Authors
Anthony T Nguyen, Jolene Viramontes, Isaiah Vazquez, Catriona McWilliam, Vaishnavi Devarakonda, Regina Henson, Wendy L Sacks, Jon Mallen-St Clair, Yufei Chen, Evan Walgama, Kevin S Scher, Justin Moyers, Howard M Sandler, Julie K Jang, Zachary S Zumsteg, Wonwoo Shon, Stephen L Shiao, Allen S Ho
Published in
Science advances. Volume 12. Issue 27. Pages eaea4727. Jul 03, 2026. Epub Jul 03, 2026.
Abstract
Lymph node (LN) metastases are a major driver of mortality across solid cancers, including thyroid carcinomas, which are known for high rates of nodal colonization. To elucidate the determinants of nodal spread, we isolated tumor-infiltrating leukocytes from primary thyroid tumors and matched metastatic LNs for single-cell RNA sequencing with validation by multiplex immunohistochemistry. Comparing the microenvironmental alterations between primary tumors and their LNs, we found that thyrocytes and tumor-associated macrophages down-regulate the expression of multiple inflammatory cytokine receptors, including TNFRSF12A and CX3CR1, upon LN colonization. LNs were associated with the induction of regulatory T cells to suppress T cell-mediated cytotoxicity compared to matched primary tumors. Notably, tumor-infiltrating lymphocytes within LNs demonstrated increased expression of activation markers, including interleukin-7 receptor (IL7R). High LN expression of IL7R was significantly correlated with improved outcomes and can serve as a biomarker in this heterogeneous disease. Our findings on the dynamic equilibrium within LN metastases may offer conserved mechanisms for nodal colonization across solid tumors.
PMID:
42397917
Bibliographic data and abstract were imported from PubMed on 04 Jul 2026.
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