Results 11 to 20 of about 20,740 (205)

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.
Weerkamp, F (Floor), Dekking, E, Ng, Peter, van der Velden, Vincent, Wai, H, Böttcher, S, Brüggemann, M, van der Sluijs, AJ, Koning, A, Boeckx, N, Van Poecke, N, Lucio, P, De Mendonca, A, Sedek, L, Szczepanski, Tomek, Kalina, T, Kovac, M, Hoogeveen, Patricia, Flores-Montero, J, Orfao, A, Macintyre, E, Lhermitte, L, Chen, Ruoqing, Brouwer - de Cock, KAJ, van der Linden, Anne, Noordijk, Rianne, Bitter, Marieke, Staal, Frank, Dongen, Jacques   +28 more
openaire   +4 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.
Y M, Lim, S, Wong, G, Lau, O N, Witte, J, Colicelli   +4 more
openaire   +2 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   +3 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 ...
Tasneem, Motiwala, Sarmila, Majumder, Kalpana, Ghoshal, Huban, Kutay, Jharna, Datta, Satavisha, Roy, David M, Lucas, Samson T, Jacob   +7 more
openaire   +4 more sources

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, Amat, Juan Carlos, Martinez-Serra, Jordi   +13 more
openaire   +3 more sources

Oncogenic fusion protein BCR-FGFR1 requires the breakpoint cluster region-mediated oligomerization and chaperonin Hsp90 for activation. [PDF]

, 2020
Mutation and translocation of fibroblast growth factor receptors often lead to aberrant signaling and cancer. This work focuses on the t(8;22)(p11;q11) chromosomal translocation which creates the breakpoint cluster region (BCR) fibroblast growth factor ...
Bisom-Rapp, Ezra W, Donoghue, Daniel J, Meyer, April N, Nelson, Katelyn N, Peiris, Malalage N   +4 more
core   +2 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

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

Transforming and tumorigenic activity of JAK2 by fusion to BCR: molecular mechanisms of action of a novel BCR-JAK2 tyrosine-kinase. [PDF]

PLoS ONE, 2012
Chromosomal translocations in tumors frequently produce fusion genes coding for chimeric proteins with a key role in oncogenesis. Recent reports described a BCR-JAK2 fusion gene in fatal chronic and acute myeloid leukemia, but the functional behavior of ...
Álvaro Cuesta-Domínguez, Mara Ortega, Cristina Ormazábal, Matilde Santos-Roncero, Marta Galán-Díez, Juan Luis Steegmann, Ángela Figuera, Eva Arranz, José Luis Vizmanos, Juan A Bueren, Paula Río, Elena Fernández-Ruiz   +11 more
doaj   +1 more source

BCR and its mutants, the reciprocal t(9;22)-associated ABL/BCR fusion proteins, differentially regulate the cytoskeleton and cell motility

BMC Cancer, 2006
Background The reciprocal (9;22) translocation fuses the bcr (breakpoint cluster region) gene on chromosome 22 to the abl (Abelson-leukemia-virus) gene on chromosome 9.
Puccetti Elena, Beissert Tim, Güller Saskia, Zheng Xiaomin, Ruthardt Martin   +4 more
doaj   +1 more source