May P. Chan

Cutaneous mucormycosis may be caused by direct inoculation or hematogenous spread of mucormycetes in immunocompromised patients. Skin biopsy is characterized by a deep fungal infection with frequent angioinvasion. The fungal hyphae can usually be identified on H&E stain. We report a case of cutaneous angioinvasive mucormycosis in which the fungi were also visualized on direct immunofluorescence. A 57‐year‐old patient with relapsed myelodysplastic syndrome status‐post allogeneic hematopoietic cell transplant, diabetes mellitus, and graft‐versus‐host disease presented with painful, palpable, dark‐red to violaceous retiform purpuric plaques. Light microscopy of punch biopsy revealed numerous broad, ribbon‐like, pauci‐septate hyphae in the dermis with angioinvasion, consistent with mucormycosis. Direct immunofluorescence performed on a concurrent biopsy to exclude immune complex vasculitis showed smooth IgG, IgA (weak), IgM (faint), and C3 deposition on the hyphal structures, compatible with antibody‐coated fungi. Tissue culture subsequently confirmed Mucor species. Although mucormycosis was readily diagnosable on routine light microscopy in this case, recognition of the unique phenomenon of antibody‐coated fungi can be crucial when the invasive fungi are sparse or only present in the direct immunofluorescence specimen.

ERG is a transcription factor encoded on chromosome 21q22.2 with important roles in hematopoiesis and oncogenesis of prostate cancer. ERG amplification has been identified as one of the most common recurrent events in acute myeloid leukemia with complex karyotype (AML‐CK). In this study, we uncover three different modes of ERG amplification in AML‐CK. Importantly, we present evidence to show that ERG amplification is distinct from intrachromosomal amplification of chromosome 21 (iAMP21), a hallmark segmental amplification frequently encompassing RUNX1 and ERG in a subset of high‐risk B‐lymphoblastic leukemia. We also characterize the association with TP53 aberrations and other chromosomal aberrations, including chromothripsis. Lastly, we show that ERG amplification can initially emerge as subclonal events in low‐grade myeloid neoplasms. These findings demonstrate that ERG amplification is a recurrent secondary driver event in AML and raise the tantalizing possibility of ERG as a therapeutic target.