Results 71 to 80 of about 125,674 (260)

The chronic myeloid leukemia stem cell: stemming the tide of persistence [PDF]

, 2017
Chronic myeloid leukaemia (CML) is caused by the acquisition of the tyrosine kinase BCR-ABL1 in a haemopoietic stem cell (HSC), transforming it into a leukaemic stem cell (LSC) that self-renews, proliferates and differentiates to give rise to a ...
Holyoake, Tessa L., Vetrie, David
core   +1 more source

MicroRNA-320a acts as a tumor suppressor by targeting BCR/ABL oncogene in chronic myeloid leukemia

Scientific Reports, 2015
Accumulating evidences demonstrated that the induction of epithelial-mesenchymal transition (EMT) and aberrant expression of microRNAs (miRNAs) are associated with tumorigenesis, tumor progression, metastasis and relapse in cancers, including chronic ...
Xishan Zhu, Ziying Lin, D. Jing, L. Gang
semanticscholar   +1 more source

Atypical Wounds in Chronic Graft‐Versus‐Host Disease and Peripheral Arterial Disease Caused by Tyrosine Kinase Inhibitors

JEADV Clinical Practice, EarlyView.
ABSTRACT The term “atypical wounds” primarily refers to lesions with immunological or cancerous etiologies. However, these wounds can also be drug‐induced. We report about a 32‐year‐old man with a 6‐year history of chronic myelogenous leukemia (CML) and chronic graft‐versus‐host disease (cGvHD) following an HLA‐compatible allogeneic stem cell ...
E. K. Stuermer, K. Malik, C. Willers, M. Augustin   +3 more
wiley   +1 more source

The FABD domain is critical for the oncogenicity of BCR/ABL in chronic myeloid leukaemia

Cell Communication and Signaling
Background Abnormally expressed BCR/ABL protein serves as the basis for the development of chronic myeloid leukaemia (CML). The F-actin binding domain (FABD), which is a crucial region of the BCR/ABL fusion protein, is also located at the carboxyl end of
Renren Zheng, Wei Wei, Suotian Liu, Dachuan Zeng, Zesong Yang, Jie Tang, Jinfeng Tan, Zhenglan Huang, Miao Gao   +8 more
doaj   +1 more source

Deletions of the derivative chromosome 9 occur at the time of the Philadelphia translocation and provide a powerful and independent prognostic indicator in chronic myeloid leukemia [PDF]

, 2001
Chronic myeloid leukemia (CML) is characterized by formation of the BCR-ABL fusion gene, usually as a consequence of the Philadelphia (Ph) translocation between chromosomes 9 and 22.
Bench, AJ, Campbell, LJ, Grace, C, Green, AR, Huntly, BJP, Nacheva, EP, Prince, HM, Reid, AG, Shepherd, P, Szer, J, Telford, N, Turner, P   +11 more
core   +1 more source

Design of substrate-based BCR-ABL kinase inhibitors using the cyclotide scaffold

Scientific Reports, 2015
The constitutively active tyrosine kinase BCR-ABL is the underlying cause of chronic myeloid leukemia (CML). Current CML treatments rely on the long-term use of tyrosine kinase inhibitors (TKIs), which target the ATP binding site of BCR-ABL.
Yen‐Hua Huang, S. Henriques, Conan K. Wang, Louise Thorstholm, N. Daly, Q. Kaas, D. Craik   +6 more
semanticscholar   +1 more source

CRISPR Enabled Precision Oncology: From Gene Editing to Tumor Microenvironment Remodeling

Med Research, EarlyView.
CRISPR technology has progressed from a prokaryotic immune system to a diverse suite of editing platforms, including Cas nucleases, base and prime editors, and RNA‐targeting enzymes. These advances enable precise genomic and epigenomic interventions, high‐throughput functional screening, and immune engineering.
Kailai Li, Peixin Huang, Yue Qian, Anqi Lin, Jingjun He, Junyi Shen, Li Chen, Kai Miao, Jian Zhang   +8 more
wiley   +1 more source

Fusion Gene Bcr-abl : From Etiopathogenesis to the Management of Chronic Myeloid Leukemia [PDF]

, 2017
Chronic Myeloid Leukemia (CML) is a myeloproliferative neoplasm. CML is relative frequent disorder. Most of CML patients have Philadelphia chromosome (Ph),which is derived from a reciprocal translocation between chromosome 9 and 22, t(9;22)(q34;ql1 ...
Sholikah, T. A. (Tri)
core   +2 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.
C, Heaney, K, Kolibaba, A, Bhat, T, Oda, S, Ohno, S, Fanning, B J, Druker   +6 more
openaire   +3 more sources

Disarming the Hsp70–Bim Alliance: Small‐Molecule and Peptidic Disruptors of a Chaperone‐Apoptotic Switch in Cancer

ChemistryOpen, EarlyView.
Targeting a nucleotide‐sensitive groove on Hsp70 that binds the Bim BH3 helix, we integrate structures, biophysics, and SAR from peptides, fragments, and phenalene‐dicarbonitrile “wedges.” These disrupt the Hsp70–Bim complex with sub‐µM cellular engagement and in vivo activity while sparing Hsp90/mortalin.
Emadeldin M. Kamel, Mohammed Al‐zharani, Lina M. Alneghery, Noha A. Ahmed, Faris F. Aba Alkhayl, Al Mokhtar Lamsabhi   +5 more
wiley   +1 more source