Results 1 to 10 of about 68,946 (284)

Differential roles of STAT1 and STAT2 in the sensitivity of JAK2V617F- vs. BCR-ABL-positive cells to interferon alpha [PDF]

Journal of Hematology & Oncology, 2019
Background Interferon alpha (IFNa) monotherapy is recommended as the standard therapy in polycythemia vera (PV) but not in chronic myeloid leukemia (CML). Here, we investigated the mechanisms of IFNa efficacy in JAK2V617F- vs.
Claudia Schubert, Manuel Allhoff, Stefan Tillmann, Tiago Maié, Ivan G. Costa, Daniel B. Lipka, Mirle Schemionek, Kristina Feldberg, Julian Baumeister, Tim H. Brümmendorf, Nicolas Chatain, Steffen Koschmieder   +11 more
doaj   +3 more sources

Tyrosine kinase inhibitors in BCR-ABL positive acute lymphoblastic leukemia. [PDF]

Haematologica, 2015
Philadelphia chromosome (Ph)/BCR/ABL-positive acute lymphoblastic leukemia (ALL) is the most common genetic abnormality associated with adult ALL and has been shown to confer the worst prognosis to both children and adults.[1][1],[2][2] Approximately 3 ...
Leoni V, Biondi A.
europepmc   +7 more sources

EPS8 regulates proliferation, apoptosis and chemosensitivity in BCR-ABL positive cells via the BCR-ABL/PI3K/AKT/mTOR pathway. [PDF]

Oncol Rep, 2018
Although the introduction of tyrosine kinase inhibitors greatly improved the survival of patients with chronic myeloid leukemia (CML), drug resistance remains a problem. Thus, mechanism-based novel therapeutic targets warrant exploration.
Huang R, Liu H, Chen Y, He Y, Kang Q, Tu S, He Y, Zhou X, Wang L, Yang J, Wu A, Li Y.   +11 more
europepmc   +5 more sources

Combination of bortezomib and mitotic inhibitors down-modulate Bcr-Abl and efficiently eliminates tyrosine-kinase inhibitor sensitive and resistant Bcr-Abl-positive leukemic cells. [PDF]

PLoS ONE, 2013
Emergence of resistance to Tyrosine-Kinase Inhibitors (TKIs), such as imatinib, dasatinib and nilotinib, in Chronic Myelogenous Leukemia (CML) demands new therapeutic strategies.
Octavian Bucur, Andreea Lucia Stancu, Ioana Goganau, Stefana Maria Petrescu, Bodvael Pennarun, Thierry Bertomeu, Rajan Dewar, Roya Khosravi-Far   +7 more
doaj   +7 more sources

Case report: BCR-ABL-positive acute lymphoblastic leukemia with bone destruction: a treatment dilemma [PDF]

Frontiers in Oncology
Although bone destruction and hypercalcemia without acute peripheral blast BCR-ABL-positive acute lymphoblastic leukemia (ALL) have been reported in children, they are rare in adults.
Shi Lijun, Ma Zhongrui, Ma Zhongrui, Wei Li, Yu Xia, Jiang Wei, Pan Yaning   +6 more
doaj   +4 more sources

Combination therapy of BCR-ABL-positive B cell acute lymphoblastic leukemia by tyrosine kinase inhibitor dasatinib and c-JUN N-terminal kinase inhibition. [PDF]

J Hematol Oncol, 2020
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 ...
Xiao X, Liu P, Li D, Xia Z, Wang P, Zhang X, Liu M, Liao L, Jiao B, Ren R.   +9 more
europepmc   +2 more sources

Regulation of hTERT by BCR-ABL at multiple levels in K562 cells [PDF]

BMC Cancer, 2011
Background The cytogenetic characteristic of Chronic Myeloid Leukemia (CML) is the formation of the Philadelphia chromosome gene product, BCR-ABL. Given that BCR-ABL is the specific target of Gleevec in CML treatment, we investigated the regulation of ...
Chai Juin Hsien, Zhang Yong, Tan Wei Han, Chng Wee Joo, Li Baojie, Wang Xueying   +5 more
doaj   +6 more sources

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   +3 more sources

p185BCR/ABL has a lower sensitivity than p210BCR/ABL to the allosteric inhibitor GNF-2 in Philadelphia chromosome-positive acute lymphatic leukemia [PDF]

Haematologica, 2012
Background The t(9;22) translocation leads to the formation of the chimeric breakpoint cluster region/c-abl oncogene 1 (BCR/ABL) fusion gene on der22, the Philadelphia chromosome. The p185BCR/ABL or the p210BCR/ABL fusion proteins are encoded as a result
Afsar A. Mian, Anna Metodieva, Yousef Najajreh, Oliver G. Ottmann, Jamal Mahajna, Martin Ruthardt   +5 more
doaj   +4 more sources

Differential effects of selective inhibitors targeting the PI3K/AKT/mTOR pathway in acute lymphoblastic leukemia. [PDF]

PLoS ONE, 2013
PurposeAberrant PI3K/AKT/mTOR signaling has been linked to oncogenesis and therapy resistance in various malignancies including leukemias. In Philadelphia chromosome (Ph) positive leukemias, activation of PI3K by dysregulated BCR-ABL tyrosine kinase (TK)
Susanne Badura, Tamara Tesanovic, Heike Pfeifer, Sylvia Wystub, Bart A Nijmeijer, Marcus Liebermann, J H Frederik Falkenburg, Martin Ruthardt, Oliver G Ottmann   +8 more
doaj   +11 more sources