Results 41 to 50 of about 128,389 (322)
Commentary to:Bortezomib treatment causes remission in a Ph+ ALL patient and reveals FoxO as a theranostic markerRajan Dewar, Sing-Tsung Chen, Heather Yeckes-Rodin, Kenneth Miller and Roya Khosravi ...
openaire +3 more sources
Background Dysregulation of long noncoding RNAs (lncRNAs) has been linked to various human cancers. Bcr-Abl oncogene that results from a reciprocal translocation between human chromosome 9 and 22, is associated with several hematological malignancies ...
Yun Ma+7 more
doaj +1 more source
Nanoparticle‐Mediated Targeted Protein Degradation: An Emerging Therapeutics Technology
Targeted protein degradation (TPD) has emerged as a powerful therapeutic approach, with numerous candidates molecules now advancing into clinical development. Recent innovations have incorporated nanoparticles to facilitate and enhance these degradation processes, yielding synergistic effects.
Andrew G. Baker+3 more
wiley +2 more sources
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
The Ins and Outs of Bcr-Abl Inhibition [PDF]
The development of inhibitors against Abl has changed the landscape for the treatment of chronic myelogenous leukemia (CML) and cancer in general. Beginning with the monumental discovery and approval of imatinib for CML, a second generation of inhibitors, nilotinib and dasatinib, has now gained approval for the treatment of CML.
E. Premkumar Reddy, Aneel K. Aggarwal
openaire +2 more sources
USP10 modulates the SKP2/Bcr-Abl axis via stabilizing SKP2 in chronic myeloid leukemia
Constitutive activation of tyrosine kinase Bcr-Abl is the leading cause of the development and progression of chronic myeloid leukemia (CML). Currently, the application of tyrosine kinase inhibitors (TKIs) targeting the Bcr-Abl is the primary therapy for
Yuning Liao+9 more
semanticscholar +1 more source
Mutations in the drug binding region of BCR-ABL lead to imatinib resistance during the management of chronic myeloid leukemia (CML). In our study, 62 Philadelphia positive (Ph+) CML patients showing conspicuous expression of BCR-ABL gene were treated ...
C. Chandrasekhar+2 more
semanticscholar +1 more source
BCR-ABL residues interacting with ponatinib are critical to preserve the tumorigenic potential of the oncoprotein [PDF]
Patients with chronic myeloid leukemia in whom tyrosine kinase inhibitors (TKIs) fail often present mutations in the BCR-ABL catalytic domain. We noticed a lack of substitutions involving 4 amino acids (E286, M318, I360, and D381) that form hydrogen ...
Alessandro Pandini+11 more
core +1 more source
Monitoring Twenty-Six Chronic Myeloid Leukemia Patients by BCR-ABL mRNA Level in Bone Marrow: A Single Hospital Experience [PDF]
Chronic myeloid leukemia (CML) is caused by the BCR-ABL oncogene. The Philadelphia chromosome (Ph) from a reciprocal translocation, t(9;22) (q34;q11) causes a fusion gene, BCR-ABL, that encodes a constitutively active tyrosine kinase. Treatment of CML by
Akagi, Tomoaki+9 more
core +1 more source
Chromosomal translocation occurs in some cancer cells, which results in the expression of aberrant oncogenic fusion proteins that include BCR‐ABL in chronic myelogenous leukemia (CML).
N. Shibata+10 more
semanticscholar +1 more source