Results 31 to 40 of about 19,722 (182)

Does thyroid dysfunction happen in CML patients receiving Imatinib for treatment? [PDF]

open access: yesReviews in Clinical Medicine, 2015
Chronic myelogenous leukemia is a myeloproliferative disorder presenting with anemia, elevated blood granulocytosis and the presence of immature granulocytes, basophilia, frequently thrombocytosis and spleen enlargement.
Hossein Rahimi   +2 more
doaj   +3 more sources

Association of HLA Class I and Class II genes with bcr-abl transcripts in leukemia patients with t(9;22) (q34;q11)

open access: yesBMC Cancer, 2004
Background Based on the site of breakpoint in t(9;22) (q34;q11), bcr-abl fusion in leukemia patients is associated with different types of transcript proteins.
Cano Pedro   +2 more
doaj   +1 more source

p185BCR/ABL has a lower sensitivity than p210BCR/ABL to the allosteric inhibitor GNF-2 in Philadelphia chromosome-positive acute lymphatic leukemia

open access: yesHaematologica, 2012
Background The t(9;22) translocation leads to the formation of the chimeric breakpoint cluster region/c-abl oncogene 1 (BCR/ABL) fusion gene on der22, the Philadelphia chromosome. The p185BCR/ABL or the p210BCR/ABL fusion proteins are encoded as a result
Afsar A. Mian   +5 more
doaj   +1 more source

Detection of derivative 9 deletion by BCR-ABL fluorescence in-situ hybridization signal pattern to evaluate treatment response in CML patients [PDF]

open access: yesArchive of Oncology, 2009
Background: To evaluate prognostic effect of submicroscopic deletions involving breakage and fusion points of the derivative chromosome 9 and 22 in chronic myeloid leukemia in untreated patients and their follow up samples to correlate with disease ...
Bakshi Sonal R.   +8 more
doaj   +1 more source

Flow Cytometric Detection of BCR-ABL Fusion Proteins in Leukemia Patients Via An Immunobead Assay [PDF]

open access: yesBlood, 2008
Abstract The BCR-ABL fusion gene results from the translocation t(9;22). It is the hallmark of chronic myeloid leukemia (CML) and is present in a poor-risk subgroup of precursor B cell acute lymphoblastic leukemia (ALL), which represents 25–30% of adult ALL and 3–5% of childhood ALL.
Flores Montero Juan Alejandro   +12 more
openaire   +2 more sources

Translational regulation of GPx-1 and GPx-4 by the mTOR pathway.

open access: yesPLoS ONE, 2014
Glutathione peroxidase activity was previously determined to be elevated in lymphocytes obtained from patients treated with the Bcr-Abl kinase inhibitor imatinib mesylate.
Emily N Reinke   +4 more
doaj   +1 more source

Tyrosine kinase chromosomal translocations mediate distinct and overlapping gene regulation events

open access: yesBMC Cancer, 2011
Background Leukemia is a heterogeneous disease commonly associated with recurrent chromosomal translocations that involve tyrosine kinases including BCR-ABL, TEL-PDGFRB and TEL-JAK2. Most studies on the activated tyrosine kinases have focused on proximal
Kim Hani   +6 more
doaj   +1 more source

The tyrosine phosphatase TC48 interacts with and inactivates the oncogenic fusion protein BCR-Abl but not cellular Abl

open access: yesBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2013
The chimeric oncoprotein BCR-Abl exhibits deregulated protein tyrosine kinase activity and is responsible for the pathogenesis of certain human leukemias, such as chronic myelogenous leukemia. The activities of cellular Abl (c-Abl) and BCR-Abl are stringently regulated and the cellular mechanisms involved in their inactivation are poorly understood ...
Kotagiri Sasikumar   +3 more
openaire   +3 more sources

Two different point mutations in ABL gene ATP-binding domain conferring Primary Imatinib resistance in a Chronic Myeloid Leukemia (CML) patient: A case report

open access: yesBiological Procedures Online, 2004
Imatinib (Gleevec) is the effective therapy for BCR-ABL positive CML patients. Point mutations have been detected in ATP-binding domain of ABL gene which disturbs the binding of Gleevec to this target leading to resistance.
Iqbal Zafar   +2 more
doaj   +1 more source

Mouse embryonic stem cells that express a NUP98–HOXD13 fusion protein are impaired in their ability to differentiate and can be complemented by BCR-ABL [PDF]

open access: yesLeukemia, 2007
NUP98-HOXD13 (NHD13) fusions have been identified in patients with myelodysplastic syndrome, acute myelogenous leukemia and chronic myeloid leukemia blast crisis. We generated 'knock-in' mouse embryonic stem (ES) cells that express a NHD13 fusion gene from the endogenous murine NUP98 promoter, and used an in vitro differentiation system to ...
Slape, C.   +4 more
openaire   +4 more sources

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