Get access

Expression of intercellular adhesion molecule (ICAM)-1 in adenoid cystic carcinoma of the head and neck

Authors

  • Akiko Shirai MD,

    1. Division of Otolaryngology, Head and Neck Surgery, Graduate School of Medicine, Kanazawa University, Kanazawa, Japan
    Search for more papers by this author
  • Mitsuru Furukawa MD,

    1. Division of Otolaryngology, Head and Neck Surgery, Graduate School of Medicine, Kanazawa University, Kanazawa, Japan
    Search for more papers by this author
  • Tomokazu Yoshizaki MD

    Corresponding author
    1. Division of Otolaryngology, Head and Neck Surgery, Graduate School of Medicine, Kanazawa University, Kanazawa, Japan
    • Dr. Tomokazu Yoshizaki, Division of Otolaryngology, Head and Neck Surgery, Graduate School of Medicine, Kanazawa University, 13–1 Takara-machi, Kanazawa 920–0934, Japan
    Search for more papers by this author

  • The contents of this manuscript were presented at the 20th conference of the Japan Society for Immunology and Allergology in Otolaryngology, Shimane, Japan, March 7–9, 2002.

Abstract

Objectives/Hypothesis: Adenoid cystic carcinoma of the head and neck (ACCHN) is characterized by late recurrence and frequent distant metastasis. Tumor attack by cytotoxic T lymphocytes and macrophages is mediated by the interaction of leukocyte function-associated antigen (LFA)-1 on lymphocytes with intercellular adhesion molecule (ICAM)-1 on the tumor surface. Thus, the reduced expression of ICAM-1 on tumor cells could contribute to their escape from host immune surveillance. To investigate the relationship between the clinical features of ACCHN and host immune surveillance, the expression of ICAM-1 and infiltration of T/natural killer (NK) cells and macrophages were immunohistochemically examined. Study Design: Retrospective analysis of immunohistochemical tumor characteristics and clinical outcome. Methods: Immunohistochemical study of ICAM-1, T/NK cells, and macrophages was performed on paraffin sections of 42 patients with ACCHN. The expression of T/NK cells and macrophages was represented by T-cell-restricted antigen (TIA)-1 and CD68 expression, respectively. The expression of these molecules and clinical features were analyzed. Results: Of 42 ACCHN cases, 15,9, and 15 patients were classified as ICAM-1 high, TIA-1 high, and CD68 high, respectively. The TIA-1 expression scores in ICAM-1-low patients were significantly lower than those in ICAM-1-high patients (1.3 ± 3.7 vs. 8.3 ± 12.7, P = .0031). The CD68 expression scores in ICAM-1-low patients were also significantly lower than those in ICAM-1-high patients (9.6 ± 9.G vs. 21.1 ± 17.6, P = .0047). Moreover, ICAM-1-high patients had a significantly better disease-free survival rate (P = .043). Conclusions: Reduced expression of ICAM-1 may promote immune evasion and metastasis, resulting in poor prognosis in ACCHN.

Ancillary