Results 41 to 50 of about 81,803 (228)

New Bcr-Abl-independent mechanisms of resistance to imatinib treatment in chronic myelogenous leukaemia patients [PDF]

, 2008
Although rare in chronic phase myeloid leukemia (CML), primary or acquired resistance to the treatment with tyrosine kinase inhibitors (TKI) may be observed in the advanced phases of disease.
Esposito, Nicola
core   +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

The Ins and Outs of Bcr-Abl Inhibition [PDF]

Genes & Cancer, 2012
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

Assembling defenses against therapy-resistant leukemic stem cells: Bcl6 joins the ranks [PDF]

, 2011
The resistance of leukemic stem cells in response to targeted therapies such as tyrosine kinase inhibitors (TKIs) relies on the cooperative activity of multiple signaling pathways and molecules, including TGFβ, AKT, and FOXO transcription factors ...
Holyoake, T.L., Tessa L. Holyoake, Pellicano, F., Francesca Pellicano   +3 more
core   +1 more source

Nilotinib concentration in cell lines and primary CD34+ chronic myeloid leukemia cells is not mediated by active uptake or efflux by major drug transporters [PDF]

, 2009
Imatinib mesylate and nilotinib are highly effective at eradicating the majority of chronic myeloid leukemia (CML) cells; however, neither agent induces apoptosis of primitive CML CD34⁺ cells.
Holyoake, T.L., Davies, A., Jordanides, N.E., Giannoudis, A., Jorgensen, H.G., Harris, R.J., Hatziieremia, S., Mountford, J.C., Pirmohamed, M., Clark, R.E., Lucas, C.M.   +10 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

Mechanisms and therapeutic opportunities of the ribotoxic stress response in cancer

Molecular Oncology, EarlyView.
Cancer cells' high translational demand creates opportunities to therapeutically target ribosome function. Ribosome stalling and collisions activate ZAKα and the ribotoxic stress response (RSR), which can trigger rapid, p53‐independent apoptosis in cancer.
Anastassiya Kim, Maryam Aslam, Elouise Torruella, Alphons Sony, Asif Rahman, Simira Smith, Columba de la Parra, Moira Sauane   +7 more
wiley   +1 more source

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

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   +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