XL BCR/ABL1/ASS consists of an aqua-labeled probe hybridizing to the ASS1 gene region at 9q34.1, an orange-labeled probe hybridizing to the ABL1 gene region at 9q34.1 and a green-labeled probe hybridizing to the BCR gene region at 22q11.2.

Probe maps are created in accordance with the intended purpose of the product. Solid colored bars do not necessarily indicate that the probe fully covers the indicated genomic region. Therefore, caution is advised when interpreting results generated through off-label use. Probe map details based on UCSC Genome Browser GRCh37/hg19. Map components not to scale. Further information is available on request.

Chronic myelogenous leukemia (CML) is genetically characterized by the presence of the reciprocal translocation t(9;22)(q34;q11), resulting in a BCR/ABL1 gene fusion on the derivative chromosome 22, called the Philadelphia (Ph) chromosome. The same translocation can also be found in acute myeloid leukemia (AML) and acute lymphocytic leukemia (ALL) with some variation in the breakpoint region. Glivec^® (imatinib mesylate) treatment targeting the BCR/ABL1 active tyrosine kinase has become a major drug in treating CML, gastrointestinal stromal tumors, and other cancers.

Deletions at the t(9;22) breakpoint regions, found in 5% of CML patients with a Ph translocation, have been associated with resistance to treatment in patients receiving tyrosine kinase inhibitors.

Clinical Applications

• Chronic Myelogenous Leukemia and Myeloproliferative Neoplasms (CML/MPN)
• Acute Lymphoblastic Leukemia (ALL)
• Acute Myelogenous Leukemia (AML)

XL BCR/ABL1/ASS hybridized to lymphocytes. One normal metaphase is shown.

• Dewald et al (1998) Blood 91:3357-3365
• DeMelo et al (2008) Canc Genet Cytogenet 182:111-115
• Luatti et al (2012) Blood 120:761-767