Perioperative Changes of Serum p53 Antibody Titer is a Predictor for Survival in Patients with Esophageal Squamous Cell Carcinoma Hideaki Shimada Æ Tooru Shiratori Æ Akihiko Takeda Æ Kazuyuki Matsushita Æ Shinichi Okazumi Æ Yasunori Akutsu Æ Hisahiro Matsubara Æ Fumio Nomura Æ Takenori Ochiai Ó Socie ´te ´ Internationale de Chirurgie 2008 Abstract Background Although the presence of serum p53 anti- body (s-p53-Abs) before treatment has been shown to correlate with poor prognosis and lymph node metastasis in esophageal cancer, there has been little information about postoperative s-p53-Abs titer and perioperative changes of s-p53-Abs titers in patients with esophageal carcinoma. Methods A highly specific enzyme-linked immunosor- bent assay was used to analyze s-p53-Abs in 110 patients with esophageal squamous cell carcinoma before and 1 month after surgery. The cutoff level of 1.3 U/ml was used to indicate seropositive patients. Impact of postoper- ative s-p53-Abs titer and perioperative changes of s-p53- Abs on survival was evaluated. Results Forty (36%) of 110 patients were positive for s-p53-Abs before surgery and 35 patients (32%) were positive after surgery. s-p53-Abs titer generally decreased after surgery. Among sero-positive patients, the patients who remained sero-positive after surgery (n = 28) had a worse prognosis than patients who showed sero-conversion (P = 0.02). Among sero-positive patients, the nonde- creased titer group showed significantly unfavorable survival (P \ 0.01). Multivariate analysis revealed that postoperative s-p53-Abs was an independent risk factor for worse overall survival (adjusted hazard ratio = 3.05; 95% confidence interval = 1.11–8.33; P = 0.03). Conclusions Perioperative monitoring of s-p53-Abs titers was useful to identify patients with esophageal cancer with a high risk for tumor recurrence and a poor prognosis. Continuous sero-positive patients and/or nondecreased titer group, even after surgery, showed significantly unfavorable survival. Introduction Alteration of the p53 gene is one of the most common genetic features of esophageal cancer, and it is detected even in a stage I patients [1]. Indeed, genomic sequencing showed that 50–60% of esophageal cancers have p53 mutations [2–5]. Most p53 mutations lead to the synthesis of a stabilized protein that has a much longer half-life than that of the wild- type p53 protein. Overexpression of mutant p53 protein has been found to induce serum p53 IgG antibodies (s-p53-Abs) in 30–48% of patients with esophageal cancer [6–11]. Due to This work was supported in part by a Grant-in-Aid from the Ministry of Education, Science and Culture of Japan (21st Century Center of Excellence Program). H. Shimada (&) Department of Gastroenterological Surgery, Chiba Cancer Center, 666-2 Nitona-cho, Chuou-ku, Chiba 260-8717, Japan e-mail: hshimada@chiba-cc.jp T. Shiratori Á Y. Akutsu Á H. Matsubara Frontier Surgery, Chiba University Graduate School of Medicine, Chiba, Japan A. Takeda Department of Digestive Surgery, Chemotherapy Research Institute Hospital International University of Health and Welfare, Ichikawa, Japan K. Matsushita Á F. Nomura Department of Molecular Diagnosis, Chiba University Graduate School of Medicine, Chiba, Japan S. Okazumi Department of Surgery, Toho Sakura Medical Center, Chiba, Japan T. Ochiai Gastroenterological Center, San-Ai Memorial Hospital, Chiba, Japan 123 World J Surg DOI 10.1007/s00268-008-9821-4