نتایج جستجو برای: bcrabl

تعداد نتایج: 84  

2016
A. ILEA A. M. VLĂDĂREANU

This article reports the molecular diagnosis findings regarding chronic myeloproliferative neoplasms made in a Molecular Biology Laboratory over a seven years’ experience (between 2009 and 2015). Ritus Biotec ltd is an ELN (European Leukemia Net) certified diagnostic laboratory for quantification of BCR-ABL. 1373 patients were subjected to Jak2 V617F testing in this time frame. The patients wer...

Journal: :Haematologica 2005
J M Perel C McCarthy O Walker I Irving B Williams G A Kennedy

To The Editor, Since the introduction of imatinib mesylate as treatment for chronic myeloid leukemia (CML) there have been increasing reports of patients developing Philadelphia (Ph) chromosome negative cytogentic clones, a rare phenomenon in the pre-imatinib era. We wish to report our experience of patients who developed Ph negative clones whilst on imatinib therapy, and briefly review the pot...

2016
Valérie Lagarde François-Xavier Mahon Jean-Max Pasquet

Targeting the tyrosine kinase activity of BCR-ABL is the gold standard strategy in Chronic Myeloid Leukemia (CML) for the last decade. Whereas inhibitors of BCR-ABL tyrosine kinase are now used in frontline therapy for CML, third generation inhibitors of BCR-ABL tyrosine kinase such as ponatinib has been developed for the treatment of BCRABL resistant mutants. In the current study, we generated...

2003
Chi Ly Adrian F. Arechiga Junia V. Melo Craig M. Walsh S. Tiong Ong

Identification of signaling pathways downstream of Abl tyrosine kinase may increase our understanding of the pathogenesis of chronic myelogenous leukemia (CML) and suggest strategies to improve clinical treatment of the disease. By combining the use of a phosphospecific antibody recognizing a substrate motif of serine/threonine kinases with bioinformatics, we found that the translational regula...

2016
Lawrence M. Agius

Contextual BCR-ABL tyrosine kinase over-activity determines in formulated fashion the emergence of proliferation and anti-apoptosis that arise largely as derived phenomena of otherwise homeostatic mechanisms of the c-ABL gene within hematopoietic stem cells and hemangioblasts in the bone marrow. The ability to suppress almost completely, both in terms of phenotype and cytogenetically, the myelo...

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 2008
Thomas O'Hare Michael W Deininger

A diagnosis of chronic myeloid leukemia (CML) remains unwelcome news. Thanks to imatinib, however, the majority of newly diagnosed patients with chronic phase CML achieve a complete cytogenetic response (CCyR) and can expect longterm survival, often without major side effects (1). Unfortunately, these responses are not equivalent to a cure because residual leukemia cells persist even in patient...

Journal: :The Journal of clinical investigation 2000
B J Druker N B Lydon

teins comprising 2 major subfamilies, the protein serine/threonine kinases and protein tyrosine kinases (PTKs). Protein kinases function as components of signal transduction pathways, playing a central role in diverse biological processes such as control of cell growth, metabolism, differentiation, and apoptosis. The development of selective protein kinase inhibitors that can block or modulate ...

2010
Nicholas B. Heaney Francesca Pellicano Bin Zhang Lisa Crawford Su Chu Syed M. A. Kazmi Elaine K. Allan Heather G. Jorgensen Alexandra E. Irvine Ravi Bhatia Tessa L. Holyoake

Chronic myeloid leukemia (CML) is treated effectively with tyrosine kinase inhibitors (TKIs); however, 2 key problems remain— the insensitivity of CML stem and progenitor cells to TKIs and the emergence of TKI-resistant BCR-ABL mutations. BCRABL activity is associated with increased proteasome activity and proteasome inhibitors (PIs) are cytotoxic against CML cell lines. We demonstrate that bor...

Journal: :Blood 2004
Yasushi Soda Kenzaburo Tani Yuansong Bai Minoru Saiki Minghan Chen Kiyoko Izawa Seiichiro Kobayashi Satoshi Takahashi Kaoru Uchimaru Tomoko Kuwabara Masaaki Warashina Tsuyoshi Tanabe Hiroyuki Miyoshi Kanji Sugita Shinpei Nakazawa Arinobu Tojo Kazunari Taira Shigetaka Asano

Patients with Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukemia (ALL) generally have a poor prognosis and would benefit from the development of new therapeutic approaches. We previously demonstrated that an allosterically controllable ribozyme, maxizyme (Mz), can induce apoptosis in chronic myelogenous leukemia (CML) cells. Ph(+) ALL cells harbor a bcrabl fusion gene (e1a2) ...

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