XL BCR/ABL1 plus consists of 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/ABL 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/ABL active tyrosine kinase has become a major drug in treating CML, gastrointestinal stromal tumors, and other cancers.

Clinical Applications

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

XL BCR/ABL1 plus hybridized to bone marrow cells. Two interphase cells with two fusion signals and separated orange and green signals each are shown, indicating a BCR::ABL1 translocation.

• Dewald et al (1998) Blood 91:3357-3365
• Huntly et al (2003) Blood 102:1160-1168
• Primo et al (2003) Leukemia 17:1124-1129