Summary of representative studies that describe use of imatinib in the treatment of CMML or atypical CMPD*
Study . | Clinical diagnosis . | No. patients . | Cytogenetic findings . | Molecular findings . | Response . | Imatinib dose, mg/d . |
|---|---|---|---|---|---|---|
| Magnusson et al80 * | CMML | 1 | t(5;17)(q33;p13) | Rab5/PDGFRB | CR | 400 |
| Pitini et al82 † | CMML | 1 | t(5;12)(q33;p13) | ETV6/PDGFRB | CR | 400 |
| Cortes et al97 | CMML | 3 | 2 normal 1 trisomy 21 | NA | 3 NR | 400 |
| Wilkinson et al18 * | aCMPD | 1 | t(1;5)(q23;q33) | PDE4DIP/PDGFRB | CR | NA |
| Trempat et al37 * | aCMPD | 1 | t(4;22)(q12;q11) | BCR/PDGFRA | CHR | 400 |
| Garcia et al67 * | aCMPD | 1 | t(5;10)(q33;q22) | H4(D10S170)/PDGFRB | CR | 400 |
| Demetri et al68 *‡ | aCMPD | 1 | Complex abnormalities | ETV6/ABL | CHR | 600 |
| Cortes97 | aCMPD | 7 | NA | NA | 1 MHR | 400 |
Study . | Clinical diagnosis . | No. patients . | Cytogenetic findings . | Molecular findings . | Response . | Imatinib dose, mg/d . |
|---|---|---|---|---|---|---|
| Magnusson et al80 * | CMML | 1 | t(5;17)(q33;p13) | Rab5/PDGFRB | CR | 400 |
| Pitini et al82 † | CMML | 1 | t(5;12)(q33;p13) | ETV6/PDGFRB | CR | 400 |
| Cortes et al97 | CMML | 3 | 2 normal 1 trisomy 21 | NA | 3 NR | 400 |
| Wilkinson et al18 * | aCMPD | 1 | t(1;5)(q23;q33) | PDE4DIP/PDGFRB | CR | NA |
| Trempat et al37 * | aCMPD | 1 | t(4;22)(q12;q11) | BCR/PDGFRA | CHR | 400 |
| Garcia et al67 * | aCMPD | 1 | t(5;10)(q33;q22) | H4(D10S170)/PDGFRB | CR | 400 |
| Demetri et al68 *‡ | aCMPD | 1 | Complex abnormalities | ETV6/ABL | CHR | 600 |
| Cortes97 | aCMPD | 7 | NA | NA | 1 MHR | 400 |
CHR indicates complete hematologic response (normalization of blood counts); MHR, major hematologic response (increase in hemoglobin concentration from 95 to 137 g/L [9.5 to 13.7/dL]); D10S170, DNA segment on chromosome 10 (unique) 170. Remaining abbreviations are explained in Tables 1 and 2.
Data supported the presence of imatinib-responsive molecular target before the start of therapy.
Some patients were described as having atypical CML based on a CML phenotype without Philadelphia chromosome or bcr/abl fusion and association with dysplasia. Does not include patients with prominent peripheral eosinophilia.
Patient was treated in chronic phase of atypical CML after receiving induction therapy for blast crisis.