title: Expression and alteration of p53 and p21(waf1/cip1) influence the sensitivity of chemoradiation therapy for esophageal cancer.
abstract: OBJECTIVE
  In vitro analyses have been demonstrated that wild type p53 and p21(waf1/cip1) proteins regulate cellular proliferation and sensitivity of anticancer agents, however, the roles of p53 and p21(waf1/cip1) expression on the response to the chemoradiation therapy for human esophageal squamous cell cancer have not been investigated.
  
  
  METHODS
  With an immunohistochemical method using specimens before and after the chemoradiation therapy, we investigate in this report the influence of the p53 and p21(waf1/cip1) expression on the chemoradiation therapy response or alteration of these protein expressions by chemoradiation therapy in thirteen esophageal squamous cell cancer patients who received our recently developed chemoradiation therapy.
  
  
  RESULTS
  In the biopsy specimens before the chemoradiation therapy, 82% of the responders and 71% of patients with down T-classification had either a p53-/p21+ or p53+/p21+ phenotype. Eighty two percent and 46% of the cases with these two phenotypes showed complete or partial response and down T-classification, respectively. After the chemoradiation therapy, 73% of the responders and 71% of the patients with down T-classification had either a p53-/p21+ or p53+/p21+ phenotype. Eighty eight percent and 56% of the cases with these two phenotypes showed complete or partial response and down T-classification, respectively. Comparative analysis before and after the chemoradiation therapy revealed that four patients had an alteration of p53 and p21(waf1/cip1) expression in association with the therapeutic response.
  
  
  CONCLUSIONS
  These results suggest that wild type p53 or p21(waf1/cip1) expression relates with and can be altered by the chemoradiation therapy, which could influence the therapeutic efficacy.
authors.affiliation: Department of Gastroenterological Surgery, University of Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Shimoyama
authors.forename: T
authors.initials: T
authors.lastname: Konishi
authors.forename: M
authors.initials: M
authors.lastname: Kawahara
authors.forename: F
authors.initials: F
authors.lastname: Aoki
authors.forename: N
authors.initials: N
authors.lastname: Harada
authors.forename: S
authors.initials: S
authors.lastname: Shimizu
authors.forename: T
authors.initials: T
authors.lastname: Murakami
authors.forename: M
authors.initials: M
authors.lastname: Kaminishi
mesh_terms: D000971:Antineoplastic Combined Chemotherapy Protocols; D002294:Carcinoma, Squamous Cell / Q000235:genetics / Q000378:metabolism / Q000628:therapy*; D002945:Cisplatin / Q000008:administration & dosage; D003131:Combined Modality Therapy; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000032:analysis* / Q000235:genetics; D019008:Drug Resistance, Neoplasm; D004938:Esophageal Neoplasms / Q000235:genetics / Q000378:metabolism / Q000628:therapy*; D005472:Fluorouracil / Q000008:administration & dosage; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D010641:Phenotype; D011836:Radiation Tolerance; D011879:Radiotherapy Dosage; D016159:Tumor Suppressor Protein p53 / Q000032:analysis* / Q000235:genetics
chemical_list: C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D016159:Tumor Suppressor Protein p53; D002945:Cisplatin; D005472:Fluorouracil