Results 21 to 30 of about 1,603 (142)
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
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 +2 more sources
Background Chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive (Ph+) acute lymphatic leukemia (Ph + ALL) are caused by the t(9;22), which fuses BCR to ABL resulting in deregulated ABL-tyrosine kinase activity.
Mian Afsar +8 more
doaj +1 more source
Induction of autophagy by Imatinib sequesters Bcr‐Abl in autophagosomes and down‐regulates Bcr‐Abl protein [PDF]
Chronic Myeloid Leukemia (CML) is a disease of hematopoietic stem cells which harbor the chimeric gene Bcr‐Abl. Expression levels of this constitutively active tyrosine kinase are critical for response to tyrosine kinase inhibitor treatment and also disease progression, yet the regulation of protein stability is poorly understood.
Elzinga, Baukje M. +5 more
openaire +5 more sources
Protein Kinase CK2: A Targetable BCR-ABL Partner in Philadelphia Positive Leukemias
BCR-ABL-mediated leukemias, either Chronic Myeloid Leukemia (CML) or Philadelphia positive Acute Lymphoblastic Leukemia (ALL), are the paradigm of targeted molecular therapy of cancer due to the impressive clinical responses obtained with BCR-ABL ...
Alessandro Morotti +6 more
doaj +1 more source
Background The BCR-ABL fusion protein is the key factor that results in the occurrence of chronic myeloid leukemia (CML). Imatinib (IM) is a targeted inhibitor of BCR-ABL to achieve complete remission.
Jianming Wang +5 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
Background Chronic myelogenous leukemia (CML) is characterized by the chimeric tyrosine kinase Bcr-Abl. Bcr-Abl-T315I is the notorious point mutation that causes resistance to imatinib and the second generation tyrosine kinase inhibitors, leading to poor
Cao Qi +5 more
doaj +1 more source
Background The Philadelphia chromosome (Ph), which leads to the creation and expression of the fusion gene product BCR-ABL, underlines the pathogenesis of chronic myelogenous leukemia (CML) and a fraction of adult and pediatric acute B-lymphoblastic ...
Xinhua Xiao +9 more
doaj +1 more source
T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities
T cell exhaustion limits immunotherapy efficacy. This article delineates its progression from stem‐like to terminally exhausted states, governed by persistent antigen, transcription factors, epigenetics, and metabolism. It maps the exhaustion landscape in the TME and proposes integrated reversal strategies, providing a translational roadmap to overcome
Yang Yu +7 more
wiley +1 more source

