Results 31 to 40 of about 60,584 (224)

Protein tyrosine phosphatase 1B antagonizes signalling by oncoprotein tyrosine kinase p210 bcr-abl in vivo [PDF]

, 1998
The p210 bcr-abl protein tyrosine kinase (PTK) appears to be directly responsible for the initial manifestations of chronic myelogenous leukemia (CML). In contrast to the extensive characterization of the PTK and its effects on cell function, relatively ...
La Montagne, K. R., Flint, A. J., Franza, B. R., Pendergast, A. M., Tonks, N. K.   +4 more
core   +1 more source

Out Foxing Bcr-Abl [PDF]

Cancer Biology & Therapy, 2011
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

Systems-pharmacology dissection of a drug synergy in imatinib-resistant CML [PDF]

, 2012
Occurrence of the BCR-ABL[superscript T315I] gatekeeper mutation is among the most pressing challenges in the therapy of chronic myeloid leukemia (CML). Several BCR-ABL inhibitors have multiple targets and pleiotropic effects that could be exploited for ...
A Quintás-Cardama, A Seth, A Subramanian, AA Borisy, AL Hopkins, André C Müller, B Benassi, B Luo, B Palsson, BJ Druker, C Pan, CA Eide, CI Bliss, CL Sawyers, D Bixby, F Grebien, Florian Grebien, Florian P Breitwieser, Forest M White, FP Breitwieser, FX Mahon, G Dennis Jr., Georg E Winter, Giulio Superti-Furga, H Kitano, IJ Griswold, J Dopazo, J Lamb, J Lehár, J Zhang, Jacques Colinge, JE Cortes, JE Delmore, Karoline V Gleixner, Keiryn L Bennett, LM Packer, M Albajar, M Azam, M Schuhmacher, Manuela Gridling, Martin Bilban, ME Gorre, N Meyer, NJ Donato, O Hantschel, P Filippakopoulos, Peter Valent, PL Ross, S Adhikary, S Gupta, S Pelengaris, Scott M Carlson, SR Hann, T O′Hare, U Rix, U Rix, Uwe Rix, X Chen, ZA Knight   +58 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]

, 2011
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, Kaimori, Mitsuomi, Kubo, Kohmei, Mariya, Yasushi, Ogura, Kazuto, Oshikiri, Toshiyuki, Sakamoto, Yuichi, Sasaki, Sumiko, Segawa, Megumi, Teshiromori, Ryuichi   +9 more
core   +1 more source

Protein Kinase CK2: A Targetable BCR-ABL Partner in Philadelphia Positive Leukemias

Advances in Hematology, 2015
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, Giovanna Carrà, Cristina Panuzzo, Sabrina Crivellaro, Riccardo Taulli, Angelo Guerrasio, Giuseppe Saglio   +6 more
doaj   +1 more source

circCRKL, a circRNA derived from CRKL, regulates BCR-ABL via sponging miR-877-5p to promote chronic myeloid leukemia cell proliferation

Journal of Translational Medicine, 2022
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, Yang Liang, Yuefeng Qin, Guoyun Jiang, Yuhang Peng, Wenli Feng   +5 more
doaj   +1 more source

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

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
Cao Qi, Li Juan, Chen Chun, Jin Yanli, Lu Zhongzheng, Pan Jingxuan   +5 more
doaj   +1 more source

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

Journal of Hematology & Oncology, 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 ...
Xinhua Xiao, Ping Liu, Donghe Li, Zhizhou Xia, Peihong Wang, Xiuli Zhang, Mingzhu Liu, Lujian Liao, Bo Jiao, Ruibao Ren   +9 more
doaj   +1 more source

The antiproliferative activity of kinase inhibitors in chronic myeloid leukemia cells is mediated by FOXO transcription factors [PDF]

, 2014
Chronic myeloid leukemia (CML) is initiated and maintained by the tyrosine kinase BCR-ABL which activates a number of signal transduction pathways, including PI3K/AKT signaling and consequently inactivates FOXO transcription factors.
Bhatia, Birkenkamp, Breitling, Bruennert, Brunet, Burgering, Chomel, Chu, Copland, Corbin, Druker, Duy, Essafi, Fernandez de Mattos, Ghaffari, Goldman, Graham, Hamilton, Hurtz, Ito, Jorgensen, Kikuchi, Komatsu, Koschmieder, Mahon, Matsumoto, Miyamoto, Naka, Pellicano, Pellicano, Pellicano, Ross, Ross, Rowley, Sarbassov, Skorski, Tothova, Tothova, Trotman   +38 more
core   +2 more sources

Induction of apoptosis in imatinib sensitive and resistant chronic myeloid leukemia cells by efficient disruption of bcr-abl oncogene with zinc finger nucleases

Journal of Experimental & Clinical Cancer Research, 2018
Background The bcr-abl fusion gene is the pathological origin of chronic myeloid leukemia (CML) and plays a critical role in the resistance of imatinib. Thus, bcr-abl disruption-based novel therapeutic strategy may warrant exploration.
Ningshu Huang, Zhenglan Huang, Miao Gao, Zhenhong Luo, Fangzhu Zhou, Lin Liu, Qing Xiao, Xin Wang, Wenli Feng   +8 more
doaj   +1 more source