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The current case-control study was conducted in order to elucidate any possible association of the single nucleotide polymorphism (SNP) of codon 72 of the p53 gene (Arg72Pro) and sporadic colorectal adenocarcinoma development in a Caucasian population in Greece. The distribution of its alleles, in relation to many clinical parameters of the cancer group, was also investigated.Genomic DNA samples from 93 sporadic colorectal adenocarcinoma cases and 95 healthy controls (age and ethnicity matched) were used to genotype the p53 codon 72 polymorphism.A strong association of the homozygous 72Arg allele with the development of colorectal cancer was observed (Chi-Square = 11,212, p = 0.001, O.R = 2.902, 95% (CI) = 1.540-5.469, for Arg/Arg vs. Arg/Pro and Pro/Pro). When tumor location was accounted for, the Arg/Arg carrier genotypes were associated with an increased incidence of left colon cancer (Chi-Square = 5.256, p = 0.026, OR = 2.975, 95% (CI) = 1.150-7.699).p53Arg homozygosity is associated with the development of sporadic colorectal adenocarcinoma, in the Greek-Caucasian population studied and this polymorphism may have a significant prognostic value, where tumor location is concerned.

Based on the hypothesis that Fractal Dimension (FD) reflects heterogeneity of tumor tissue, we performed an image analysis study to calculate FD of tissue specimens from patients with laryngeal carcinomas in order to investigate its prognostic value.Laryngectomy specimens from 52 patients, who had previously undergone total laryngectomy for squamous cell carcinomas, were examined and their history files reviewed. Ten patients were lost from follow-up. Fractal Analysis software was used to estimate FD of histology sections by the box-counting method. FD of carcinomatous areas was correlated with survival.Patients with a FD lower than the median value of the sample, estimated in sections of carcinomas, had statistically significant higher survival rates.Within the sample of patients studied, FD could be used as a prognostic factor.

E2F-1 is an intriguing transcription factor that accumulates the integrated signal of the G1-S transition regulators. Its role in cell fate, as depicted from in vivo models and a few studies on human tissues, is a matter of debate, since it confers a tissue-specific oncogenic or tumor suppressor behavior. In the present work, in an attempt to shed light on the role of E2F-1 in colon cancer, we examined E2F-1 expression in a series of 45 colon carcinomas and we further correlated it with tumor kinetics. E2F-1 expression and proliferation were evaluated by immunohistochemistry as the percentage of E2F-1 (E2F-1 index: EI) and Ki-67 (Proliferation index: PI)-positive cells, respectively; whereas apoptosis was estimated as the percentage of positive, by TUNEL assay, cells (Apoptotic index: AI). The relationship between E2F-1 expression and tumor kinetics was assessed by microscopical evaluation in semi-serial tissue sections and statistical analysis. Our results demonstrated that E2F-1 expression was inversely correlated with tumor growth (GI=PI/AI) (p=0.002). Specifically, the histological observations showed that E2F-1 was expressed in lesions with high apoptotic incidence and low proliferation. These results also supported the statistical findings showing that EI was inversely correlated with PI (p0.001) and positively associated with AI (p = 0.013). In conclusion, we suggest a tumor-suppressive behavior of E2F-1 in colon carcinomas.

p53 is an oncosuppressor protein, which acts via transcriptional and non-transcriptional mechanisms. The transcriptional function of p53 is mediated by specific responsive elements. In the present study we found active responsive elements, specific for the p53 within the 5'flanking region and within the first intron of the gene encoding for the CD59 membrane inhibitor of reactive lysis, and within the first intron of the gene encoding for the CD58 membrane protein (LFA-3). The results suggest that p53 may enhance the transcription of both CD59 and CD58 and imply a novel role for p53 as a direct regulator of the immune response.

This review aims in presenting the established and putative prognostic markers in non-small cell lung carcinoma (NSCLC). We have focused on the molecular/genetic alterations accompanying the pathogenesis of this malignancy, which may derange the cellular response to external and internal stimuli. A variety of factors influencing cell cycle progression, programmed cell death, drug resistance and immune evasion seem to obtain a predictive--though sometimes argued--role. Taking into account that a great number of these factors develope "cross-talking" protein-complex networks, their combined evaluation is likely to contribute towards a more accurate prediction of the clinical outcome in NSCLC patients.