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.