Cytogenetically complex SEC31A-ALK fusions are recurrent in ALK-positive large B-cell lymphomas

do well on imatinib 400mg/day with no evidence of ETV6-ABL1 transcript by qRT-PCR for the past five years.Somatic mutations in UTX, ASXL1, and TET2 have been reported in chronic myeloid leukemia and mutations in EZH2 and IDH1/2 in myeloid malignancies other than CML.We found no somatic alterations in these genes in the DNA extracted from whole blood prior to imatinib treatment, nor when the patient was in a molecular remission.Our studies indicate that ETV6-ABL1 + "chronic myeloid leukemia" can be sensitive to imatinib and there is significant overlap of molecular targets of ETV6-ABL1 with those of BCR-ABL1, suggesting that the ETV6-ABL1 fusion protein may trigger similar oncogenic cascades as BCR-ABL1.Finally, we were able to exclude mutations in any of the recently identified "myeloid" genes including UTX, ASXL1, EZH2, TET2 and IDH1/2 suggesting that the pathogenesis of ETV6-ABL1 + "chronic myeloid leukemia" may be as tyrosine kinase focused as BCR-ABL1 driven disease.