A CDKN2B-Associated Immune Prognostic Model for Predicting Immune Cell Infiltration and Prognosis in Esophageal Carcinoma.

Objective: Studies have indicated that cyclin dependent protein kinase inhibitor 2B (CDKN2B) deletion is one of the most common changes in esophageal cancer (EC) which affects its progression and prognosis. This study explored the association between CDKN2B deletion, immunophenotype, and the prognosis of EC.

Methods: We investigated CDKN2B status and RNA expression, identified differentially expressed immune-associated genes between wild-type CDKN2B (CDKN2B^WT) and deleted CDKN2B (CDKN2B^deletion) in Cancer Genome Atlas (TCGA) EC samples. We also a constructed an immune prognostic model (IPM) based on these genes. Thereafter, the effects of IPM on the immune microenvironment of EC were analyzed. Finally, we established a nomogram by integrating the IPM and other clinical factors.

Results: CDKN2B deletion leads to downregulation of the immune response in EC. A total of 136 immune-associated genes were identified based on the CDKN2B deletion status, and three genes with remarkable potential as individual targets were selected for model construction. An IPM was developed and validated, it showed good performance in differentiating patients with a low or high risk of poor prognosis, and its predictive ability was independent of traditional clinical features. High-risk patients with EC had increased T follicular helper cells (Tfh) and M0 macrophages, and lower infiltration levels of resting CD4 memory T cells resting, and naive B cells. The nomogram developed for clinical application showed good predictive performance.

Conclusions: Our results suggested that CDKN2B deletion was associated with the survival and immune microenvironment in EC. IPM is not only an effective indicator of the immune response and prognosis, but also suggest potential targets for immunotherapy in patients with EC.