More than 95% of CML patients are diagnosed with the e13a2 or e14a2 BCR-ABL1 fusion transcripts while, in about 1% of these individuals, the break generates the e1a2 rearrangement.
Rapid decline of Philadelphia-positive metaphases after nilotinib treatment in a CML patient expressing a rare e14a3 <i>BCR-ABL1</i> fusion transcript: A case report.
In chronic myeloid leukemia (CML), the duration of deep molecular response (MR) before treatment cessation (MR4 or deeper, corresponding to BCR-ABL1 ≤ 0.01% on the International Scale (IS)) is considered as a prognostic factor for treatment free remission in stopping trials.
Leukemia stem cells contribute to drug-resistance and relapse in chronic myeloid leukemia and BCR-ABL1 inhibitor monotherapy fails to eliminate them, thereby necessitating alternate therapeutic strategies.
Treatment-free remission in chronic myeloid leukaemia-ie, achievement of a sustained deep molecular response leading to discontinuation of BCR-ABL1 tyrosine kinase inhibitor (TKI) therapy-has become a potential aim of therapy.
Chronic myeloid leukemia (CML) is characterized by the constitutive tyrosine kinase activity of the oncoprotein BCR-ABL1 in myeloid progenitor cells that activates multiple signal transduction pathways leading to the leukemic phenotype.
In our study population, patients in progressive stage CML and in IM resistant CP with multiple copies of BCR-ABL1 fusion gene displayed a poor response to targeted treatment with IM.
Chronic myeloid leukemia (CML) originates in a hematopoietic stem cell (HSC) transformed by the breakpoint cluster region (BCR)-abelson (ABL) oncogene and is effectively treated with tyrosine kinase inhibitors (TKIs).
The BCR-ABL1 oncogene is associated with chronic myeloid leukemia (CML) pathogenesis, but the molecular mechanisms that initiate leukemogenesis are still unclear.
We explore the potential pathways and events that may cooperate with BCR-ABL1 to answer these questions but also challenge the fundamental tenet that BCR-ABL1 is always the sole event initiating CML.
Using mouse models and patient-derived samples, we identified an essential role for γ-catenin in the initiation and maintenance of BCR-ABL1<sup>+</sup> B-ALL but not CML.
Chronic myeloid leukemia (CML) is a myeloproliferative disease caused by the constitutive tyrosine kinase (TK) activity of the BCR-ABL1 fusion protein.
BCR-ABL1 tyrosine kinase inhibitors (TKIs) are selective therapies for patients with chronic myeloid leukemia (CML) and induce deep molecular response (DMR).
The emergence of additional chromosomal abnormalities (ACAs) in Philadelphia chromosome/<i>BCR-ABL1</i> positive chronic myeloid leukemia (CML), is considered to be a feature of disease evolution.
Philadelphia chromosome, reciprocal translocation between chromosome 9 and 22, leading to a constitutively active fusion protein BCR-ABL1 is the common feature among Philadelphia positive acute lymphoblastic leukemia (Ph+ ALL) and chronic myeloid leukemia (CML).
BCR/ABL<sup>p210</sup> fusion gene, the characteristic biomarker of chronic myelogenous leukemia (CML), contains two different transcription isoforms, e13a2 and e14a2, which lead to differences in the pathological features and response to targeted drug.
Chronic myeloid leukemia is characterized by a t(9;22)(q34;q11.2) resulting in BCR/ABL1 fusion located on the derivative chromosome 22, also known as the Philadelphia chromosome.
CML transformation to lymphoid blast phase (BP) is associated with copy number abnormalities, characteristic of BCR-ABL1 positive acute lymphoblastic leukemia, but not of CML in the chronic phase.