Apoptosis and cell proliferation in esophageal squamous cell carcinoma treated by chemotherapy

The p53 gene is associated with G1 arrest during the cell cycle and with ap optosis. To evaluate the preoperative chemotherapeutic effect in esophageal squamous cell carcinoma, we retrospectively investigated the apoptotic ind ex (AI) and Ki-67 labeling index (Ki-67LI) in relation to the expression of p53. Thirty patients with esophageal carcinoma who had received chemothera py prior to surgery a ere examined using the terminal deoxynucleotidyl-tran sferase-mediated in-situ end-labeling (TUNEL) method for evaluating AI and immunohistochemical staining with anti Ki-67 and anti p53 antibody for eval uating Ki-67LI and p53 expression, respectively. The histological response rate of chemotherapy was 20.0%. A significant correlation between p53-negat ive expression and response to chemotherapy was found (P < 0.01). The AIs a nd Ki-67LIs in p53-negative tumors with ineffective responses to chemothera py were significantly higher than those in p53-positive tumors with ineffec tive responses (P < 0.05). The AIs and Ki-67LIs were significantly lower in p53-negative tumors with effective responses to chemotherapy than those in p53-negative tumors with ineffective responses (P ( 0.05 and P < 0.01. res pectively), Further more. significant correlations were found between AIs a nd Ki-67LIs in p53 negative tumors (r = 0.60. P < 0.05). In esophageal carc inoma, p53-negative tumors with highly proliferative cells might be suscept ible to apoptosis induced by chemotherapy. (C) 2000 Elsevier Science irelan d Ltd. All rights reserved.