6533b7d2fe1ef96bd125edc9

RESEARCH PRODUCT

BCR-ABL as a target for novel therapeutic interventions.

Thomas FischerT KindlerRg Meyer

subject

medicine.drug_classmedicine.medical_treatmentT-LymphocytesClinical BiochemistryFusion Proteins bcr-ablChromosomal translocationChromosome 9Antineoplastic AgentsBiologyGenes ablTyrosine-kinase inhibitorhemic and lymphatic diseasesNeoplasmsDrug DiscoverymedicineAnimalsHumansneoplasmsGenePharmacologyOncogeneImmunotherapyProtein-Tyrosine KinasesFusion proteinCell Transformation NeoplasticImmunologyMolecular MedicineSignal transductionSignal Transduction

description

The BCR-ABL oncogene is the result of a reciprocal translocation between the long arms of chromosome 9 and 22 t(9; 22). There is good experimental evidence demonstrating that BCR-ABL is the single causative abnormality in chronic myeloid leukaemia (CML), making it a unique model for the development of molecular targets. In addition to CML, BCR-ABL transcripts can be found in a minority of acute lymphoblastic leukaemias and very rarely in acute myeloid leukaemia (AML). Elucidating the molecular mechanisms and downstream pathways of BCR-ABL has led to the design of several novel therapeutic approaches. In this review, molecular targeting of BCR-ABL will be discussed based on the inhibition of protein tyrosine kinase activity, antisense strategies and immunomodulation.

10.1517/14728222.6.1.85https://pubmed.ncbi.nlm.nih.gov/11901483