title: Correlation of p53 status with the response to chemotherapy-based treatment in esophageal cancer: a meta-analysis.
abstract: BACKGROUND
  The value of p53 status for predicting response to chemotherapy-based treatment in patients with esophageal cancer has been controversial. We conducted a meta-analysis to elucidate the correlation of p53 status with the response to chemotherapy-based treatment.
  
  
  METHODS
  Studies were searched in PubMed, Embase, and Web of Science (up to September 2012). The p53 status and response to therapy were defined and standardized. Subgroup analyses based on the treatment and histopathology were performed to explore the usefulness of p53 status for predicting response to therapy in esophageal cancer. Sensitivity analyses were conducted by removing specific studies to assess the effects of study quality.
  
  
  RESULTS
  We included 28 studies with 1497 cases in our meta-analysis. Wild-type form of p53 status (low expression of p53 protein and/or wild-type p53 gene) was associated with high response to chemotherapy-based treatment in esophageal cancer (total major response [MR]: risk ratio [RR] = 1.09, 95 % CI = 1.03-1.16, P = .003; pathological MR: RR = 1.15, 95 % CI = 1.06-1.25, P = .001; total complete response [CR]: RR = 1.08, 95 % CI = 1.00-1.17, P = .040). The similar correlation between the wild-type form p53 and response to therapy were also detected in subgroup analyses (total MR, pathological MR, and total CR in chemoradiotherapy subgroup; total MR in chemotherapy subgroup; total MR and pathological CR in esophageal squamous cell carcinoma [ESCC]). Additionally, patients with wild-type form p53 status had high pathological complete response rate to neoadjuvant chemoradiotherapy in ESCC.
  
  
  CONCLUSIONS
  The current meta-analysis suggested that p53 status might be a predictive biomarker for response to chemotherapy-based treatment in esophageal cancer.
authors.affiliation: State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, People's Republic of China.
authors.forename: Shui-Shen
authors.initials: SS
authors.lastname: Zhang
authors.forename: Qing-Yuan
authors.initials: QY
authors.lastname: Huang
authors.forename: Hong
authors.initials: H
authors.lastname: Yang
authors.forename: Xuan
authors.initials: X
authors.lastname: Xie
authors.forename: Kong-Jia
authors.initials: KJ
authors.lastname: Luo
authors.forename: Jing
authors.initials: J
authors.lastname: Wen
authors.forename: Xiao-Li
authors.initials: XL
authors.lastname: Cai
authors.forename: Fu
authors.initials: F
authors.lastname: Yang
authors.forename: Yi
authors.initials: Y
authors.lastname: Hu
authors.forename: Jian-Hua
authors.initials: JH
authors.lastname: Fu
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy / Q000235:genetics*; D014408:Biomarkers, Tumor / Q000235:genetics*; D002294:Carcinoma, Squamous Cell / Q000188:drug therapy / Q000235:genetics*; D059186:Chemoradiotherapy, Adjuvant; D017024:Chemotherapy, Adjuvant; D004938:Esophageal Neoplasms / Q000188:drug therapy / Q000235:genetics*; D006801:Humans; D020360:Neoadjuvant Therapy; D016896:Treatment Outcome; D016159:Tumor Suppressor Protein p53 / Q000235:genetics*
chemical_list: D014408:Biomarkers, Tumor; D016159:Tumor Suppressor Protein p53