The reciprocal (9;22) translocation fuses the bcr (breakpoint cluster region) gene on chromosome 22 to the abl (Abelson-leukemia-virus) gene on chromosome 9.
Martin Ruthardt   +14 more
core   +2 more sources

Effect of HSP90AB1 and CC domain interaction on Bcr-Abl protein cytoplasm localization and function in chronic myeloid leukemia cells

open access: yesCell Communication and Signaling, 2021
Background The fusion oncoprotein Bcr-Abl is mostly located in the cytoplasm, which causes chronic myeloid leukemia (CML). After moving into the nucleus, the fusion protein can induce apoptosis of CML cells.
Yuhang Peng   +5 more
doaj   +1 more source

Interactions of CBL with BCR-ABL and CRKL in BCR-ABL-transformed Myeloid Cells [PDF]

open access: yesJournal of Biological Chemistry, 1997
The Philadelphia chromosome, detected in virtually all cases of chronic myelogenous leukemia (CML), is formed by a reciprocal translocation between chromosomes 9 and 22 that fuses BCR-encoded sequences upstream of exon 2 of c-ABL. The BCR-ABL fusion creates a gene whose protein product, p210BCR-ABL, has been implicated as the cause of the disease ...
A, Bhat   +5 more
openaire   +2 more sources

Targeting the oligomerization of BCR/ABL by membrane permeable competitive peptides inhibits the proliferation of Philadelphia Chromosome positive leukemic cells [PDF]

open access: yes, 2013
The BCR/ABL fusion protein is the hallmark of Philadelphia Chromosome positive (Ph+) leukemia. The constitutive activation of the ABL-kinase in BCR/ABL cells induces the leukemic phenotype.
Mahajna, Jamal   +8 more
core   +1 more source

I13 overrides resistance mediated by the T315I mutation in chronic myeloid leukemia by direct BCR-ABL inhibition

open access: yesFrontiers in Pharmacology, 2023
Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm caused by a BCR-ABL fusion gene. Imatinib has significantly improved the treatment of CML as a first-generation tyrosine kinase inhibitor (TKIs). The T315I mutant form of BCR-ABL is the most
Congying Gao   +6 more
doaj   +1 more source

Chronic myeloid leukemia stem cells are not dependent on Bcr-Abl kinase activity for their survival [PDF]

open access: yes, 2012
Recent evidence suggests CML stem cells are insensitive to kinase inhibitors and responsible for minimal residual disease in treated patients. We investigated whether CML stem cells, in a transgenic mouse model of CML-like disease or derived from ...
Allan, Elaine K.   +18 more
core   +1 more source

Bcr/Abl Interferes with the Fanconi Anemia/BRCA Pathway: Implications in the Chromosomal Instability of Chronic Myeloid Leukemia Cells [PDF]

open access: yes, 2010
Chronic myeloid leukemia (CML) is a malignant clonal disorder of the hematopoietic system caused by the expression of the BCR/ABL fusion oncogene. Although it is well known that CML cells are genetically unstable, the mechanisms accounting for this ...
Valeri, Antonio   +71 more
core   +2 more sources

Pterostilbene downregulates BCR/ABL and induces apoptosis of T315I-mutated BCR/ABL-positive leukemic cells

open access: yesScientific Reports, 2022
In this study, we examined the antileukemic effects of pterostilbene, a natural methylated polyphenol analog of resveratrol that is predominantly found in berries and nuts, using various human and murine leukemic cells, as well as bone marrow samples ...
Shohei Kawakami   +11 more
doaj   +1 more source

Association of Clinical Features and Hematological Laboratories between Ph (+)/BCR-ABL (+) Chronic Myeloid Leukemia and Other Type of Ph/BCR-ABL Chronic Myeloid Leukemia

open access: yesJurnal Penyakit Dalam Indonesia, 2018
Introduction. Patients with chronic phase Chronic Myeloid Leukemia (CML) at Hematology-Medical Oncology Clinic Department of Internal Medicine dr. Cipto Mangunkusumo National Hospital who haveperformed cytogenetic and RTPCR BCR-ABL examination showed: Ph
Wulyo Rajabto   +3 more
doaj   +1 more source

Suppression of autophagy by BCR ABL

open access: yesFrontiers in Bioscience, 2012
Imatinib and second generation BCR/ABL tyrosine kinase inhibitors (TKIs) serve now as standard therapies for patients with chronic myelogenous leukemia (CML); however, CML stem cells are intrinsically insensitive to the cell death-inducing effects of TKIs, allowing the persistence of a "reservoir" of BCR/ABL-expressing CML-initiating cells potentially ...
CALABRETTA, Bruno, SALOMONI, Paolo
openaire   +4 more sources

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