We found that follicular B cells (clusters 0, 1, and 3) and plasma cells (cluster 7) located in the core of the tumor were significantly more active in immune depletion-related pathways than the B cell subsets located at the edge of the tumor; these pathways included epithelial cell adhesion, fibroblast growth factor binding, VEGFR2-mediated cell proliferation, oxidative stress-stimulated hypoxia, and stress-inhibited cytokine synthesis (Figure 5D). Here, KDR is linked to neoplasm.