Since γ-catenin was dispensable for normal hematopoiesis, these lineage- and disease-specific features of canonical Wnt signaling identified a potential therapeutic target for the treatment of BCR-ABL1<sup>+</sup> B-ALL.
High-risk subtypes of B-cell acute lymphoblastic leukemia (B-ALL) include Philadelphia chromosome-positive (Ph+) B-ALL driven by the <i>BCR-ABL1</i> oncogene and a more recently identified subtype known as <i>BCR-ABL</i>-like or Ph-like B-ALL.
The aberrant expression and mutation of CFTR have been observed in several tumor, but not in philadelphia chromosome-positive(Ph+) acute leukemia, including Ph+ B cell acute lymphoblastic leukemia(Ph+ B-ALL) and chronic myelogenous leukemia blast crisis phases (CML-BC).
Our meta-analysis suggests that IKZF1 deletion is a poor prognostic factor for adults with B cell ALL and may be more valuable in BCR-ABL1-negative B cell ALL patients.
BCR-ABL1(+) precursor B-cell acute lymphoblastic leukemia (BCR-ABL1(+) B-ALL) is an aggressive hematopoietic neoplasm characterized by a block in differentiation due in part to the somatic loss of transcription factors required for B-cell development.
Expression of CD25 is a specific and relatively sensitive marker for the Philadelphia chromosome (BCR-ABL1) translocation in pediatric B acute lymphoblastic leukemia.
A 74-year-old man was previously diagnosed with BCR-ABL1-positive pre-B cell acute lymphoblastic leukaemia (pre-B ALL) based on bone marrow cytology, flow cytometry, cytogenetics and fluorescent in situ hybridisation findings.
A diagnosis of BCR-ABL1 (p190)-positive and ETV6-RUNX1-positive B-ALL was made, and treatment was initiated according to the AIEOP-BFM-ALL2000 protocol.
A diagnosis of BCR-ABL1 (p190)-positive and ETV6-RUNX1-positive B-ALL was made, and treatment was initiated according to the AIEOP-BFM-ALL2000 protocol.
The presence of the type A fusion transcript strongly implies ALL manifestation in ETV6/ABL1-positive hematologic malignancies as minor BCR breakpoint in BCR/ABL1-positive ALL.
However, BCR-ABL1 was expressed and active in Stat5-null leukemic stem cells, and Stat5 deletion did not prevent progression to lymphoid blast crisis or abolish establishedB-cell acute lymphoblastic leukemia.
The abnormal Ph chromosome, which arises from a translocation creating the BCR-ABL1 fusion gene, is most commonly associated with chronic myelogenous leukemia (CML) and precursor B cell acute lymphoblastic leukemia (B-ALL).
Chromosomal rearrangements involving the ABL1 gene, leading to a BCR-ABL1 fusion gene, have been mainly associated with chronic myeloid leukemia and B-cell acute lymphoblastic leukemia (ALL).
Here we describe a fifth case of ABL1 deletion without BCR/ABL1 rearrangement in an adolescent patient with precursor B-cell lymphoblastic leukemia (B-ALL) and review the relevant literature.
The BCR-ABL1 fusion kinase is frequently associated with chronic myeloid leukemia and B-cell acute lymphoblastic leukemia but is rare in T-cell acute lymphoblastic leukemia (T-ALL).
These findings suggest a role for the pre-BCR complex in the response of ALL cells to treatment and provide insight into the mechanism of steroid response in the treatment of pre-B ALL.