Results 81 to 90 of about 125,674 (260)

Donor chimerism and bcr-abl gene status following non-myeloablative peripheral blood stem cell transplantation in chronic myeloid leukaemia patients in HUKM [PDF]

open access: yes, 2008
Objective: This study was done to determine the relationship between donor chimerism and the presence of bcr-abl gene in chronic myeloid leukaemia (CML) patients post-transplantation.
Cheong, Soon Keng   +4 more
core  

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

Multi-Lineage BCR-ABL Expression in Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia Is Associated With Improved Prognosis but No Specific Molecular Features

open access: yesFrontiers in Oncology, 2020
BackgroundRecently, various blood cell lineages expressing the BCR-ABL fusion gene in Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL) have been reported. However, the biological and clinical significance of these BCR-ABL lineages
Satoshi Nishiwaki   +14 more
doaj   +1 more source

Clinical implications of discordant early molecular responses in CML patients treated with imatinib [PDF]

open access: yes, 2019
A reduction in BCR-ABL1/ABL1IS transcript levels to <10% after 3 months or <1% after 6 months of tyrosine kinase inhibitor therapy are associated with superior clinical outcomes in chronic myeloid leukemia (CML) patients.
Accurso V.   +23 more
core   +1 more source

Clinical Applications of Phosphoproteomics: Illuminating Cancer Signaling and Enabling Rational Therapeutic Strategies

open access: yesCancer Science, EarlyView.
Mass spectrometry‐based phosphoproteomics for mechanistic dissection of cancer signaling pathways and uncovering therapeutic vulnerabilities. ABSTRACT Protein phosphorylation is a central post‐translational modification regulating cellular signaling, frequently dysregulated in cancer.
Hirokazu Shoji   +2 more
wiley   +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

Roles of TIF1β in Leukemic Stem Cell Through SETDB1‐Dependent and Independent Mechanisms

open access: yesCancer Science, EarlyView.
In leukemic stem cell, BCR::ABL cooperates with TIF1β to open chromatin at oncogenes and close chromatin at differentiation regulators, driving leukemic reprogramming. In TIF1β‐deficient stem cell, the loss of TIF1β inverts this balance, showing closed chromatin at oncogenes and open chromatin at differentiation regulators.
Mariko Morii, Sho Kubota, Goro Sashida
wiley   +1 more source

Contribution of BCR-ABL kinase domain mutations to imatinib mesylate resistance in Philadelphia chromosome positive Malaysian chronic myeloid leukemia patients

open access: yesHematology Reports, 2012
Development of resistance to imatinib mesylate (IM) in chronic myeloid leukemia (CML) patients is mediated by different mechanisms that can be classified as BCR-ABL dependent or BCR-ABL independent pathways.
Marjanu Hikmah Elias   +7 more
doaj   +1 more source

Kill Two Birds with One Stone: A Multifunctional Dual‐Targeting Protein Drug to Overcome Imatinib Resistance in Philadelphia Chromosome‐Positive Leukemia

open access: yesAdvanced Science, 2022
The Bcr/Abl plays a central role in Philadelphia chromosome‐positive (Ph+) leukemia because of the constitutively activated Abl tyrosine kinase and its downstream pathways.
Bohan Ma   +8 more
doaj   +1 more source

Celecoxib inhibits proliferation and survival of chronic myelogeous leukemia (CML) cells via AMPK-dependent regulation of β-catenin and mTORC1/2. [PDF]

open access: yes, 2016
CML is effectively treated with tyrosine kinase inhibitors (TKIs). However, the efficacy of these drugs is confined to the chronic phase of the disease and development of resistance to TKIs remains a pressing issue.
Calabretta, Bruno   +10 more
core   +2 more sources

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