Results 121 to 130 of about 128,389 (322)

Unraveling the complexity of tyrosine kinase inhibitor-resistant populations by ultra-deep sequencing of the BCR-ABL kinase domain.

open access: yesBlood, 2013
In chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia, tyrosine kinase inhibitor (TKI) therapy may select for drug-resistant BCR-ABL mutants. We used an ultra-deep sequencing (UDS) approach to resolve qualitatively
S. Soverini   +25 more
semanticscholar   +1 more source

What Is Acute Myeloid Leukemia?

open access: yeseJHaem, Volume 6, Issue 3, June 2025.
ABSTRACT Background The recently published fifth edition of the World Health Organization (WHO) Classification and the International Consensus Classification (ICC) of myeloid neoplasms diverge in their definitions of acute myeloid leukemia (AML). Fundamentally, this current situation is problematic for two main reasons.
Daniel Mazza Matos   +1 more
wiley   +1 more source

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

open access: yesBMC Cancer, 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.
Puccetti Elena   +4 more
doaj   +1 more source

In Vivo Eradication of Human BCR/ABL-Positive Leukemia Cells With an ABLKinase Inhibitor [PDF]

open access: yes, 2017
BACKGROUND: The leukemia cells of approximately 95% of patients with chronic myeloid leukemia and 30%-50% of adult patients with acute lymphoblastic leukemia express the Bcr/Abl oncoprotein, which is the product of a fusion gene created by a chromosomal ...
Buchdunger, Elisabeth   +7 more
core  

Overcoming Bcr-Abl T315I mutation by combination of GNF-2 and ATP competitors in an Abl-independent mechanism

open access: yesBMC Cancer, 2012
Background Philadelphia positive leukemias are characterized by the presence of Bcr-Abl fusion protein which exhibits an abnormal kinase activity. Selective Abl kinase inhibitors have been successfully established for the treatment of Ph (+) leukemias ...
Khateb Mamduh   +7 more
doaj   +1 more source

Tumor angiogenic switch determines sustained proliferative malignant transformation in tumorigenesis and overlaps with para-inflammatory phenomena [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  

Identification of novel posttranscriptional targets of the BCR/ABL oncoprotein by ribonomics: requirement of E2F3 for BCR/ABL leukemogenesis

open access: yesBlood, 2008
Several RNA binding proteins (RBPs) have been implicated in the progression of chronic myelogenous leukemia (CML) from the indolent chronic phase to the aggressively fatal blast crisis. In the latter phase, expression and function of specific RBPs are aberrantly regulated at transcriptional or posttranslational levels by the constitutive kinase ...
Stefano Volinia   +13 more
openaire   +6 more sources

Minimal Residual Disease Detection: Implications for Clinical Diagnosis and Cancer Patient Treatment

open access: yesMedComm, Volume 6, Issue 6, June 2025.
Currently, a variety of methods such as flow cytometry, polymerase chain reaction, next‐generation sequencing, and other emerging methods are used for the detection of minimal residual disease, each of which has its own unique strengths and limitations and, more importantly, promising clinical applications.
Meiling Song   +10 more
wiley   +1 more source

bcr rearrangement and translocation of the c-abl oncogene in Philadelphia positive acute lymphoblastic leukemia [PDF]

open access: bronze, 1986
A De Klein   +9 more
openalex   +1 more source

Targeting Primitive Chronic Myeloid Leukemia Cells by Effective Inhibition of a New AHI-1–BCR-ABL–JAK2 Complex

open access: yesJournal of the National Cancer Institute, 2013
Background Imatinib mesylate (IM) induces clinical remission of chronic myeloid leukemia (CML). The Abelson helper integration site 1 (AHI-1) oncoprotein interacts with BCR-ABL and Janus kinase 2 (JAK2) to mediate IM response of primitive CML cells, but ...
Min Chen   +21 more
semanticscholar   +1 more source

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