To compare the fits of various normal tissue complication probability (NTCP) models to a common set of late rectal toxicity data, with the aim of identifying the best model for predicting late rectal injury after irradiation.
Those variables that were found to contribute substantially (P<0.10) to the multivariate model for colon and/or rectal cancer (age, sex, QI, smoking, energy intake and family history of CRC) were included as covariates in all multivariate analyses.
The covariates included in the multivariate analyses were those found to significantly (p < 0.05) contribute to the multivariate model for colon and/or rectal cancer (age at baseline, sex, body mass index, family history of colorectal cancer, and smoking status) or to influence the RR by more than ten percent, as well as energy intake.
Our findings of high frequencies of MSS (27/30) tumors, aneuploidy (21/30), immunohistochemical p53 expression (18/30) and increased β-catenin expression (25/30) (Table 3) is in line with previous reports of genetic alterations in rectal cancer, but support such a model for the development of rectal cancer also in the majority of young patients.
The variety of tumor response has increased the need to find a useful predictive model for the response of rectal cancer to nCRT, which may be helpful in the design of individualized treatment or early surgery in non-responders.
†Comparison in AUC between the best models obtained with our strategy (MPT1 for rectal cancer, MG for prostate cancer) and the corresponding ensemble models based on the same number of features [ 46] We additionally verified whether, in both cases, data from multiple layers of molecular biology were complementary.
Our objective was to generate an up-to-date estimate of the cost of traditional radiotherapy for rectal cancer and model the impact of a range of potential efficiency improvements.
Recently, Watanabe conducted a new study to establish a prediction model for response to chemoradiotherapy in rectal cancer based on gene expression by RT-PCR analysis as it allows accurate and reproducible quantification of genes [ 16].
On the basis of our data we propose a model for the host response in rectal cancer, in which there is an interaction between the specific and the nonspecific inflammatory reaction (figure 3).
For example, neoadjuvant radiotherapy or chemoradiotherapy is administered solely for rectal cancer.
