Results 131 to 140 of about 29,567 (180)
BCR-ABL kinase domain mutations in CML patients, experience from a tertiary care center in North India. [PDF]
Leuk Res RepS A +6 more
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Editor's Note to: Targeting Primitive Chronic Myeloid Leukemia Cells by Effective Inhibition of a New AHI-1-BCR-ABL-JAK2 Complex. [PDF]
J Natl Cancer Insteuropepmc +1 more source
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Leukemia Research, 1996
This review focuses on the role of the chimeric BCR/ABL gene in leukemia development. First, we discuss and update knowledge regarding the molecular biology of BCR/ABL. We then review data regarding transforming activity of BCR/ABL. Third, we discuss the complex interactions between BCR/ABL and leukemia phenotype. We conclude with a brief discussion of
, Ralph B Arlinghaus, R B Arlinghaus
exaly +3 more sources
This review focuses on the role of the chimeric BCR/ABL gene in leukemia development. First, we discuss and update knowledge regarding the molecular biology of BCR/ABL. We then review data regarding transforming activity of BCR/ABL. Third, we discuss the complex interactions between BCR/ABL and leukemia phenotype. We conclude with a brief discussion of
, Ralph B Arlinghaus, R B Arlinghaus
exaly +3 more sources
CRKL Binding to BCR-ABL and BCR-ABL Transformation
Leukemia & Lymphoma, 1999The SH2-SH3 domain-containing adaptor protein CRKL is the predominant tyrosine phosphorylated protein in chronic myelogenous leukemia (CML) neutrophils and BCR-ABL-expressing cell lines. The amino terminal CRKL SH3 domain binds directly to a proline-rich region in the C-terminus of BCR-ABL. BCR-ABL mutants with deletions of this region were constructed
K S, Kolibaba +4 more
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Blood Reviews, 1999
gene on chromosome 9 is the humanhomologue of a gene originally identified in a murineoncogenic virus, the Abelson murine leukaemia virus(A-MuLV). This retrovirus was isolated from a pred-nisolone treated mouse which developed lymphomafollowing innoculation with Moloney murineleukaemia virus (M-MuLV).
R, Chopra, Q Q, Pu, A G, Elefanty
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gene on chromosome 9 is the humanhomologue of a gene originally identified in a murineoncogenic virus, the Abelson murine leukaemia virus(A-MuLV). This retrovirus was isolated from a pred-nisolone treated mouse which developed lymphomafollowing innoculation with Moloney murineleukaemia virus (M-MuLV).
R, Chopra, Q Q, Pu, A G, Elefanty
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Baillière's Clinical Haematology, 1987
A DNA region on chromosome 22, designated M-BCR, contains the chromosomal breakpoint of the Philadelphia (Ph) translocation in all Ph positive CML patients studied to date. M-BCR is part of a gene, BCR, oriented with its 5' end towards the centromere of chromosome 22. All of the CML DNAs analysed have a breakpoint within introns of the BCR gene.
J, Groffen, N, Heisterkamp
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A DNA region on chromosome 22, designated M-BCR, contains the chromosomal breakpoint of the Philadelphia (Ph) translocation in all Ph positive CML patients studied to date. M-BCR is part of a gene, BCR, oriented with its 5' end towards the centromere of chromosome 22. All of the CML DNAs analysed have a breakpoint within introns of the BCR gene.
J, Groffen, N, Heisterkamp
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Osteopontin is upregulated by BCR-ABL
Biochemical and Biophysical Research Communications, 2005Chronic myelogenous leukemia (CML) is characterized by its hallmark oncogene BCR-ABL and the progression from a chronic phase toward an acute leukemia, with a differentiation arrest of the leukemic clone. In the present study, we conducted a microarray analysis using an inducible model of BCR-ABL expression based on the TET-OFF system, and we found ...
S, Flamant +9 more
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Blood, 2007
In Ph+ chronic myeloid leukemia (CML), the constitutively active Bcr-Abl kinase leads to the up-regulation and activation of multiple genes, which may subsequently result in the expression of leukemia-associated antigens. In this study, we investigated the immunogenicity of Bcr-Abl–regulated antigens by stimulating CD8+ T lymphocytes with autologous ...
Florian, Scheich +3 more
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In Ph+ chronic myeloid leukemia (CML), the constitutively active Bcr-Abl kinase leads to the up-regulation and activation of multiple genes, which may subsequently result in the expression of leukemia-associated antigens. In this study, we investigated the immunogenicity of Bcr-Abl–regulated antigens by stimulating CD8+ T lymphocytes with autologous ...
Florian, Scheich +3 more
openaire +2 more sources
Blood, 2006
Abstract The inhibition of BCR/ABL kinase activity by imatinib mesylate (IM, STI571, Gleevec®) is the standard therapy for patients with Philadelphia chromosome+ (Ph+) chronic myeloid leukemia (CML). However, the long term treatment with IM or other BCR/ABL kinase inhibitors may be limited due to the development of resistant disease and ...
Florian Scheich +2 more
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Abstract The inhibition of BCR/ABL kinase activity by imatinib mesylate (IM, STI571, Gleevec®) is the standard therapy for patients with Philadelphia chromosome+ (Ph+) chronic myeloid leukemia (CML). However, the long term treatment with IM or other BCR/ABL kinase inhibitors may be limited due to the development of resistant disease and ...
Florian Scheich +2 more
openaire +1 more source