نتایج جستجو برای: abl positive

تعداد نتایج: 663991  

2015
Anahita Rafiei Afsar Ali Mian Claudia Döring Anna Metodieva Claudia Oancea Frederic B. Thalheimer Martin Leo Hansmann Oliver Gerhard Ottmann Martin Ruthardt

The hallmark of Philadelphia chromosome positive (Ph(+)) leukemia is the BCR/ABL kinase, which is successfully targeted by selective ATP competitors. However, inhibition of BCR/ABL alone is unable to eradicate Ph(+) leukemia. The t(9;22) is a reciprocal translocation which encodes not only for the der22 (Philadelphia chromosome) related BCR/ABL, but also for der9 related ABL/BCR fusion proteins...

Journal: :Blood 2008
Artur Gontarewicz Stefan Balabanov Gunhild Keller Riccardo Colombo Alessio Graziano Enrico Pesenti Daniel Benten Carsten Bokemeyer Walter Fiedler Jürgen Moll Tim H Brümmendorf

The emergence of resistance to imatinib (IM) mediated by mutations in the BCR-ABL domain has become a major challenge in the treatment of chronic myeloid leukemia (CML). Here, we report on studies performed with a novel small molecule inhibitor, PHA-739358, which selectively targets Bcr-Abl and Aurora kinases A to C. PHA-739358 exhibits strong antiproliferative and proapoptotic activity against...

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 2001
R Nimmanapalli M Porosnicu D Nguyen E Worthington E O'Bryan C Perkins K Bhalla

Bcr-Abl tyrosine kinase inhibitor STI-571 induces differentiation and apoptosis of HL-60/Bcr-Abl (with ectopic expression of p190 Bcr-Abl) and K562 (with endogenous expression of p210 Bcr-Abl) cells (Blood, 96: 2246-2253, 2000). Cotreatment with STI-571 partially overcomes the resistance to antileukemic drug-induced apoptosis of HL-60/Bcr-Abl and K562 cells. Tumor necrosis factor (TNF) alpha-re...

2016
Fabienne Lamballe Sara Toscano Filippo Conti Maria Arechederra Nathalie Baeza Dominique Figarella-Branger Françoise Helmbacher Flavio Maina

The cytoplasmic tyrosine kinase ABL exerts positive or negative effects in solid tumours according to the cellular context, thus functioning as a "switch modulator". The therapeutic effects of drugs targeting a set of signals encompassing ABL have been explored in several solid tumours. However, the net contribution of ABL inhibition by these agents remains elusive as these drugs also act on ot...

Journal: :Blood 2010
Cong Peng Yaoyu Chen Zhongfa Yang Haojian Zhang Lori Osterby Alan G Rosmarin Shaoguang Li

The tumor suppressor gene phosphatase and tensin homolog (PTEN) is inactivated in many human cancers. However, it is unknown whether PTEN functions as a tumor suppressor in human Philadelphia chromosome-positive leukemia that includes chronic myeloid leukemia (CML) and B-cell acute lymphoblastic leukemia (B-ALL) and is induced by the BCR-ABL oncogene. By using our mouse model of BCR-ABL-induced...

Journal: :Journal of periodontology 2015
Shawneen M Gonzalez Jeffrey B Payne Fang Yu Geoffrey M Thiele Alan R Erickson Paul G Johnson Marian J Schmid Grant W Cannon Gail S Kerr Andreas M Reimold Jeremy Sokolove William H Robinson Ted R Mikuls

BACKGROUND This study examines: 1) alveolar bone loss (ABL), a hallmark of periodontitis, in anti-citrullinated protein antibody (ACPA)-positive rheumatoid arthritis (RA) patients versus control patients with osteoarthritis (OA); and 2) the association of ABL with RA disease activity and ACPA concentrations, including multiple antigen-specific ACPA. METHODS This multicenter case-control study...

2011
Vilas Wagh Shailaja Chile Sonal Monahar Bikas Chandra Pal Santu Bandyopadhyay Somesh Sharma Kalpana Joshi

1. Abstract 2. Introduction 3. Materials and Methods 3.1. Plant material, extraction and purification 3.2. Reagents 3.3. Cell lines 3.4. Clinical Samples 3.4. Cytotoxicity assay/proliferation assay 3.5. Cell cycle analysis apoptosis assay 3.6. In-vitro kinase assay 3.7. Data analysis 4. Results 4.1. Discovery and preparation of NPB001-05 4.2. Effect of NPB001-05 on growth of Bcr-Abl positive an...

Journal: :Cancer research 2001
B Sun G Jiang M A Zaydan V F La Russa H Safah M Ehrlich

Formation of the hybrid BCR-ABL gene is responsible for >95% of chronic myeloid leukemia (CML). The alternative, downstream ABL promoter (Pa), which is usually retained in this chimeric oncogene, was reported to be methylated in many CML patients, but there has been controversy as to whether this methylation is a frequent change in bone marrow (BM) in early chronic phase (CP) or only past this ...

Journal: :Blood 1995
T Skorski P Kanakaraj M Nieborowska-Skorska M Z Ratajczak S C Wen G Zon A M Gewirtz B Perussia B Calabretta

The BCR/ABL oncogenic tyrosine kinase is responsible for initiating and maintaining the leukemic phenotype of Philadelphia chromosome (Ph1)-positive cells. Phosphatidylinositol-3 (PI-3) kinase is known to interact with and be activated by receptor and nonreceptor tyrosine kinases. We investigated whether PI-3 kinase associates with and/or is regulated by BCR/ABL, whether this interaction is fun...

Journal: :The New England journal of medicine 2006
Moshe Talpaz Neil P Shah Hagop Kantarjian Nicholas Donato John Nicoll Ron Paquette Jorge Cortes Susan O'Brien Claude Nicaise Eric Bleickardt M Anne Blackwood-Chirchir Vishwanath Iyer Tai-Tsang Chen Fei Huang Arthur P Decillis Charles L Sawyers

BACKGROUND The BCR-ABL tyrosine kinase inhibitor imatinib is effective in Philadelphia chromosome-positive (Ph-positive) leukemias, but relapse occurs, mainly as a result of the outgrowth of leukemic subclones with imatinib-resistant BCR-ABL mutations. We evaluated dasatinib, a BCR-ABL inhibitor that targets most imatinib-resistant BCR-ABL mutations, in patients with chronic myelogenous leukemi...

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