Table 10

Molecular genetic abnormalities in myeloid/lymphoid neoplasms associated with eosinophilia

DiseasePresentationGeneticsTreatment
PDGFRA Eosinophilia Cryptic deletion at 4q12 Respond to TKI 
↑Serum tryptase FIP1L1-PDGFRA, at least 66 other partners 
↑Marrow mast cells 
PDGFRB Eosinophilia t(5;12)(q32;p13.2) ETV6-PDGFRB, at least 25 other partners Respond to TKI 
Monocytosis mimicking CMML 
FGFR1 Eosinophilia Translocations of 8p11.2 Poor prognosis; do not respond to TKI 
Often presents with T-ALL or AML FGFR1-various partners 
PCM1-JAK2 Eosinophilia t(8;9)(p22;p24.1) PCM1-JAK2 May respond to JAK2 inhibitors 
Rarely presents with T-LBL or B-ALL 
Bone marrow shows left-shifted erythroid predominance and lymphoid aggregates 
DiseasePresentationGeneticsTreatment
PDGFRA Eosinophilia Cryptic deletion at 4q12 Respond to TKI 
↑Serum tryptase FIP1L1-PDGFRA, at least 66 other partners 
↑Marrow mast cells 
PDGFRB Eosinophilia t(5;12)(q32;p13.2) ETV6-PDGFRB, at least 25 other partners Respond to TKI 
Monocytosis mimicking CMML 
FGFR1 Eosinophilia Translocations of 8p11.2 Poor prognosis; do not respond to TKI 
Often presents with T-ALL or AML FGFR1-various partners 
PCM1-JAK2 Eosinophilia t(8;9)(p22;p24.1) PCM1-JAK2 May respond to JAK2 inhibitors 
Rarely presents with T-LBL or B-ALL 
Bone marrow shows left-shifted erythroid predominance and lymphoid aggregates 

↑, Increased.

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