Robert Peter Gale1, Jane Apperley2. 1. Department of Immunology and Inflammation, Centre for Haematology Research, Imperial College London, London, SW7 2AZ, UK. robertpetergale@alumni.ucla.edu. 2. Department of Immunology and Inflammation, Centre for Haematology Research, Imperial College London, London, SW7 2AZ, UK.
Abstract
PURPOSE OF REVIEW: Determine if therapy of chronic myeloid leukaemia (CML) is a model for treating other cancers. RECENT FINDINGS: CML has a relatively homogeneous phenotype and genotype and is caused by one mutation, BCRABL1, in every instance. In contrast, most other leukaemias, haematologic cancers and solid cancer have more heterogeneous phenotypes and extraordinarily greater genotypic diversity and mutational complexity. Lesions learned from treating CML have little applicability to other leukaemias, haematologic cancers or solid cancer.
PURPOSE OF REVIEW: Determine if therapy of chronic myeloid leukaemia (CML) is a model for treating other cancers. RECENT FINDINGS:CML has a relatively homogeneous phenotype and genotype and is caused by one mutation, BCRABL1, in every instance. In contrast, most other leukaemias, haematologic cancers and solid cancer have more heterogeneous phenotypes and extraordinarily greater genotypic diversity and mutational complexity. Lesions learned from treating CML have little applicability to other leukaemias, haematologic cancers or solid cancer.
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