Different characteristics of the tumor immune microenvironment among subtypes of salivary gland cancer.

Autor: Nagatani Y; Department of Medical Oncology and Hematology, Kobe University Graduate School of Medicine, Kobe, Japan., Kiyota N; Department of Medical Oncology and Hematology, Kobe University Graduate School of Medicine, Kobe, Japan.; Kobe University Hospital Cancer Center, Kobe, Japan., Imamura Y; Department of Medical Oncology and Hematology, Kobe University Graduate School of Medicine, Kobe, Japan., Koyama T; Department of Medical Oncology and Hematology, Kobe University Graduate School of Medicine, Kobe, Japan., Funakoshi Y; Department of Medical Oncology and Hematology, Kobe University Graduate School of Medicine, Kobe, Japan., Komatsu M; Department of Diagnostic Pathology, Kobe University Graduate School of Medicine, Kobe, Japan., Itoh T; Department of Diagnostic Pathology, Kobe University Graduate School of Medicine, Kobe, Japan., Teshima M; Department of Otorhinolaryngology-Head and Neck Surgery, Kobe University Graduate School of Medicine, Kobe, Japan., Nibu KI; Department of Otorhinolaryngology-Head and Neck Surgery, Kobe University Graduate School of Medicine, Kobe, Japan., Sakai K; Department of Genome Biology, Kindai University Faculty of Medicine, Sayama, Japan., Nishio K; Department of Genome Biology, Kindai University Faculty of Medicine, Sayama, Japan., Shimomura M; Division of Cancer Immunotherapy (Kashiwa), Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Japan., Nakatsura T; Division of Cancer Immunotherapy (Kashiwa), Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Japan., Ikarashi D; Division of Cancer Immunotherapy (Kashiwa), Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Japan., Nakayama T; Division of Cancer Immunotherapy (Kashiwa), Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Kashiwa, Japan., Kitano S; Division of Cancer Immunotherapy Development, Center for Advanced Medical Development, The Cancer Institute Hospital of Japanese Foundation for Cancer Research, Tokyo, Japan., Minami H; Department of Medical Oncology and Hematology, Kobe University Graduate School of Medicine, Kobe, Japan.; Kobe University Hospital Cancer Center, Kobe, Japan.
Jazyk: angličtina
Zdroj: Asia-Pacific journal of clinical oncology [Asia Pac J Clin Oncol] 2024 Dec; Vol. 20 (6), pp. 779-788. Date of Electronic Publication: 2024 Sep 04.
DOI: 10.1111/ajco.14108
Abstrakt: Aim: Although immune checkpoint inhibitors (ICPi) for salivary gland cancer (SGC) have been investigated in clinical trials, details of the tumor immune microenvironment (TIME) remain unclear. This research aimed to elucidate the TIME of SGC and its relationship with tumor mutation burden (TMB) and to explore the rationale for the applicability of ICPi.
Materials and Methods: We selected five pathological types, namely adenoid cystic carcinoma (ACC); adenocarcinoma, not otherwise specified (ANOS); salivary duct carcinoma (SDC); and low/high-grade mucoepidermoid carcinoma (MEC low/high ). We investigated the TIME and TMB of each pathological type. TIME was evaluated by multiplexed fluorescent immunohistochemistry. TMB was measured by next-generation sequencing.
Results: ACC and MEC high showed the lowest and highest infiltration of immune effector and suppressor cells in both tumor and stroma. ANOS, SDC, and MEC low showed modest infiltration of immune effector cells in tumors. Correlation analysis showed a positive correlation between CD3 + CD8 + T cells in tumor and TMB (r = 0.647). CD3 + CD8 + T cells in tumors showed a positive correlation with programmed cell death-ligand 1 expression in tumor cells (r = 0.513) and a weak positive correlation with CD3 + CD4 + Foxp3 + cells in tumors (r = 0.399). However, no correlation was observed between CD3 + CD8 + T cells and CD204 + cells in tumors (r = -0.049).
Conclusion: The TIME of ACC was the so-called immune desert type, which may explain the mechanisms of the poor response to ICPi in previous clinical trials. On the other hand, MEC high was the immune-inflamed type, and this may support the rationale of ICPi for this pathological subtype.
(© 2024 John Wiley & Sons Australia, Ltd.)
Databáze: MEDLINE
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