We wish to thank Josette Noletti and Michle Radal for excellent technical assistance, and Dr Sharon Lynn Salhi for crucial comments and excellent editorial assistance.. no fibrosis in the presence of abundant macroscopic tumour. In our study, RCRG 1 patients were considered as histological responders, while histological non-responders corresponded to patients with RCRG 2 or RCRG 3. The same pathologist, blinded to the result of the p53 analysis, classified all tumours. Statistical analyses To investigate the association between parameters, univariate statistical analyses were performed using Pearson’s computation for categorical variables or Fisher’s exact test if applicable. Multivariate analyses for response, by logistic regression, were carried out to evaluate the effect of interactions between the different variables. Owing to the small number of patients and the fact that some patients did not have measurements for all those variables, the power of analysis was reduced. All 56.3% of p53-Ab-negative patients. We noticed that one patient with circulating p53-Ab had no gene alteration and no p53 nuclear overexpression. One p53-Ab-positive patient was IHC positive with a wild-type gene, and one patient was IHC unfavorable with a codon 175 mutation. Table 3 Univariate analysis of the four levels of p53 analysis for pattern for pattern (mean, s.d., years)65.28.963.0710.19NS???? for pattern for trend other postsurgical stages demonstrated a pattern to correlation (1994; Poller (2004) in a series of 220 colorectal cancer patients detected p53-Ab mainly in Dukes B and C stages. Moreover, Tang (2001), in a large study of 998 colorectal patients demonstrated that the presence of p53-Ab correlates with tumour progression in colorectal carcinogenesis and an increase with Pyrotinib Racemate advanced node metastasis. However, in these studies, both colon and rectal cancers were analysed as a single entity, whereas our work was focalised only on rectal carcinoma. Allelic loss of 17p is usually a frequent event associated with colorectal carcinogenesis (Baker (2002) showed by sequence analysis in a retrospective series of 86 rectal CSF3R tumours with 41% responders that the presence of p53 mutations correlated with sensitivity to radiotherapy. However, Rodel (2002) analysed the histopathological response to radiotherapy in a series of 44 patients and exhibited that neither the p53 nor the bcl-2 status was correlated with a response to radiotherapy, but they found that the apoptotic index may help to tailor therapy with regard to neoadjuvant treatment of rectal cancer. Similarly, Saw (2003), in a Pyrotinib Racemate series of 60 low rectal tumours locally advanced, concluded that neither p53 by IHC and PCRCSSCP (single-strand conformation polymorphism), nor DCC (deleted in colon cancer) by IHC was associated with tumour downstaging. Although no correlation was obtained for pretreated tissues in our study, a pattern to correlation was observed on surgical Pyrotinib Racemate samples where retention of heterozygosity was associated with em p /em T0C em p /em T1 stages. When cells are exposed to ionising radiation, a complex response is initiated including cell cycle arrest in the G1 and the G2 phases, apoptosis, and DNA repair. Wild-type p53 is usually a cell cycle checkpoint determinant following irradiation (Kuerbitz em et al /em , 1992); and in response to ionising radiation (Buschmann em et al /em , 2000), p53 is usually stabilised through phosphorylation, inhibition of Mdm2-mediated degradation, and reduction in Mdm2 sumoylation. The consequence is usually promotion of either cell cycle arrest or apoptosis. Following gamma-irradiation-induced cell death, striking tissue specificity is usually observed, with distinct regulation of target p53-induced genes (Fei and El Deiry, 2003). Instead of static analyses, dynamic immunohistochemical studies, comparing expression Pyrotinib Racemate of apoptosis-releated genes (Tannapfel em et al /em , 1998; Rau em et al /em , 2003) in pretherapy biopsies and the final resected specimen after neoadjuvant treatment, could contribute to molecular marker positioning. Furthermore, other components such as EGFR and cyclin D1 could play active functions in tumour response to radiotherapy (Milas em et al /em , 2004). Our analysis of rectal cancers investigated the implication of p53 dysregulation with relation to the response to neoadjuvant therapy. The strength of our study was three-fold. First, p53 was.