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Case Report

JAK2 V617f in chronic myeloid leukemia: driving force or passive bystander?

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Figures & data

Figure 1. Different possible scenarios of BCR-ABL1 and JAK2 (V617F) co-occurrence in MPNs. (A) A CML patient can show the JAK2 mutation at diagnosis and present a ‘hybrid’ phenotype. (B) A CML patient can acquire the JAK2 mutation during follow-up, together with a phenotype change. (C) A JAK2 mutated Ph-MPN can acquire BCR-ABL1 during follow-up and change the phenotype. CML: chronic myeloid leukemia; Ph-MPN: Philadelphia-negative myeloproliferative neoplasm; PLT: platelets; HCT: hematocrit; WBC: white blood cells.

Figure 1. Different possible scenarios of BCR-ABL1 and JAK2 (V617F) co-occurrence in MPNs. (A) A CML patient can show the JAK2 mutation at diagnosis and present a ‘hybrid’ phenotype. (B) A CML patient can acquire the JAK2 mutation during follow-up, together with a phenotype change. (C) A JAK2 mutated Ph-MPN can acquire BCR-ABL1 during follow-up and change the phenotype. CML: chronic myeloid leukemia; Ph-MPN: Philadelphia-negative myeloproliferative neoplasm; PLT: platelets; HCT: hematocrit; WBC: white blood cells.

Figure 2. BCR-ABL1 and JAK2 (V617F) kinetics during the CML follow-up. JAK2 V617F remained stable with minor fluctuations independent of BCR-ABL1 kinetics. The evaluations shown refer to the 2016–2022 time range. IS: international scale; MR: molecular response; NR: non responder; VAF: variant allele frequency.

Figure 2. BCR-ABL1 and JAK2 (V617F) kinetics during the CML follow-up. JAK2 V617F remained stable with minor fluctuations independent of BCR-ABL1 kinetics. The evaluations shown refer to the 2016–2022 time range. IS: international scale; MR: molecular response; NR: non responder; VAF: variant allele frequency.
Supplemental material

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