title: [Posttranslational p53 phosphorylation in non small cell lung cancer cells after radio/chemotherapy].
abstract: BACKGROUND
  p53 protein is a critical regulator of cell cycle and apoptosis. Many stimuli change its expression and modify its functions. The aim of our work was to determine stability and chosen posttranslational modification of p53 protein during the treatment of lung cancer.
  
  
  METHODS
  We investigated levels of poly-ADP-ribose- a marker of cellular DNA damage, DNA ploidy, Ki-67 expression, wild type and mutated p53 protein expression and intensity of phosphorylation of chosen p53 serine sites: C-terminal Ser392, and N-terminal Ser15, and Ser20 in fiberoptic bronchoscopy biopsy samples taken from patients suffering from recurrent squamous cell lung cancer before and after radio/chemotherapy. Analysis was based on results obtained from 23 patients after surgery in I-IIIA clinical stage of the disease.
  
  
  RESULTS
  Therapy lowered the number of G2/M cells, but increased S fraction cell population in about 50%. Therapy increased p53 expression and p53 phosphorylation at Ser392 and Ser20, and these changes correlated with poly-ADP-ribose levels and Ki-67 expression.
  
  
  CONCLUSIONS
  Our results indicate that apart from changes in p53 quantity, p53 posttranslational phosphorylation play a role in regulation of neoplastic cells proliferation in response to drugs.
authors.affiliation: Zakład Farmakologii Klinicznej, Akademia Medyczna w Białymstoku, Białystok, Poland. holow_sinai@hotmail.com
authors.forename: Adam
authors.initials: A
authors.lastname: Hołownia
authors.forename: Robert Marek
authors.initials: RM
authors.lastname: Mróz
authors.forename: Mirosław
authors.initials: M
authors.lastname: Kozłowski
authors.forename: Elzbieta
authors.initials: E
authors.lastname: Chyczewska
authors.forename: Jerzy
authors.initials: J
authors.lastname: Laudański
authors.forename: Lech
authors.initials: L
authors.lastname: Chyczewski
authors.forename: Jan Józef
authors.initials: JJ
authors.lastname: Braszko
mesh_terms: D000368:Aged; D000970:Antineoplastic Agents / Q000627:therapeutic use; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy / Q000378:metabolism* / Q000532:radiotherapy; D005260:Female; D006801:Humans; D019394:Ki-67 Antigen / Q000096:biosynthesis; D008175:Lung Neoplasms / Q000188:drug therapy / Q000378:metabolism* / Q000532:radiotherapy; D008297:Male; D008875:Middle Aged; D010766:Phosphorylation; D011064:Poly Adenosine Diphosphate Ribose / Q000378:metabolism; D011499:Protein Processing, Post-Translational; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
chemical_list: D000970:Antineoplastic Agents; D019394:Ki-67 Antigen; D016159:Tumor Suppressor Protein p53; D011064:Poly Adenosine Diphosphate Ribose