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
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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 +5 more
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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 +4 more
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Association of HLA Class I and Class II genes with
BMC Cancer, 2004 Background Based on the site of breakpoint in t(9;22) (q34;q11), bcr-abl fusion in leukemia patients is associated with different types of transcript proteins.
Cano Pedro +2 more
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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 +4 more
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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 +11 more
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Light-Activating PROTACs in Cancer: Chemical Design, Challenges, and Applications
Applied Sciences, 2022 Nonselective cell damage remains a significant limitation of radiation therapies in cancer. Decades of successful integration of radiation therapies with other medicinal chemistry strategies significantly improved therapeutic benefits in cancer ...
Arvind Negi +2 more
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Chronic myeloid leukemia with an e1a3 BCR-ABL fusion protein: transformation to lymphoid blast crisis [PDF]
Biomarker Research, 2014 Chronic myelogenous leukemia (CML) results from the neoplastic transformation of a hematopoietic stem cell. CML is cytogenetically characterized by the presence of the Philadelphia chromosome (Ph'). Most patients with CML express e13a2 or e14a2 mRNAs that result from a rearrangement of the major breakpoint cluster regions (M-BCR) generating the 210-kDa
Martinez-Serra, Jordi +12 more
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A combined computational and experimental strategy identifies mutations conferring resistance to drugs targeting the BCR-ABL fusion protein [PDF]
Communications Biology, 2020 AbstractDrug resistance is of increasing concern, especially during the treatments of infectious diseases and cancer. To accelerate the drug discovery process in combating issues of drug resistance, here we developed a computational and experimental strategy to predict drug resistance mutations. Using BCR-ABL as a case study, we successfully recaptured
Jinxin Liu, Jianfeng Pei, Luhua Lai
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Intrinsic structural disorder confers cellular viability on oncogenic fusion proteins. [PDF]
PLoS Computational Biology, 2009 Chromosomal translocations, which often generate chimeric proteins by fusing segments of two distinct genes, represent the single major genetic aberration leading to cancer.
Hedi Hegyi, László Buday, Peter Tompa
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