Modification of p53 expression levels and its principle apoptosis and cell cycle regulatory partners, mouse double minute 2 homolog (MDM-2) and p21, has been previously reported in various types of cancer. In the current study, the expression of Delta 133p53 isoforms was investigated in lung carcinomas with respect to the expression of the aforementioned genes. The expression of p53 full-length transcript and Delta 133p53 isoforms alpha, beta and gamma transcripts, MDM-2 and p21 transcripts were determined by reverse transcription-quantitative polymerase chain reaction, in total RNA isolated from 17 lung carcinoma specimens and 17 corresponding adjacent non-cancerous tissues. RNA expression analysis was performed according to the Pfaffl equation and Rest tool using beta-actin as a reference gene. Detection of the above proteins was additionally performed by western blotting. Significant overexpression of the Delta 133p53 mRNAs was observed in cancerous as compared with adjacent non-cancerous tissues (3.94-fold), whereas full-length p53 and MDM-2 expression exhibited a smaller, however significant, increase. The expression of the p21 transcript was significantly reduced in cancerous specimens. Delta 133p53 and p21 expression levels varied in parallel, however were not significantly correlated. p53 full-length protein expression observed by western blot analysis strongly varied from the Delta 133p53 isoforms, however MDM-2 protein isoforms were not detectable and p21 protein was more abundant in non-cancerous tissues. In conclusion, Delta 133p53 mRNA levels is suggested as a potentially useful marker of malignancy in lung cancer. The absence of Delta 133p53 protein in lung carcinomas, which overexpress Delta 133p53 transcripts, may indicate the role of the latter in post-transcriptional regulation through RNA interference in the cell cycle and apoptosis.