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Acute Myeloid Leukemia in an Infant with t(8;19)(p11.2;q13) Translocation: Case Report and a Review of the Literature
Ashley C Eason1, Silvia T Bunting2, Jess F Peterson3
1Department of Pediatrics, Aflac Cancer and Blood Disorders Center, Children's Healthcare of Atlanta and Emory University, Atlanta, GA, USA.
Insights
A rare genetic variation in infant acute myeloid leukemia (AML), t(8;19), was observed in the youngest patient documented. This case highlights the distinct clinical profile and treatment response in this AML subgroup.
Area of Science:
- Hematology
- Oncology
- Genetics
Background:
- Acute myeloid leukemia (AML) with t(8;16)(p11.2;p13) is a rare subgroup with unique characteristics.
- The t(8;19)(p11.2;q13.3) translocation is a rarely reported variation of t(8;16).
Observation:
- A female infant presented with monocytic AML and leukemia cutis.
- Erythrophagocytosis was noted in the diagnostic bone marrow aspirate.
- The patient was the youngest reported with the t(8;19) translocation.
Findings:
- The patient responded well to standard AML chemotherapy.
- The infant achieved remission.
- The case provides insights into the clinical presentation of this specific AML genetic variant.
Implications:
- This case expands the understanding of AML genetic variations.
- It highlights the prognostic significance of the t(8;19) translocation.
- Further research into 8p11.2 fusion proteins in AML is warranted.
Abstract:
Acute myeloid leukemia (AML) patients with t(8;16)(p11.2;p13) constitute a small subgroup with a distinct genetic and clinical profile. We present a unique case of a female infant with monocytic AML associated with t(8;19)(p11.2;q13.3), a rarely reported variation of t(8;16)(p11.2;p13). The patient presented with leukemia cutis and demonstrated erythrophagocytosis in the diagnostic bone marrow. She responded well to standard AML chemotherapy and is currently in remission. Here, we highlight her case as the youngest AML patient with t(8;19) described in the literature, discuss the significance and prognostic implications of this genetic variant, and review 8p11.2 fusion proteins in AML.
