Shin-Ichi Yamada1, Mitsunobu Otsuru2, Souichi Yanamoto3, Takumi Hasegawa4, Hitoshi Aizawa5, Takahiro Kamata5, Nobuhiro Yamakawa6, Tomoyuki Kohgo7, Akira Ito8, Yuri Noda9, Chihoko Hirai10, Tetsuya Kitamura11, Masaya Okura8, Tadaaki Kirita6, Michihiro Ueda7, Tetsuro Yamashita7, Yoshihide Ota2, Takahide Komori4, Masahiro Umeda3, Hiroshi Kurita5. 1. Department of Dentistry and Oral Surgery, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano, 390-8621, Japan. yshinshin@shinshu-u.ac.jp. 2. Department of Oral and Maxillofacial Surgery, Division of Surgery, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa, 253-1193, Japan. 3. Department of Clinical Oral Oncology, Unit of Translational Medicine, Course of Medical and Dental Sciences, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto., Nagasaki, Nagasaki, 852-8588, Japan. 4. Department of Oral and Maxillofacial Surgery, Kobe University Graduate School of Medicine, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan. 5. Department of Dentistry and Oral Surgery, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, Nagano, 390-8621, Japan. 6. Department of Oral and Maxillofacial Surgery, School of Medicine, Nara Medical University, 840 Shijo-cho, Kashihara, Nara, 634-8522, Japan. 7. Department of Oral and Maxillofacial Surgery, Keiyukai Sapporo Hospital, Kita 1-1, Hondori 14, Shiraishi-ku, Sapporo, 003-0027, Japan. 8. The 1st Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University, 1-8, Yamadaoka, Suita, Osaka, 565-0871, Japan. 9. Department of Oral Pathology, Osaka University Graduate School of Dentistry, 1-8, Yamadaoka, Suita, Osaka, 565-0871, Japan. 10. Department of Diagnostic Pathology, Kobe University Hospital, 7-5-1, Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan. 11. Department of Oral Pathology and Biology, Hokkaido University Graduate School of Dental Medicine, Kita 13, Nishi 7, Kita-ku, Sapporo, 060-8586, Japan.
Abstract
OBJECTIVES: The progression level of extracapsular spread (ECS) for cervical lymph node metastasis of oral squamous cell carcinoma (OSCC) was previously divided into three types, and their relationships with the prognosis of patients were re-examined. PATIENTS AND METHODS: The Kaplan-Meier method was used to examine overall survival (OS) and relapse-free survival (RFS) curves. Prognosis factor for recurrence was analyzed with univariate and multivariate analysis. RESULTS: ECS was detected in 216 cases of OSCC and analyzed. The 5-year overall survival and RFS rates of patients with type C, which was microscopically defined as tumor invasion to perinodal fat or muscle tissue, were significantly poor at 40.6 and 37.8%, respectively. The results of a univariate analysis suggested that the prognosis of ECS in OSCC patients is associated with its progression level, particularly type C. The 5-year RFS rate of type C with tumor budding was significantly poor at 31.5%. Type C with tumor budding correlated with local and regional recurrence as well as distant metastasis. In a multivariate analysis, tumor budding was identified as an independent prognostic factor. CONCLUSIONS: These results suggest that the progression level of ECS and tumor budding are useful prognostic factors in OSCC patients. CLINICAL RELEVANCE: This study indicated that the progression level and tumor budding of ECS for cervical lymph node metastasis were useful prognostic factors in OSCC patients.
OBJECTIVES: The progression level of extracapsular spread (ECS) for cervical lymph node metastasis of oral squamous cell carcinoma (OSCC) was previously divided into three types, and their relationships with the prognosis of patients were re-examined. PATIENTS AND METHODS: The Kaplan-Meier method was used to examine overall survival (OS) and relapse-free survival (RFS) curves. Prognosis factor for recurrence was analyzed with univariate and multivariate analysis. RESULTS: ECS was detected in 216 cases of OSCC and analyzed. The 5-year overall survival and RFS rates of patients with type C, which was microscopically defined as tumor invasion to perinodal fat or muscle tissue, were significantly poor at 40.6 and 37.8%, respectively. The results of a univariate analysis suggested that the prognosis of ECS in OSCC patients is associated with its progression level, particularly type C. The 5-year RFS rate of type C with tumor budding was significantly poor at 31.5%. Type C with tumor budding correlated with local and regional recurrence as well as distant metastasis. In a multivariate analysis, tumor budding was identified as an independent prognostic factor. CONCLUSIONS: These results suggest that the progression level of ECS and tumor budding are useful prognostic factors in OSCC patients. CLINICAL RELEVANCE: This study indicated that the progression level and tumor budding of ECS for cervical lymph node metastasis were useful prognostic factors in OSCC patients.
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