Results 21 to 30 of about 9,645 (157)

Influence of BCR/ABL fusion proteins on the course of Ph leukemias.

open access: yesActa Biochimica Polonica, 2004
The hallmark of chronic myeloid leukemia (CML) and a subset of acute lymphoblastic leukemia (ALL) is the presence of the Philadelphia chromosome as a result of the t(9;22) translocation. This gene rearrangement results in the production of a novel oncoprotein, BCR/ABL, a constitutively active tyrosine kinase.
S. S. Maliuta   +3 more
openaire   +4 more sources

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

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

BCR-ABL1 tyrosine kinase sustained MECOM expression in chronic myeloid leukaemia [PDF]

open access: yes, 2012
MECOM oncogene expression correlates with chronic myeloid leukaemia (CML) progression. Here we show that the knockdown of MECOM (E) and MECOM (ME) isoforms reduces cell division at low cell density, inhibits colony-forming cells by 34% and moderately ...
Alzuherri   +53 more
core   +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

Targeting the phosphatidylinositol 3-kinase/Akt/mechanistic target of rapamycin signaling pathway in B-lineage acute lymphoblastic leukemia: An update [PDF]

open access: yes, 2018
Despite considerable progress in treatment protocols, B-lineage acute lymphoblastic leukemia (B-ALL) displays a poor prognosis in about 15–20% of pediatric cases and about 60% of adult patients. In addition, life-long irreversible late effects from chemo-
Capitani, Silvano   +6 more
core   +1 more source

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

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