Results 1 to 10 of about 128,389 (322)

Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I [PDF]

BMC Cancer, 2012
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, Metodieva Anna, Badura Susanne, Khateb Mamduh, Ruimi Nili, Najajreh Yousef, Ottmann Oliver, Mahajna Jamal, Ruthardt Martin   +8 more
doaj   +9 more sources

Pterostilbene downregulates BCR/ABL and induces apoptosis of T315I-mutated BCR/ABL-positive leukemic cells [PDF]

Scientific Reports, 2022
In this study, we examined the antileukemic effects of pterostilbene, a natural methylated polyphenol analog of resveratrol that is predominantly found in berries and nuts, using various human and murine leukemic cells, as well as bone marrow samples ...
Shohei Kawakami, Mitsuyo Tsuma-Kaneko, Masakazu Sawanobori, Tomoko Uno, Yoshihiko Nakamura, Hideyuki Matsuzawa, Rikio Suzuki, Makoto Onizuka, Takashi Yahata, Kazuhito Naka, Kiyoshi Ando, Hiroshi Kawada   +11 more
doaj   +5 more sources

Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-κB signaling and depleting Bcr-Abl [PDF]

Molecular Cancer, 2010
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
Jingxuan Pan
exaly   +6 more sources

Direct Binding of CRKL to BCR-ABL Is Not Required for BCR-ABL Transformation [PDF]

Blood, 1997
AbstractCRKL has previously been shown to be a major tyrosine phosphorylated protein in neutrophils of patients with BCR-ABL+ chronic myelogenous leukemia and in cell lines expressing BCR-ABL. CRKL and BCR-ABL form a complex as demonstrated by coimmunoprecipitation and are capable of a direct interaction in a yeast two-hybrid assay.
Conor Heaney, Kathryn S. Kolibaba, Arun Bhat, Tsukasa Oda, Sayuri Ohno, Shane Fanning, Brian J. Druker   +6 more
openalex   +5 more sources

Past, present, and future of Bcr-Abl inhibitors: from chemical development to clinical efficacy

Journal of Hematology and Oncology, 2018
Bcr-Abl inhibitors paved the way of targeted therapy epoch. Imatinib was the first tyrosine kinase inhibitor to be discovered with high specificity for Bcr-Abl protein resulting from t(9, 22)-derived Philadelphia chromosome.
Federico Rossari, Filippo Minutolo, Enrico Orciuolo   +2 more
exaly   +2 more sources

Nickel pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via both Bcr/Abl-dependent and Bcr/Abl-independent mechanisms [PDF]

Journal of Hematology & Oncology, 2016
Background Acquired imatinib (IM) resistance is frequently characterized by Bcr-Abl mutations that affect IM binding and kinase inhibition in patients with chronic myelogenous leukemia (CML).
Xiaoying Lan, Chong Zhao, Xin Chen, Peiquan Zhang, Dan Zang, Jinjie Wu, Jinghong Chen, Huidan Long, Li Yang, Hongbiao Huang, Bing Z. Carter, Xuejun Wang, Xianping Shi, Jinbao Liu   +13 more
doaj   +3 more sources

Reciprocal t(9;22) ABL/BCR fusion proteins: leukemogenic potential and effects on B cell commitment. [PDF]

PLoS ONE, 2009
BACKGROUND:t(9;22) is a balanced translocation, and the chromosome 22 breakpoints (Philadelphia chromosome--Ph+) determine formation of different fusion genes that are associated with either Ph+ acute lymphatic leukemia (Ph+ ALL) or chronic myeloid ...
Xiaomin Zheng, Claudia Oancea, Reinhard Henschler, Malcolm A S Moore, Martin Ruthardt   +4 more
doaj   +5 more sources

I13 overrides resistance mediated by the T315I mutation in chronic myeloid leukemia by direct BCR-ABL inhibition [PDF]

Frontiers in Pharmacology, 2023
Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm caused by a BCR-ABL fusion gene. Imatinib has significantly improved the treatment of CML as a first-generation tyrosine kinase inhibitor (TKIs). The T315I mutant form of BCR-ABL is the most
Congying Gao, Lei Zhang, Yun Xu, Xiangyu Ma, Peilei Chen, Zhe-Sheng Chen, Liuya Wei   +6 more
doaj   +2 more sources

Activity of a Specific Inhibitor of the BCR-ABL Tyrosine Kinase in the Blast Crisis of Chronic Myeloid Leukemia and Acute Lymphoblastic Leukemia with the Philadelphia Chromosome

New England Journal of Medicine, 2001
BACKGROUND BCR-ABL, a constitutively activated tyrosine kinase, is the product of the Philadelphia chromosome. This enzyme is present in virtually all cases of chronic myeloid leukemia (CML) throughout the course of the disease, and in 20 percent of ...
Hagop Kantarjian, Brian J Druker, Charles L Sawyers   +2 more
exaly   +2 more sources

An In-house Method for Molecular Monitoring of BCR-ABL [PDF]

Turkish Journal of Hematology, 2012
OBJECTIVE: At present in Turkey, centers that are able to give reliable RQ-PCR BCR-ABL results are limited in number. We aimed to describe a cost-effective, in-house method for BCR-ABL quantification and to illustrate an example for RQ-PCR validation ...
Hakkı Ogun Sercan, Ilgın Öztürk, Ceyda Çalışkan, Melek Pehlivan, Zeynep Sercan   +4 more
doaj   +4 more sources