Myeloid-derived TGFβ1 and oncostatin M establish two distinct stromal niches controlling late and hybrid EMT states.

In mouse skin tumors, hybrid and late EMT states are linked to distinct stromal niches marked by oncostatin M–rich neutrophil areas and TGFβ1–rich macrophage areas, respectively.

• Why it matters: EMT spans multiple tumor programs, but how microenvironmental signals map onto specific EMT states—and how those states are maintained—remains unclear.
• What they did: Using single-cell and spatial transcriptomics in mouse skin tumors, the study compared stromal composition across EMT-associated niches and tested how oncostatin M and TGFβ1 sustain EMT programs via feed-forward inflammatory signaling.
• The result: Neutrophils are enriched in oncostatin M niches that partially activate EMT while sustaining epithelial features, promoting hybrid EMT and metastasis, whereas macrophages are enriched in TGFβ1 niches that support late EMT.

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