With abundant experience in antibody development, Creative Biolabs is able to provide a full range of marker-specific IVD (in vitro diagnostic) antibody development services. Here, we focus on the BCR-ABL as a marker of myeloma.
BCR-ABL
BCR-ABL gene forms when pieces of chromosomes 9 and 22 break off and trade positions. The ABL gene from chromosome 9 is linked to the BCR gene on chromosome 22 to form a BCR-ABL fusion gene. The changed chromosome 22 with the fusion gene is called the Philadelphia chromosome. The gene encodes a hybrid protein: the "always-on" tyrosine kinase signaling protein, leading to uncontrolled cell division. Philadelphia chromosome or Philadelphia translocation (Ph) is a specific genetic abnormality in chromosome 22 of leukemia cancer cells (especially chronic myelogenous leukemia (CML) cells). The BCR-ABL fusion gene has been found in most patients with chronic myelogenous leukemia and in certain patients with acute lymphoblastic leukemia (ALL) or acute myeloid leukemia (AML). The presence of this translocation is a highly sensitive assay for CML because all CML cases are positive for BCR-ABL1.
Fig.1 Locations of the breakpoints in the ABL and BCR genes and structure of the chimeric BCR/ABL mRNA transcripts derived from the various breaks. (Salesse S., 2002)
BCR-ABL Marker of Lymph Cancer
Chronic myelogenous leukemia (CML) is a myeloproliferative disorder resulting from the clonal expansion of a transformed multipotent hematopoietic stem cell. At the molecular level, CML is characterized by the Philadelphia chromosome (Ph) resulting from a balanced translocation between chromosome 9 and 22 which leads to the formation of the BCR/ABL fusion gene. BCR-ABL1 is present in all cases of chronic myeloid leukemia, but it is also involved in other cancers. These include pediatric B-cell acute lymphoblastic leukemia (3-5%), adult B-cell acute lymphoblastic leukemia (25-30%), acute myeloid leukemia (rare), and T-cell acute lymphoblastic leukemia. ABL1 kinase inhibitors have been developed as targeted therapies against BCR-ABL1 positive malignancies.
BCR-ABL Marker of Chronic Myeloid Leukemia
CML is a myeloproliferative disorder resulting from the clonal expansion of a transformed multipotent hematopoietic stem cell. CML is a biphasic disease with an initial chronic phase characterized by a massive expansion of myeloid precursors and mature cells that leave the bone marrow (BM) prematurely but retain their capacity to differentiate normally. Current National Comprehensive Cancer Network recommended that, in addition to complete cytogenetic response and mutational status, molecular endpoints should be regarded as aids in the management of patients considered for first-line and second-line therapy. It is worth noting that high BCR-ABL1 radios are not reliable when the AB1 gene is applied as an internal control gene. There raised the concerns that the primer/probe amplifies both the wild-type and translocated ABL1 genes. In this way, the result underestimates the actual amount of BCR-ABL1, particularly when BCR-ABL1 levels are high when the individuals are going through diagnosis process.
Fig. 2 Signaling pathways of p210BCR/ABL. (Salesse S., 2002)
IVD antibodies are extensively used in diagnostic immunoassays (e.g., ELISA, lateral flow, western blot) for disease screening and therapeutic monitoring. Through our role as a leading antibody service provider, Creative Biolabs is well-positioned to offer high-quality IVD antibody development and immunoassay development services to clients across the global. Our expertise lies in antibody conjugation, antibody pair screening, assay design, validation, and production.
Having successfully accomplished numerous projects, Creative Biolabs is confident in offering services of the best quality and finest results to our customers. If you are interested in our services, please contact us for more details.
Reference
For Research Use Only.
