Source: Annual Congress 2002 - Lung cancer biology
Disease area: Thoracic oncology

Abstract

P53 protein is critical regulator of cell cycle and apoptosis in genotoxic stress and its levels, distribution and functions changing in response to many stimuli. To assess whether C-terminal or N-terminal phosphorylations of p53 protein and poly(ADP-ribosyl)ation might serve as an index of recurrent lung cancer progression we examined DNA ploidy, poly(ADP-ribose) levels, the expression of total (wild type + mutated) and mutated p53 protein only, as well as its Ser-392 and Ser-20 phosphate levels in fiberoptic bronchoscopy biopsy samples taken before and after treatment with radiotherapy/cisplatin/vinorelbine of patients suffering from recurrent squamous cell lung cancer. All 31 patients included in this study had similar clinical stage and alike, mostly aneuploid DNA ploidy irrespectively on the therapy. The treatment decreased G2/M cell numbers but increased S-phase cells by almost 50% comparing to ploidy status before therapy, while median p53 expression was doubled and represented mostly mutated protein. p53 phosphorylated on Ser20 and Ser392 was also increased by approximately 120% and 70%, respectively after radiotherapy/ chemotherapy, but only p53-Ser392~P alterations correlated with elevated poly(ADP-ribose) levels. Our data indicate that apart from changes in p53 quantity, posttranslational phosphorylation/dephosphorylation-mediated alterations may play a role in neoplastic cell growth and antiproliferative activity of drugs inducing DNA damage and apoptosis.

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R. M. Mroz, A. Holownia, E. Chyczewska, L. Chyczewski, J. J. Braszko (Bialystok, Poland). Therapy increases poly(ADP-ribose), p53 expression, p53-Ser392 –P, and p53-Ser2 –P levels in recurrent squamous cell lung cancer. Eur Respir J 2002; 20: Suppl. 38, 223

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