Results 1 to 10 of about 11,727 (181)

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

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   +2 more sources

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

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   +2 more sources

p185BCR/ABL has a lower sensitivity than p210BCR/ABL to the allosteric inhibitor GNF-2 in Philadelphia chromosome-positive acute lymphatic leukemia [PDF]

Haematologica, 2012
Background The t(9;22) translocation leads to the formation of the chimeric breakpoint cluster region/c-abl oncogene 1 (BCR/ABL) fusion gene on der22, the Philadelphia chromosome. The p185BCR/ABL or the p210BCR/ABL fusion proteins are encoded as a result
Afsar A. Mian, Anna Metodieva, Yousef Najajreh, Oliver G. Ottmann, Jamal Mahajna, Martin Ruthardt   +5 more
doaj   +2 more sources

Direct evidence that leukemic cells present HLA-associated immunogenic peptides derived from the BCR-ABL b3a2 fusion protein [PDF]

Blood, 2001
Abstract The BCR-ABL oncogene is central in the pathogenesis of chronic myeloid leukemia (CML). Here, tandem nanospray mass spectrometry was used to demonstrate cell surface HLA-associated expression of the BCR-ABL peptide KQSSKALQR on class I-negative CML cells transfected with HLA-A*0301, and on primary CML cells from HLA-A3–positive ...
Clark, Richard E, Dodi, I. Anthony, Hill, Seran C, Lill, Jennie L, Aubert, Geraldine, Macintyre, Andrew R, Rojas, José Manuel, Bourdon, Audrey, Bonner, Philip LR, Wang, Lihui, Christmas, Stephen E, Travers, Paul J, Creaser, Colin S, Rees, Robert C, Madrigal, Alejandro   +14 more
openaire   +4 more sources

Fusion gene bcr-abl: From etiopathogenesis to the management of chronic myeloid leukemia [PDF]

JKKI (Jurnal Kedokteran dan Kesehatan Indonesia), 2017
Chronic Myeloid Leukemia (CML) is a myeloproliferative neoplasm. CML is relative frequent disorder. Most of CML patients have Philadelphia chromosome (Ph),which is derived from a reciprocal translocation between chromosome 9 and 22, t(9;22)(q34;ql1 ...
Tri Agusti Sholikah
doaj   +3 more sources

Characterization of a Monoclonal Antibody Specific for Novel Bcr/Abl Out-of-Frame Fusion Proteins

Hybridoma, 2011
The new tumor-specific antigens Bcr/Abl-OOF, identified in Philadelphia chromosome (Ph)-positive leukemia cells, are derived from an alternative splicing event involving BCR exons 1, 13, or 14 and ABL exons 4 and 5. The COOH-terminus of these transcription products contain an amino acid portion derived from an out-of-frame (OOF) reading of the ABL gene;
C. Casnici, G. Volpe, K. Crotta, C. Panuzzo, D. Lattuada, C. A. Cabras, R. Longhi, G. Saglio, O. Marelli   +8 more
openaire   +5 more sources

Peptides spanning the junctional region of both the abl/bcr and the bcr/abl fusion proteins bind common HLA class I molecules [PDF]

Leukemia, 2000
The Philadelphia (Ph) chromosome, resulting from the t(9;22) translocation, is characteristic of chronic myeloid leukemia (CML). As a result of this translocation, two novel chimeric genes are generated and the bcr/abl and abl/bcr fusion proteins expressed.
Berke, Z., Andersen, M.H., Pedersen, M., Fugger, L., Zeuthen, J.and, Haurum, J.S.   +5 more
openaire   +4 more sources

Influence of BCR/ABL fusion proteins on the course of Ph leukemias.

Acta Biochimica Polonica, 2004
The hallmark of chronic myeloid leukemia (CML) and a subset of acute lymphoblastic leukemia (ALL) is the presence of the Philadelphia chromosome as a result of the t(9;22) translocation. This gene rearrangement results in the production of a novel oncoprotein, BCR/ABL, a constitutively active tyrosine kinase.
Gennady D, Telegeev, Anna N, Dubrovska, Mykhaylo V, Dybkov, Stanislav S, Maliuta   +3 more
openaire   +4 more sources

Integrating dual convolutional networks and BiLSTM for precision prediction of chronic myeloid leukemia from protein sequences [PDF]

Frontiers in Genetics
IntroductionChronic Myeloid Leukemia (CML) is a hematologic malignancy characterized by the occurrence of the Philadelphia chromosome [t(9; 22)(q34; q11)], leading to the creation of the BCR–ABL fusion gene.
Hend Khalid Alkahtani, Ayman Qahmash
doaj   +2 more sources