Clonal evolution in a patient with CML detected by FISH precedes imatinib treatment failure
BMC Cancer volume 7, Article number: A41 (2007)
Imatinib (IM) inhibits the TK protein from chromosome Philadelphia (Ph). However, less than 10% of IM-treated patients become resistant. Second generation TK inhibitors are on active clinical research aimed to overcome most, but not all, important mutations.
A 61 year-old male was diagnosed on Sep/98 with CML chronic phase, he was treated with hydroxiurea, interferon and Ara-C. On July/01 the patient was on complete hematological response (CHR), but Ph positive in karyotyping (Ky) and fluorescence in-situ hybridization (FISH), there were not additional abnormalities. Patient began IM treatment, 400 mg/day. After 4 months of treatment, +der(22) was detected, but the patient was still on CHR. On subsequent visits, the patient had an increased frequency of chromosomal abnormalities, and after 2 years he lost CHR, regardless of the increase IM dose and the concomitant use of Ara-C. The patient was included on a dasatinib phase II protocol. 2 weeks after he had a profound cytopenia and 2 months after had CHR. Table 1 shows clinical and hematological and Ky and FISH follow-up.
Additional abnormalities found on Ky and FISH could preceed treatment failure. Molecular monitoring is required to guide treatment decisions. The role of second generation TK inhibitors needs to be defined.
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Enriquez, V., Cruz, J., Gutierrez, O. et al. Clonal evolution in a patient with CML detected by FISH precedes imatinib treatment failure. BMC Cancer 7 (Suppl 1), A41 (2007). https://doi.org/10.1186/1471-2407-7-S1-A41