The functional interplay between the t(9;22)-associated fusion proteins BCR/ABL and ABL/BCR in Philadelphia chromosome-positive acute lymphatic leukemia. [PDF]
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 +8 more
doaj +7 more sources
Reciprocal t(9;22) ABL/BCR fusion proteins: leukemogenic potential and effects on B cell commitment. [PDF]
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 +4 more
doaj +8 more sources
Lactate-mediated activation of GPR81 regulates BCR/Abl protein expression in chronic myeloid leukemia cells selected under low oxygen tension. [PDF]
Abstract Chronic myeloid leukemia (CML) is a stem cell‐driven neoplasia characterized by the expression of the constitutively active tyrosine kinase (TK) BCR/Abl. Under low oxygen, a condition that characterizes stem cell niches (SCNs) in vivo, the oncogenic BCR/Ablprotein is suppressed.
Menegazzi G +5 more
europepmc +2 more sources
Predictors of Response to Imatinib Therapy and Long-Term Outcomes in Paediatric and Adolescent Patients With Chronic Myeloid Leukaemia. [PDF]
ABSTRACT Background Chronic myeloid leukaemia (CML) is an infrequent myeloproliferative neoplasm in the paediatric population as compared to adults. Despite vast progress in understanding the disease biology and therapy of CML‐chronic phase (CML CP), the applicability of risk scoring systems in practice and prognostic factors in children remain grey ...
Saha S +6 more
europepmc +2 more sources
Flow cytometric immunobead assay for the detection of BCR–ABL fusion proteins in leukemia patients [PDF]
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) +28 more
openaire +4 more sources
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.
Y M, Lim +4 more
openaire +2 more sources
Relationship Between BCR/ABL Fusion Proteins and Leukemia Phenotype [PDF]
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 +3 more
openaire +3 more sources
Background The fusion oncoprotein Bcr-Abl is mostly located in the cytoplasm, which causes chronic myeloid leukemia (CML). After moving into the nucleus, the fusion protein can induce apoptosis of CML cells.
Yuhang Peng +5 more
doaj +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 ...
Tasneem, Motiwala +7 more
openaire +4 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

