Abstract

Case report 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.

Highlights

  • Imatinib (IM) inhibits the TK protein from chromosome Philadelphia (Ph)

  • 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

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Summary

Open Access

Clonal evolution in a patient with CML detected by FISH precedes imatinib treatment failure. Virginia Enriquez[1], Judith Cruz[1], Olga Gutierrez[1], Maria Teresa Salles[1], Pablo Vargas[2], Arturo Martínez[2], Myrna Candelaria[1], Rafael Hurtado[2] and Eduardo Cervera*1. Address: 1Instituto Nacional de Cancerología, México, D.F and 2Hospital Angeles del Pedregal, México, D.F. Published: 5 February 2007 BMC Cancer 2007, 7(Suppl 1):A41 doi:10.1186/1471-2407-7-S1-A41. islen2t4iilathbleohr>erAelso.s-lores Gallardo-Rincon, Luis A Herrera, Myrna Candelaria, Adolfo Fuentes-Alburo Meeting abstracts – A single PDF containing all

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