نتایج جستجو برای: BCR-ABL1

تعداد نتایج: 11415  

Objective(s): Chronic myeloid leukemia (CML) is a myeloid clonal proliferation disease defining by the presence of the Philadelphia chromosome that shows the movement of BCR-ABL1. In this study, the critical role of the Musashi2-Numb axis in determining cell fate and relationship of the axis to important signaling pathways such as Hedgehog and Notch that are essential ...

Journal: :Blood 2011
Arelis Salas Suriyan Ponnusamy Can E Senkal Marisa Meyers-Needham Shanmugam Panneer Selvam Sahar A Saddoughi Elif Apohan R David Sentelle Charles Smith Christopher R Gault Lina M Obeid Hesham M El-Shewy Joshua Oaks Ramasamy Santhanam Guido Marcucci Yusuf Baran Sandeep Mahajan Daniel Fernandes Robert Stuart Danilo Perrotti Besim Ogretmen

The mechanisms by which sphingosine kinase-1 (SK-1)/sphingosine 1-phosphate (S1P) activation contributes to imatinib resistance in chronic myeloid leukemia (CML) are unknown. We show herein that increased SK-1/S1P enhances Bcr-Abl1 protein stability, through inhibition of its proteasomal degradation in imatinib-resistant K562/IMA-3 and LAMA-4/IMA human CML cells. In fact, Bcr-Abl1 stability was...

2017
Masanobu Tsubaki Tomoya Takeda Toshiki Kino Kazuko Sakai Tatsuki Itoh Motohiro Imano Takashi Nakayama Kazuto Nishio Takao Satou Shozo Nishida

Resistance to the breakpoint cluster region-abelson 1 (BCR-ABL1) tyrosine kinase inhibitor (TKI) imatinib poses a major problem when treating chronic myeloid leukemia (CML). Imatinib resistance often results from a secondary mutation in BCR-ABL1. However, in the absence of a mutation in BCR-ABL1, the basis of BCR-ABL1-independent resistance must be elucidated. To gain insight into the mechanism...

Journal: :Blood 2016
Yashodhara Dasgupta Mateusz Koptyra Grazyna Hoser Kanchan Kantekure Darshan Roy Barbara Gornicka Margaret Nieborowska-Skorska Elisabeth Bolton-Gillespie Sabine Cerny-Reiterer Markus Müschen Peter Valent Mariusz A Wasik Christine Richardson Oliver Hantschel Heiko van der Kuip Tomasz Stoklosa Tomasz Skorski

Leukemias expressing constitutively activated mutants of ABL1 tyrosine kinase (BCR-ABL1, TEL-ABL1, NUP214-ABL1) usually contain at least 1 normal ABL1 allele. Because oncogenic and normal ABL1 kinases may exert opposite effects on cell behavior, we examined the role of normal ABL1 in leukemias induced by oncogenic ABL1 kinases. BCR-ABL1-Abl1(-/-) cells generated highly aggressive chronic myeloi...

2016
Sanaz Tabarestani Abolfazl Movafagh

CONTEXT Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by overproduction of immature and matured myeloid cells in the peripheral blood, bone marrow and spleen. EVIDENCE ACQUISITION A hallmark of CML is the presence of (9; 22) (q34; q11) reciprocal translocation, which is cytogenetically visible as Philadelphia chromosome (Ph) and results in the formation of BCR-...

Journal: :The Journal of Experimental Medicine 2005
Niklas Feldhahn Florian Klein Jana L. Mooster Paul Hadweh Mieke Sprangers Maria Wartenberg Mohamed M. Bekhite Wolf-Karsten Hofmann Sebastian Herzog Hassan Jumaa Janet D. Rowley Markus Müschen

Pre-B cells undergo apoptosis unless they are rescued by pre-B cell receptor-dependent survival signals. We previously showed that the BCR-ABL1 kinase that is expressed in pre-B lymphoblastic leukemia bypasses selection for pre-B cell receptor-dependent survival signals. Investigating possible interference of BCR-ABL1 with pre-B cell receptor signaling, we found that neither SYK nor SLP65 can b...

2017
Soo In Choi Mi-Ae Jang Woo Joon Jeong Byung Ryul Jeon Yong-Wha Lee Hee Bong Shin Dae-Sik Hong You Kyoung Lee

Dear Editor, The translocation (9;12)(q34;p13) ETV6/ABL1 rearrangement is a rare but recurrent chromosomal translocation associated with a variety of hematological malignancies, including CML, atypical CML, AML, and ALL [1]. The structure of the ETV6/ABL1 oncoprotein is similar to that of BCR/ABL1, and they initiate similar downstream pathways [2]. There are two ETV6/ABL1 fusion isoforms: the t...

2017
Judith M. Boer Elisabeth M.P. Steeghs João R.M. Marchante Aurélie Boeree James J. Beaudoin H. Berna Beverloo Roland P. Kuiper Gabriele Escherich Vincent H.J. van der Velden C. Ellen van der Schoot Hester A. de Groot-Kruseman Rob Pieters Monique L. den Boer

Approximately 15% of pediatric B cell precursor acute lymphoblastic leukemia (BCP-ALL) is characterized by gene expression similar to that of BCR-ABL1-positive disease and unfavorable prognosis. This BCR-ABL1-like subtype shows a high frequency of B-cell development gene aberrations and tyrosine kinase-activating lesions. To evaluate the clinical significance of tyrosine kinase gene fusions in ...

Journal: :Blood 2014
Mo-Ying Hsieh Richard A Van Etten

The product of the Ph chromosome, the BCR-ABL1 tyrosine kinase activates diverse signaling pathways in leukemic cells from patients with chronic myeloid leukemia (CML) and Ph(+) B-cell acute lymphoblastic leukemia (B-ALL). Previous studies showed that nuclear factor κB (NF-κB) is activated in BCR-ABL1-expressing cells, but the mechanism of activation and importance of NF-κB to the pathogenesis ...

2012
Wolfgang Warsch Eva Grundschober Angelika Berger Lars Gille Sabine Cerny-Reiterer Anca-Sarmiza Tigan Andrea Hoelbl-Kovacic Peter Valent Richard Moriggl Veronika Sexl

We recently reported that chronic myeloid leukaemia (CML) patients harbour high levels of STAT5 when they progress to advanced phases of disease. Advanced disease is characterized by an increased incidence of BCR-ABL1 mutations. We now describe a highly significant correlation between STAT5 expression and the incidence of BCR-ABL1 mutations in primary CML. Forced expression of STAT5 in murine B...

نمودار تعداد نتایج جستجو در هر سال

با کلیک روی نمودار نتایج را به سال انتشار فیلتر کنید