Feb 15, 2012 · Aberrant tyrosine kinase activity plays a critical role in many hematologic disorders, including chronic myeloid leukemia characterized by the constitutive activity of BCR-ABL. ABL therefore represents a crucial target for new therapeutic strategies.

Targeted therapies based on tyrosine kinase inhibitors (TKIs), such as imatinib, dasatinib, nilotinib, bosutinib, and ponatinib, have revolutionized the treatment of BCR-ABL1-driven leukemia, particularly chronic myeloid leukemia (CML).

Feb 14, 2012 · Aberrant tyrosine kinase activity plays a critical role in many hematologic disorders, including chronic myeloid leukemia characterized by the constitutive activity of BCR-ABL. ABL therefore represents a crucial target for new therapeutic strategies. Here, we summarize the molecular pathways that are abnormally activated by the oncoprotein.

Abl kinases are prototypic cytoplasmic tyrosine kinases and are involved in a variety of chromosomal aberrations in different cancers. This causes the expression of Abl fusion proteins, such as Bcr-Abl, that are constitutively activated and drivers of tumorigenesis.

BCR-ABL activates pathways mediating cytokine independence and protection against apoptosis in murine hematopoietic cells in a dose-dependent manner. Oncogene. 1998;16:335–348. doi: 10.1038/sj.onc.1201490.

Jan 16, 2011 · We provide an up-to-date synopsis of BCR-ABL signaling pathways, highlight new findings on mechanisms underlying BCR-ABL mutation acquisition and disease progression, discuss the use of nilotinib and dasatinib in a first-line capacity, and evaluate ponatinib, DCC-2036, and other ABL kinase inhibitors with activity against BCR-ABL T315I in the ...

Feb 1, 2024 · The BCR-ABL oncogene stands as a pivotal genetic anomaly with profound implications for the pathogenesis and progression of specific leukemia forms, notably chronic myeloid leukemia (CML) and a distinct subset of acute lymphoblastic leukemia (ALL).

Jan 1, 2004 · The prototypic non-receptor tyrosine kinase c-Abl is implicated in various cellular processes. Its oncogenic counterpart, the Bcr–Abl fusion protein, causes certain human leukaemias.

Jun 1, 1997 · Current research efforts are focused on defining the mechanism by which BCR-ABL transforms cells, with a view toward applying insights from these studies to the treatment of CML patients. BCR-ABL contains tyrosine residues, an SH2 domain, an …

The Abl protein intricately regulates the cell cycle by phosphorylating protein tyrosine residues through diverse signaling pathways. In CML, the BCR-ABL fusion protein disrupts the first exon of Abl, leading to sustained activation of tyrosine kinase and resistance to deactivation mechanisms.