Results 1 to 10 of about 9,645 (157)

Reciprocal t(9;22) ABL/BCR fusion proteins: leukemogenic potential and effects on B cell commitment. [PDF]

PLoS ONE, 2009
BACKGROUND:t(9;22) is a balanced translocation, and the chromosome 22 breakpoints (Philadelphia chromosome--Ph+) determine formation of different fusion genes that are associated with either Ph+ acute lymphatic leukemia (Ph+ ALL) or chronic myeloid ...
Xiaomin Zheng, Claudia Oancea, Reinhard Henschler, Malcolm A S Moore, Martin Ruthardt   +4 more
doaj   +8 more sources

The functional interplay between the t(9;22)-associated fusion proteins BCR/ABL and ABL/BCR in Philadelphia chromosome-positive acute lymphatic leukemia. [PDF]

PLoS Genetics, 2015
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.
Anahita Rafiei, Afsar Ali Mian, Claudia Döring, Anna Metodieva, Claudia Oancea, Frederic B Thalheimer, Martin Leo Hansmann, Oliver Gerhard Ottmann, Martin Ruthardt   +8 more
doaj   +7 more sources

BCR/ABL inhibition by an escort/phosphatase fusion protein [PDF]

Proceedings of the National Academy of Sciences, 2000
Cellular transformation by the BCR/ABL oncogene depends on the ABL-encoded tyrosine kinase activity. To block BCR/ABL function, we created a unique tyrosine phosphatase by fusing the catalytic domain of SHP1 (SHP1c) to the ABL binding domain (ABD) of RIN1, an established binding partner and substrate for c-ABL and BCR/ABL.
John Colicelli, Stephane Wong, Owen N. Witte, Gary Lau, Young-Mi Lim   +4 more
openaire   +3 more sources

Relationship Between BCR/ABL Fusion Proteins and Leukemia Phenotype [PDF]

Blood, 1997
To the Editor: We read with interest the recent Editorial in Blood by Melo[1][1] concerning the relationship between BCR/ABL variant transcripts and the leukemia phenotype determination. Regarding the chronic myeloid leukemia (CML), a strict correlation was suggested between at least three ...
Emilia G, LUPPI, Mario, MARASCA, Roberto, TORELLI, Giuseppe   +3 more
openaire   +4 more sources

Effect of HSP90AB1 and CC domain interaction on Bcr-Abl protein cytoplasm localization and function in chronic myeloid leukemia cells

Cell Communication and Signaling, 2021
Background The fusion oncoprotein Bcr-Abl is mostly located in the cytoplasm, which causes chronic myeloid leukemia (CML). After moving into the nucleus, the fusion protein can induce apoptosis of CML cells.
Yuhang Peng, Zhenglan Huang, Fangzhu Zhou, Teng Wang, Ke Mou, Wenli Feng   +5 more
doaj   +1 more source

Acute lymphoblastic leukemia with e1a3 BCR/ABL fusion protein. A report of two cases [PDF]

Experimental Hematology & Oncology, 2015
B Acute Lymphoblastic leukemia (B-ALL) with Philadelphia chromosome (Ph') is a neoplasm of lymphoblast committed to the B cell lineage. The clinical presentation of B-ALL Ph'+ is similar to B-ALL, but is more common in adults than in children. The e1a3 rare variant is produced by the fusion of BCR exon 1 to ABL exon 3.
Lopez-Andrade, Bernardo, Sartori, Francesca, Gutiérrez, Antonio, Garcia, Lucia, Cunill Monjo, Vanesa, Duran Pastor, Maria Antonia, Sampol Mayol, Antonia, Bernues, Marta, Iglesias, Julio, Ramos-Asensio, Rafael, Llado, Josep, Sanchez, Maria, Carlos Amat, Juan, Martinez-Serra, Jordi   +13 more
openaire   +4 more sources

Interplay between kinase domain autophosphorylation and F-actin binding domain in regulating imatinib sensitivity and nuclear import of BCR-ABL. [PDF]

PLoS ONE, 2011
The constitutively activated BCR-ABL tyrosine kinase of chronic myeloid leukemia (CML) is localized exclusively to the cytoplasm despite the three nuclear localization signals (NLS) in the ABL portion of this fusion protein.
Martin Preyer, Paolo Vigneri, Jean Y J Wang   +2 more
doaj   +1 more source

Flow cytometric immunobead assay for the detection of BCR–ABL fusion proteins in leukemia patients [PDF]

Leukemia, 2009
BCR-ABL fusion proteins show increased signaling through their ABL tyrosine kinase domain, which can be blocked by specific inhibitors, thereby providing effective treatment. This makes detection of BCR-ABL aberrations of utmost importance for diagnosis, classification and treatment of leukemia patients.
Nancy Boeckx, Tomasz Szczepański, Paulo Sérgio Lucio, Lukasz Sedek, A Mendonça, S Böttcher, Monika Brüggemann, Frank J. T. Staal, R Chen, Y Y Ng, Martin Kovac, V H J van der Velden, H Wai, Elisabeth Macintyre, A. van der Linden, P G Hoogeveen, N Van Poecke, Juan Flores-Montero, Tomas Kalina, W.M. Comans-Bitter, A Koning, K.A.J. Brouwer-de Cock, A J van der Sluijs, J. J. M. Van Dongen, A L Noordijk, Ludovic Lhermitte, Alberto Orfao, E Dekking, Floor Weerkamp   +28 more
openaire   +4 more sources

PTPROt Inactivates the Oncogenic Fusion Protein BCR/ABL and Suppresses Transformation of K562 Cells [PDF]

Journal of Biological Chemistry, 2009
Chronic myelogenous leukemia is typified by constitutive activation of the c-abl kinase as a result of its fusion to the breakpoint cluster region (BCR). Because the truncated isoform of protein-tyrosine phosphatase receptor-type O (PTPROt) is specifically expressed in hematopoietic cells, we tested the possibility that it could potentially ...
Huban Kutay, Kalpana Ghoshal, Jharna Datta, Samson T. Jacob, Satavisha Roy, David M. Lucas, Tasneem Motiwala, Sarmila Majumder   +7 more
openaire   +5 more sources

Spontaneous Soft Tissue Haematomas-A Rare Presentation of Chronic Myeloid Leukemia (CML) [PDF]

Journal of Clinical and Diagnostic Research, 2015
Spontaneous soft tissue haematomas are rarely found in haematological malignancies. Chronic myeloid leukemia (CML) is a myeloproliferative disorder which rarely present with thrombo-haemorrhagic phenomenon.
Manoj Lakhotia, Hans Raj Pahadiya, Gopal Raj Prajapati, Akanksha Choudhary, Ronak Gandhi   +4 more
doaj   +1 more source