نتایج جستجو برای: abl positive

تعداد نتایج: 663991  

Journal: :The Journal of biological chemistry 1997
R de Jong A van Wijk L Haataja N Heisterkamp J Groffen

BCR/ABL is considered responsible for the development of Philadelphia chromosome-positive leukemia. Experimental animal models, such as transgenic mice, have demonstrated unambiguously that Bcr/Abl is capable of inducing leukemogenesis. The adaptor molecule Crkl is a major in vivo substrate of the deregulated Bcr/Abl tyrosine kinase and functions as a molecular link with other signaling protein...

Journal: :Cancer research 2009
Tetsuya Kurosu Manabu Ohki Nan Wu Hiroyuki Kagechika Osamu Miura

Although the BCR/ABL tyrosine kinase inhibitor imatinib is highly effective for treatment of chronic myelogenous leukemia and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia, relapse with emerging imatinib resistance mutations in the BCR/ABL kinase domain poses a significant problem. Here, we show that the multikinase inhibitor sorafenib inhibits proliferation and induces ap...

Journal: :Oncoscience 2015
Cristina Panuzzo Gisella Volpe Elisa Cibrario Rocchietti Claudia Casnici Katia Crotta Sabrina Crivellaro Giovanna Carrà Roberta Lorenzatti Barbara Peracino Davide Torti Alessandro Morotti Maria Pilar Camacho-Leal Paola Defilippi Ornella Marelli Giuseppe Saglio

In Chronic Myeloid Leukemia 80% of patients present alternative splice variants involving BCR exons 1, 13 or 14 and ABL exon 4, with a consequent impairment in the reading frame of the ABL gene. Therefore BCR/ABL fusion proteins (BCR/ABL-OOF) are characterized by an in-frame BCR portion followed by an amino acids sequence arising from the out of frame (OOF) reading of the ABL gene. The product ...

2011
Afsar Ali Mian Marion Schüll Claudia Oancea Yousef Najajreh Jamal Mahajna Amiram Goldblum Oliver Gerhard Ottmann Tim Beissert Martin Ruthardt

The BCR/ABL fusion protein is the hallmark of Philadelphia Chromosome positive (Ph+) leukemia. The constitutive activation of the ABL-kinase in BCR/ABL cells induces the leukemic phenotype. Targeted inhibition of BCR/ABL by small molecule inhibitors reverses the transformation potential of BCR/ABL. Recently, we definitively proved that targeting the tetramerization of BCR/ABL mediated by the N-...

Journal: :Blood 1993
J V Melo D E Gordon A Tuszynski S Dhut B D Young J M Goldman

We have previously shown that the chimeric gene ABL-BCR, formed on the derivative chromosome 9q+ as a result of the t(9;22) translocation, is transcriptionally active in 65% of chronic myeloid leukemia patients. We have now used the same technique, reverse transcription/polymerase chain reaction amplification of ABL-BCR transcripts, to study nine patients with Philadelphia (Ph) chromosome-posit...

Journal: :Blood 1998
H Honda H Oda T Suzuki T Takahashi O N Witte K Ozawa T Ishikawa Y Yazaki H Hirai

The Philadelphia (Ph) chromosome can be detected in chronic myelogenous leukemia (CML) and a significant number of acute lymphoblastic leukemia (ALL) cases. Generation of p210bcr/abl, a chimeric protein with enhanced kinase activity, is thought to be involved in the pathogenesis of these diseases. To elucidate the biological properties of p210bcr/abl and to create an animal model for human Ph1-...

Journal: :Revista medica de Chile 2006
Carmen Gloria Artigas A María Elena Cabrera C Angélica Melo A Eduardo Páez F Mónica Arriagada M Carmen Astete A Iván Roa E Juan Carlos Roa S

BACKGROUND t(12;21) (p12;q22) and t(9;22) (q34;q11) translocations have prognostic significance in acute lymphoblastic leukemia (ALL). The fusion genes TEL/AML1 y BCR/ABL, generated by these translocations, can be easily detected using molecular biology technique. AIM To study the frequency of TEL/AML1 y BCR/ABL fusion genes in children with ALL. MATERIAL AND METHODS Fifty-six children with...

Journal: :Cancer research and treatment : official journal of Korean Cancer Association 2010
Jae-Sook Ahn Yeo-Kyeoung Kim Se Ryeon Lee Li Yu Deok-Hwan Yang Sang-Hee Cho Hyun Jeong Shim Woo Kyun Bae Je-Jung Lee Ik-Joo Chung Myung Gun Shin Hyeoung-Joon Kim

PURPOSE Second-generation tyrosine kinase inhibitors (second TKIs) such as nilotinib and dasatinib control the activity of most ABL kinase domain mutations observed in patients with imatinib resistance. Although in vitro data show that both agents can inhibit all mutations except T315I, some discrepancies have been observed in a small subset of mutation clones. Cytogenetic clonal evolution is t...

Journal: :Blood 2005
Shinya Kimura Haruna Naito Hidekazu Segawa Junya Kuroda Takeshi Yuasa Kiyoshi Sato Asumi Yokota Yuri Kamitsuji Eri Kawata Eishi Ashihara Yohei Nakaya Haruna Naruoka Tatsushi Wakayama Kimio Nasu Tetsuo Asaki Tomoko Niwa Kazuko Hirabayashi Taira Maekawa

Although the Abelson (Abl) tyrosine kinase inhibitor imatinib mesylate has improved the treatment of breakpoint cluster region-Abl (Bcr-Abl)-positive leukemia, resistance is often reported in patients with advanced-stage disease. Although several Src inhibitors are more effective than imatinib and simultaneously inhibit Lyn, whose overexpression is associated with imatinib resistance, these inh...

Journal: :The Journal of clinical investigation 2007
Paolo Neviani Ramasamy Santhanam Joshua J Oaks Anna M Eiring Mario Notari Bradley W Blaser Shujun Liu Rossana Trotta Natarajan Muthusamy Carlo Gambacorti-Passerini Brian J Druker Jorge Cortes Guido Marcucci Ching-Shih Chen Nicole M Verrills Denis C Roy Michael A Caligiuri Clara D Bloomfield John C Byrd Danilo Perrotti

Blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia chromosome-positive (Ph1-positive) acute lymphocytic leukemia (ALL) are 2 fatal BCR/ABL-driven leukemias against which Abl kinase inhibitors fail to induce a long-term response. We recently reported that functional loss of protein phosphatase 2A (PP2A) activity is important for CML blastic transformation. We assessed the therap...

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