3.1 Nasopharyngeal carcinoma
Nasopharyngeal carcinoma (NPC) is a genetically related squamous cell carcinoma of nasopharyngeal epithelial origin with a different immune infiltration and a lower degree of differentiation than other carcinomas. It occurs mainly in Southeast Asia and North Africa [54]. Clinical observations have shown that malignantly transformed nasopharyngeal epithelial cells are often mixed with large numbers of stromal cells. Lanqi Gong et al. used scRNA seq to confirm the presence of large numbers of anisotropic stromal cells in malignant tumors, and discovered that an important component of stromal cells was fibroblasts (CAFs), which can alter the immune microenvironment by inhibiting the activity of immune effector cells and recruiting immunosuppressive cells. The immune microenvironment can be altered by inhibiting the activity of immune effector cells and recruiting immunosuppressive cells, thereby enabling cancer cells to evade immune surveillance [55-57]. The tumor microenvironment in NPC predominantly undergoes changes in T cells and B cells. Five major stromal populations and 36 different subpopulations were identified by use of scRNA-seq combined with the clonal identification of T and B cells, and the results were further verified by constructing a map of nasopharyngeal carcinoma infiltration into stromal cells. The map showed that the CD45+ immune cells included T cells, B cells, natural killer cells (NK cells), and myeloid cells, with the T cells being mainly characterized by a significant up-regulation of CXCL1 3 and LGALS1 gene expression. The differentially expressed genes for B cells were mainly interferon-induced and immunoglobulin-encoded, including IFITM1 ,IFI44L , IGHA1 , IGKC , and IGHG . Both the T and B cells were affected by IFN-γ and IFN-α over-release [58]. In terms of cellular interactions, three clusters of depleted T cells (HAVCR2, TOX, and LAG3) were found to preferentially interact with memory B cells, innate-like B cells, inactivated B cells, and IFN-induced B cells in NPC [59, 60]. These studies elucidated the degree of tumor heterogeneity and the intercellular network of NPC at the level of single-cell resolution. They also provided insights into the mechanisms of NPC progression and suggested strategies for developing precise therapies for NPC.