Protein kinases have grown over the past few years as a crucial target for different cancer
types. With the multifactorial nature of cancer, and the fast development of drug resistance …

Deregulated activity of BCR-ABL1, a nonreceptor tyrosine kinase encoded by the fusion
gene resulting from the t (9; 22)(q34; q11) chromosomal translocation, is thought to be the …

Abstract c-Abl is activated in the brain of Parkinson's disease (PD) patients and in 1-methyl-4-
phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-intoxicated mice where it inhibits parkin through …

The oncogenic fusion protein BCR-ABL is the driving force of leukemogenesis in chronic
myeloid leukemia (CML). Despite great progress for CML treatment through application of …

Abstract The Philadelphia (Ph) chromosome, resulting from the t (9; 22)(q34; q11)
translocation, can be found in chronic myeloid leukemia (CML) as well as in a subset of …

In chronic myeloid leukemia (CML) patients, tyrosine kinase inhibitors (TKIs) may select for
drug-resistant BCR-ABL1 kinase domain (KD) mutants. Although Sanger sequencing (SS) is …

Accumulating evidence suggests that the non-receptor tyrosine kinase c-Abl plays an
important role in the progression of Parkinson's disease (PD) and c-Abl inhibition could be …

Chronic myeloid leukemia (CML) has been the first human malignancy to be associated,
more than 50 years ago, with a consistent chromosomal abnormality—the t (9; 22)(q34; q11) …

Optimal use of current therapeutic opportunities for chronic myeloid leukemia patients
requires integration of clinical and laboratory monitoring. Assessment of molecular response …

In chronic myeloid leukemia (CML) and Philadelphia-positive (Ph+) acute lymphoblastic
leukemia (ALL) patients who fail imatinib treatment, BCR-ABL1 mutation profiling by Sanger …