The abl oncogene is translocated from chromosome 9 to 22 in the creation of the Philadelphia (Ph1) chromosome. This article describes new translocation breakpoints identified in two patients with chronic myelogenous leukemia using Southern blotting and cloned human DNA probes from chromosome 9. The translocation breakpoints on chromosome 9 in both of these patients lie closer to the human cellu...

BACKGROUND In 5%-10% of patients with of chronic myelogenous leukemia (CML), the Philadelphia chromosome (Ph) is not identified, despite the presence of the associated BCR-ABL molecular abnormality (Ph-negative, BCR-ABL-positive CML) because of sub-microscopic rearrangements. PATIENTS AND METHODS Six patients with Ph-negative, BCR-ABL-positive CML were investigated. The Ph chromosome detectio...

acute lymphoblastic leukemia(all) is due to early stage arrest of lymphoblast development. the translocation of philadelphia (ph) chromosome occurs as a result of the bcr-abl fusion gene, which constitutively produced activated tyrosine kinase. this gene fusion is an important indicator for prognosis in all and is associated with poor overall survival and remission duration. bcr-abl could inter...

Chronic myeloid leukemia (CML) accounts for twenty percent of the incidence of leukemia in adults. The disease begins as a chronic low grade leukemia but frequently progresses to an accelerated transformation stage and then to blast crisis. The driving force behind CML is the Philadelphia chromosome (Ph), a reciprocal translocation t(9;22)(q34;q11) which forms the BCR-ABL fusion gene. Although ...

The consistent cytogenetic translocation of chronic myelogenous leukemia (the Philadelphia chromosome, Ph1) has been observed in cells of multiple hematopoietic lineages. This translocation creates a chimeric gene composed of breakpoint-cluster-region (bcr) sequences from chromosome 22 fused to a portion of the abl oncogene on chromosome 9. The resulting gene product (P210c-abl) resembles the t...

We report the transient response of a patient with the ETV6-ABL fusion gene to imatinib mesylate (STI571). A 38-year-old man was referred with an erroneous diagnosis of Philadelphia-positive chronic myeloid leukemia in blastic transformation for treatment with the ABL tyrosine kinase inhibitor, STI571. Further investigation indicated that the patient in fact had acute myeloid leukemia; no evide...

We previously demonstrated that activation of v-ABL protein tyrosine kinase resulted in suppression of apoptosis following interleukin-3 removal using an interleukin-3-dependent haemopoietic cell line transfected with a temperature-sensitive mutant of the v-abl oncoprotein (IC.DP). Cellular signalling events associated with the activation of v-ABL included increased levels of sn-1,2-diacylglyce...

The BCR-ABL oncogene was the first chromosomal abnormality shown to be associated with a specific human malignancy, the chronic myelogenous leukemia (CML), resulting from a reciprocal t(9;22) translocation characterized by the formation of a shortened chromosome, named Philadelphia chromosome (Ph), in which the tyrosine kinase of c-ABL is constitutively activated. This chromosomal translocation...

A chromosomal translocation uniquely associated with chronic myeloid leukemia leads to the formation of a chimeric gene, bcr-abl, on the Philadelphia chromosome. The BRC-ABL protein displays an uncontrolled tyrosine kinase activity similar to that seen with the transforming oncogene of the Abelson murine leukemia (ABL) virus (v-abl). An interleukin 3 dependent cell line, IC.DP, has been transfe...

The identical cytogenetic marker, t(9;22)(q34;q11) (Philadelphia [Ph] translocation), is found in approximately 90%, 20%, and 2% of adult patients with chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), and acute myelogenous leukemia (AML), respectively. In CML, the molecular events resulting from the Ph translocation include a break within the bcr locus on chromosome 22, t...