BCR/ABL inhibition by an escort/phosphatase fusion protein [PDF]
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+4 more
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BCR-ABL is the oncogenic fusion product of tyrosine kinase ABL1 and a highly frequent driver of acute lymphocytic leukemia (ALL) and chronic myeloid leukemia (CML).
Martin Smolnig+2 more
semanticscholar +1 more source
PTPROt Inactivates the Oncogenic Fusion Protein BCR/ABL and Suppresses Transformation of K562 Cells [PDF]
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+7 more
openaire +5 more sources
Acute lymphoblastic leukemia with e1a3 BCR/ABL fusion protein. A report of two cases [PDF]
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+13 more
openaire +3 more sources
Spontaneous Soft Tissue Haematomas-A Rare Presentation of Chronic Myeloid Leukemia (CML) [PDF]
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+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]
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
doaj +1 more source
Light-Activating PROTACs in Cancer: Chemical Design, Challenges, and Applications
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
doaj +1 more source
A combined computational and experimental strategy identifies mutations conferring resistance to drugs targeting the BCR-ABL fusion protein [PDF]
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
openaire +3 more sources
The oncoprotein BCR-ABL has distinct fusion proteins generated from the Philadelphia chromosome translocation, depending on the site of the breakpoint on chromosome 22. The p210 is the hallmark of chronic myeloid leukemia.
Nalinikumari Gandhe+2 more
semanticscholar +1 more source
Intrinsic structural disorder confers cellular viability on oncogenic fusion proteins. [PDF]
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
doaj +1 more source