Results 291 to 300 of about 128,389 (322)

BCR-ABL and Human Cancer [PDF]

open access: possible, 2007
The BCR-ABL oncogene was the first chromosomal abnormality shown to be associated with a specific human malignancy, the chronic myelogenous leukemia (CML), resulting from a reciprocal t(9;22) translocation characterized by the formation of a shortened chromosome, named Philadelphia chromosome (Ph), in which the tyrosine kinase of c-ABL is ...
Maria Perez-Caro   +1 more
openaire   +1 more source
Some of the next articles are maybe not open access.

Related searches:

2 BCR-ABL gene variants

Baillière's Clinical Haematology, 1997
The BCR-ABL hybrid gene, the main product of the t(9;22)(q34;q11) translocation, is found in the leukaemic clone of at least 95% of CML patients. The fusion protein encoded by BCR-ABL varies in size, depending on the breakpoint in the BCR gene. Three breakpoint cluster regions have been characterized to date: major (M-bcr), minor (m-bcr) and micro (mu ...
openaire   +3 more sources

Bcr-Abl and Signal Transduction [PDF]

open access: possible, 2007
The BCR-ABL oncogene is generated by the Philadelphia (Ph) chromosome translocation, fusing the BCR to the ABL gene. The Bcr-Abl fusion protein has constitutive and deregulated tyrosine kinase activity that is critical for transformation of hematopoietic cells.
Giuseppe Saglio, Daniela Cilloni
openaire   +1 more source

The Role of MYC in Transformation by BCR-ABL

Leukemia & Lymphoma, 1993
The BCR-ABL gene plays a central role in the pathogenesis of chronic myelogenous leukemia. Despite a detailed understanding of the regions of BCR and ABL required for transformation by BCR-ABL, little is known about the signalling pathway by which BCR-ABL causes transformation. The nuclear oncogene c-myc plays a critical role in BCR-ABL transformation.
openaire   +2 more sources

Identification of GZD824 as an orally bioavailable inhibitor that targets phosphorylated and nonphosphorylated breakpoint cluster region-Abelson (Bcr-Abl) kinase and overcomes clinically acquired mutation-induced resistance against imatinib.

Journal of Medicinal Chemistry, 2013
Bcr-Abl(T315I) mutation-induced imatinib resistance remains a major challenge for clinical management of chronic myelogenous leukemia (CML). Herein, we report GZD824 (10a) as a novel orally bioavailable inhibitor against a broad spectrum of Bcr-Abl ...
Xiaomei Ren   +19 more
semanticscholar   +1 more source

Breaking the Back of BCR-ABL

Science, 2008
BIOCHEMISTRY One of the advances in the war on cancer has been the development of small molecules that target protein tyrosine kinases; one such drug, imatinib, is used to inhibit the BCR-ABL kinase in the treatment of chronic myelogenous leukemia.
openaire   +2 more sources

Direct Interaction of Ahi-1 with BCR-ABL Modulates BCR-ABL Transforming Activity and Imatinib Response in a BCR-ABL Inducible Cell Line Model

Blood, 2008
Abstract (Abelson helper integration site-1) is a novel oncogene that was initially identified by provirus insertional mutagenesis in v-abl-induced murine pre-B cell lymphoma as a candidate cooperate oncogene. The Ahi-1 protein has a SH3 domain, multiple SH3 binding sites and WD-repeat domains, suggesting novel signaling activities.
Donna DeGeer   +5 more
openaire   +2 more sources

Effects of a selective inhibitor of the Abl tyrosine kinase on the growth of Bcr–Abl positive cells

Nature Network Boston, 1996
B. Druker   +7 more
semanticscholar   +1 more source

Deubiquitylase USP25 prevents degradation of BCR-ABL protein and ensures proliferation of Ph-positive leukemia cells

Oncogene, 2020
N. Shibata   +7 more
semanticscholar   +1 more source

Bcr-Abl Kinase Inhibitors

2006
The hallmark of chronic myelogenous leukemia (CML) is the expression of Bcr-Abl, a constitutivelyactive form of the Abl tyrosine kinase. Imatinib, a 2-phenyl aminopyrimidine Bcr-Abl inhibitor developedby Novartis and marketed under the tradename of Gleevec (Glivec), is highly effective in treating CML patientswith early stage disease. However, patients
openaire   +2 more sources

Home - About - Disclaimer - Privacy