title: p53 expression and p21 expression are mutually exclusive in esophageal squamous cell carcinoma.
abstract: The accumulation of p53 protein, which is considered to be caused by a p53 gene mutation, is closely associated with poor prognosis in patients with certain types of carcinomas. The progression of esophageal squamous cell carcinoma (ESCC) is also suspected to depend on p53 gene status. We analyzed the relationship between p53 and p21 protein accumulation in ESCC, and simultaneously analyzed the frequency of apoptosis. Formalin-fixed paraffin-embedded sections were taken from 46 patients who underwent esophagectomy for ESCC. These sections were examined by immunostaining with monoclonal antibodies PAb1801 and EA10 to determine p53 and p21 protein accumulation, respectively. We also analyzed the frequency of apoptosis by TdT-mediated dUTP-biotin nick end-labeling (TUNEL). For estimation of the proportion of stained cells, we used computer analysis with NIH image analysis software. p21 protein accumulation showed an almost inverse distribution to that of p53 protein. In areas where both p53 and p21 proteins were accumulated, few apoptotic cells were observed. Particularly in cases of mucosal tumors, p53 protein was prominently accumulated in the lower layer of the tumor, whereas p21 protein accumulation was confined to the upper layer. Our results suggest that progression of esophageal squamous cell carcinoma is controlled by a p53-dependent pathway.
authors.affiliation: Department of Gastroenterological Surgery Transplant and Surgical Oncology, Graduate School of Medicine and Dentistry, Okayama University, 2-5-1 Shikatacho, Okayama 700-8558, Japan.
authors.forename: Madoka
authors.initials: M
authors.lastname: Hamada
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Naomoto
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Shirakawa
authors.forename: Tomoki
authors.initials: T
authors.lastname: Yamatsuji
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Noma
authors.forename: Takayuki
authors.initials: T
authors.lastname: Motoki
authors.forename: Tetsuji
authors.initials: T
authors.lastname: Nobuhisa
authors.forename: Takaomi
authors.initials: T
authors.lastname: Okawa
authors.forename: Minoru
authors.initials: M
authors.lastname: Haisa
authors.forename: Mehmet
authors.initials: M
authors.lastname: Gunduz
authors.forename: Junji
authors.initials: J
authors.lastname: Matsuoka
authors.forename: Noriaki
authors.initials: N
authors.lastname: Tanaka
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis; D002294:Carcinoma, Squamous Cell / Q000378:metabolism / Q000473:pathology*; D004938:Esophageal Neoplasms / Q000378:metabolism / Q000473:pathology*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D008875:Middle Aged; D009367:Neoplasm Staging; D015689:Oncogene Protein p21(ras) / Q000096:biosynthesis*; D012189:Retrospective Studies; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*
chemical_list: D016159:Tumor Suppressor Protein p53; D015689:Oncogene Protein p21(ras)