Results 11 to 20 of about 19,722 (182)

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   +2 more sources

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

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   +2 more sources

Structure and Dynamics of the ABL1 Tyrosine Kinase and Its Important Role in Chronic Myeloid Leukemia. [PDF]

Arch Pharm (Weinheim)
Tyrosine kinase inhibitors (TKIs) targeting the ABL1 tyrosine kinase are playing a critical role in the treatment of chronic myeloid leukemia (CML) through the inhibition of persistently activated signaling pathways mediated by the BCR‐ABL1 fusion protein.
Irgit A, Kamıs R, Sever B, Tuyun AF, Otsuka M, Fujita M, Demirci H, Ciftci H.   +7 more
europepmc   +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   +2 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   +5 more sources

Flow Cytometric Immunobead Assay for Detection of BCR-ABL1 Fusion Proteins in Chronic Myleoid Leukemia: Comparison with FISH and PCR Techniques.

PLoS ONE, 2015
Chronic Myeloid Leukemia (CML) is characterized by a balanced translocation juxtaposing the Abelson (ABL) and breakpoint cluster region (BCR) genes.
Anna Grazia Recchia, Nadia Caruso, Sabrina Bossio, Mariavaleria Pellicanò, Laura De Stefano, Stefania Franzese, Angela Palummo, Vincenzo Abbadessa, Eugenio Lucia, Massimo Gentile, Ernesto Vigna, Clementina Caracciolo, Antolino Agostino, Sara Galimberti, Luciano Levato, Fabio Stagno, Stefano Molica, Bruno Martino, Paolo Vigneri, Francesco Di Raimondo, Fortunato Morabito   +20 more
doaj   +2 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]

Blood, 2014
Abstract The successful targeting of BCR/ABL by selective ABL-kinase inhibitors (AKI) such as Imatinib, Nilotinib, or Dasatinib alone is unable to eradicate the leukemic clone in Philadelphia chromosome positive (Ph+ ) leukemia. The t(9;22)(q34;q11) is a balanced translocation.
Anahita Rafiei, Oliver G. Ottmann, Claudia Oancea, Martin Ruthardt, Afsar Ali Mian   +4 more
openaire   +3 more sources

Leukemia-associated fusion proteins, dek-can and bcr-abl, represent immunogenic HLA-DR-restricted epitopes recognized by fusion peptide-specific CD4+ T lymphocytes [PDF]

Leukemia, 2002
Although CD4(+) helper T lymphocytes have been demonstrated to play an important role in antitumor immune response, only a few epitopes of tumor-associated antigens recognized by HLA class II-restricted CD4(+) T lymphocytes have been identified.
Shigeru Fujita, Masaki Yasukawa, Kensuke Kojima, Mine Harada, Mitsune Tanimoto, H Hamaguchi, Masanori Makita, Hironari Niiya, Taichi Azuma   +8 more
openaire   +3 more sources

Alternative BCR/ABL Splice Variants in Philadelphia Chromosome–Positive Leukemias Result in Novel Tumor-Specific Fusion Proteins that May Represent Potential Targets for Immunotherapy Approaches

Cancer Research, 2007
Abstract Imatinib currently represents the standard treatment in the early chronic phase of chronic myelogenous leukemia (CML), thanks to the high percentage of cytogenetic complete remission achieved, but it is yet unclear to what extent it can eradicate leukemia.
Volpe G, Cignetti A, Panuzzo C, Kuka M, Vitaggio K, Brancaccio M, Perrone G, Rinaldi M, Prato G, Fava M, Geuna M, Pautasso M, Casnici C, Signori E, Tonon G, Tarone G, Marelli O, Fazio VM, Saglio G   +18 more
openaire   +8 more sources

Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent. [PDF]

Cell Biol Int
ABSTRACT Chronic Myeloid Leukemia (CML) is characterized by the BCR::ABL1 fusion gene, driving uncontrolled myeloid cell proliferation. Furthermore, metabolic dysregulation contributes to disease progression. Despite the efficacy of tyrosine kinase inhibitors (TKIs), unresolved clinical needs persist, necessitating refined preclinical models.
Cavalleri A, Xhahysa B, Mutti S, Ferraro RM, Mazzoldi EL, Farina M, Leoni A, Garuffo L, Trenta F, Re F, Radici V, Buttini EA, Morello E, Magliano G, Cancelli V, Giliani SC, Malagola M, Russo D, Bernardi S.   +18 more
europepmc   +2 more sources