Published online Jun 6, 2022. doi: 10.12998/wjcc.v10.i16.5446
Peer-review started: October 10, 2021
First decision: January 13, 2022
Revised: January 21, 2022
Accepted: April 21, 2022
Article in press: April 21, 2022
Published online: June 6, 2022
Processing time: 235 Days and 7.8 Hours
Chromosome i(17)(q10) abnormality is mainly associated with chronic myeloid leukemia (CML), myelodysplastic syndrome/myeloproliferative tumors (MDS/MPD), and acute myeloid leukemia (AML). The role of i(17)(q10) in AML is still unknown, the differences between AML and acute promyelocytic leukemia (APL)-like AML with i(17)(q10) need more research. This study aimed to investigate the clinical characteristics and laboratory evidence of 2 AML cases with i(17)(q10), similar to APL phenotype.
Both pediatric patients were males; case 1 had newly diagnosed AML, and case 2 showed relapsed tumor after 1 year of drug withdrawal. Bone marrow cell morphology, chromosome karyotype analysis, Fully-instrumented submersible housing test, immunological assays, molecular biological methods, and blood tumor panoramic gene test were performed. All-trans retinoic acid (ATRA) combined with arsenic acid (As2O3) were used in the first course of treatment. Bone marrow was dominated by abnormal promyelocytic granulocytes. Karyotype test revealed i(17)(q10) isochromosome. Immunological phenotype mainly included positive expressions of CD9, CD13, CD33, and CD38. Case 1 suffered intracranial hemorrhage after re-chemotherapy and died on D162. For case 2, on D145 and D265, bone marrow promyelocytic granulocytes accounted for 2%. Flow cytometric residual lesion detection showed no abnormal immuno
ATRA, As2O3, and chemotherapy may be ineffective in treating APL-like AML with i(17)(q10) but without t(15;17) and PML-RARA fusion gene.
Core Tip: Herein we reported two cases of acute myeloid leukemia (AML) mimicking APL after the same treatment protocols. A rare chromosomal abnormality, i(17)(q10), was observed in two pediatric patients, which mimicked acute promyelocytic leukemia (APL) phenotype. Both patients showed no responses to all-trans retinoic acid and arsenic trioxide induction therapy. One patient with i(17)(q10) died after 5 mo, and the other patient with i(17)(q10) add (14)14 had been medication free more than 10 mo and achieved complete tumor remission for 3 years since drugs were withdrawn. Pediatric AML mimicking APL is difficult to treat and additional cases should be studied to provide better treatment strategies for these patients.