Germ layer specification and organotropism in lymphoma invasion - PubMed
5 hours ago
- #Lymphoma
- #Organotropism
- #Germ Layer
- Study identifies germ layer-dependent extranodal invasion (ENI) in diffuse large B-cell lymphoma, linked to embryonic development.
- Mesoderm-originating ENI correlates with worse survival post-R-CHOP treatment vs. ectoderm- or endoderm-originating ENI.
- Distinct oncogenic mutations vary by germ layer: ENI-ectoderm has MYD88, PIM1, TBL1XR1; ENI-endoderm has TP53, TET2; ENI-mesoderm has MYD88, PIM1, TBL1XR1, CD79B.
- Organotropic migration follows a temporal pattern matching germ layer development: ectoderm to endoderm to mesoderm.
- Single-cell RNA-seq shows malignant B cells differentiate from a progenitor via NF-κB/T-cell activation into branches upregulating B-cell receptor or T-cell activation signaling.
- Immune checkpoints differ by germ layer: LGALS9 up in ENI-ectoderm, PD-L1 in ENI-endoderm, B7-H3 in ENI-mesoderm, aiding targeted cancer therapy insights.