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Editorial
. 2024 Aug 1;109(8):2385-2387.
doi: 10.3324/haematol.2024.285081.

Rethinking paraneoplastic eosinophilia

Kathrin M Bernt  1
Affiliations
Editorial

Rethinking paraneoplastic eosinophilia

Kathrin M Bernt. Haematologica. .
No abstract available

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Figures

Figure 1.
Figure 1.
The ACSL6::ETV6 fusion. (Top) In the patient with an ACSL6::ETV6 fusion acute lymphoblastic leukemia described by Xu and colleagues, the ETV6 breakpoint is located within Intron 1. (Center) The 5’ portion of ETV6 if fused to the intergenic region 5’ to the ACSL6 gene. The fusion event results in transcription of a fusion RNA, whereby exon 1 of ACSL6 is skipped, and ETV6 exon 1 is fused to ACSL6 exon 2. This induces a frameshift and premature stop; no ETV6-ACSL6 fusion protein is expressed. (Bottom) The reciprocal translocation places the large 3’ super enhancer of ETV6 in the vicinity of the IL5, SLC22A5, P4HA2, and IL3 genes, which are over-expressed as a result. ETV6 haploinsufficiency and IL3 overexpression likely cause or contribute to leukemic transformation. In parallel, the high levels of IL3 produced by the leukemia cells result in paraneoplastic eosinophilia.
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References

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