Chromosomol translocations in chronic myeloproliferative diseases (CMPD) almost invariably result in epxression of constitutively activated fusion tyrosine kinases. The hallmark of these diseases is CML, where the BCR/ABL activated tyrosine kinase results from the balanced reciprocal Philadelphia chromosome translocation t(9;22).
Leukemia and Lymphomas
Chronic Myelogenous Leukenia (CML)
CML is a malignant chronic myeloproliferative disorder (MPD) of the hematopoietic stem cell. All CML have a t(9;22) causing fusion of the 3’ ABL region at 9q34 with the 5’ BCR region at 22q11. This chimeric BCR/ABL gene encodes a constitutively activated protein tyrosine kinase with profound effects on cell cycle, adhesion, and apoptosis. Understanding this process has led to the development of the drug imatinib mesylate (Gleevec™), the first in a new class of genetically targeted agents, this is a major advance in cancer treatment. Several different approaches are used to analyze the BCR/ABL t(9;22)(q34;q11) by FISH each providing different details about this translocation.
BCR/ABL Product Family
The Philadelphia chromosome is an abnormally short chromosome 22 that is one of the two chromosomes involved in a translocation with chromosome 9. This translocation t(9;22)(q34;q11) takes place in a single bone marrow cell and, through the process of clonal expansion, gives rise to the leukemia. ABL and BCR are normal genes on chromosomes 9 and 22, respectively. The ABL gene encodes a tyrosine kinase enzyme whose activity is tightly controlled. In the formation of the Ph translocation, two fusion genes are generated: BCR-ABL on the Ph chromosome and ABL-BCR on the chromosome 9 participating in the translocation. The BCR-ABL gene encodes a protein with deregulated tyrosine kinase activity. The presence of this protein in the CML cells is strong evidence of its pathogenetic role. The efficacy in CML of a drug that inhibits the BCRABL tyrosine kinase has provided the final proof that the BCR-ABL oncoprotein is the unique cause of CML. The Poseidon portfolio contains now 4 different probes for BCR/ABL to suit all needs for the detection of t(9;22) by FISH:
Chromosomol translocations in chronic myeloproliferative diseases (CMPD) almost invariably result in epxression of constitutively activated fusion tyrosine kinases. The hallmark of these diseases is CML, where the BCR/ABL activated tyrosine kinase results from the balanced reciprocal Philadelphia chromosome translocation t(9;22).
Leukemia and Lymphomas
Chronic Myelogenous Leukenia (CML)
CML is a malignant chronic myeloproliferative disorder (MPD) of the hematopoietic stem cell. All CML have a t(9;22) causing fusion of the 3’ ABL region at 9q34 with the 5’ BCR region at 22q11. This chimeric BCR/ABL gene encodes a constitutively activated protein tyrosine kinase with profound effects on cell cycle, adhesion, and apoptosis. Understanding this process has led to the development of the drug imatinib mesylate (Gleevec™), the first in a new class of genetically targeted agents, this is a major advance in cancer treatment. Several different approaches are used to analyze the BCR/ABL t(9;22)(q34;q11) by FISH each providing different details about this translocation.
BCR/ABL Product Family
The Philadelphia chromosome is an abnormally short chromosome 22 that is one of the two chromosomes involved in a translocation with chromosome 9. This translocation t(9;22)(q34;q11) takes place in a single bone marrow cell and, through the process of clonal expansion, gives rise to the leukemia. ABL and BCR are normal genes on chromosomes 9 and 22, respectively. The ABL gene encodes a tyrosine kinase enzyme whose activity is tightly controlled. In the formation of the Ph translocation, two fusion genes are generated: BCR-ABL on the Ph chromosome and ABL-BCR on the chromosome 9 participating in the translocation. The BCR-ABL gene encodes a protein with deregulated tyrosine kinase activity. The presence of this protein in the CML cells is strong evidence of its pathogenetic role. The efficacy in CML of a drug that inhibits the BCRABL tyrosine kinase has provided the final proof that the BCR-ABL oncoprotein is the unique cause of CML. The Poseidon portfolio contains now 4 different probes for BCR/ABL to suit all needs for the detection of t(9;22) by FISH: