Personalized risk prediction for prolonged ileus after minimally invasive colorectal cancer surgery: in-depth risk factor analysis and model development.

PURPOSE: Despite the increasing preference for minimally invasive surgery for colorectal cancer (CRC), the incidence of prolonged postoperative ileus (PPOI) remains high. Thus, this study aimed to identify risk factors for PPOI in patients with CRC who underwent minimally invasive surgery (MICRS) and to develop a practical nomogram for predicting individual PPOI risk. METHODS: A consecutive series of 2368 patients who underwent MICRS between 2013 and 2023 at two tertiary academic centers were retrospectively studied. Using the data from 1895 patients in the training cohort, a multivariable logistic regression model was employed to select significant variables for the construction of a best-fit nomogram. The nomogram was internally and externally validated. RESULTS: PPOI occurred in 9.5% of patients. Six independent risk factors were identified to construct a nomogram: advanced age (OR 1.055, P = 0.002), male sex (OR 2.914, P = 0.011), age-adjusted Charlson comorbidity index ≥ 6 (OR 2.643, P = 0.025), preoperative sarcopenia (OR 0.857, P = 0.02), preoperative prognostic nutritional index (OR 2.206, P = 0.047), and intraoperative fluid overload (OR 2.227, P = 0.045). The AUCs of the model for predicting PPOI in the training and external validation cohorts were 0.887 and 0.838, respectively. The calibration curves demonstrated excellent consistency between the nomogram-predicted and observed probabilities in both cohorts. Individuals with a total nomogram score of < 197 or ≥ 197 were considered to be at low or high risk for PPOI, respectively. CONCLUSIONS: The integrated nomogram we developed could provide personalized risk prediction of PPOI after MICRS. This quantification enables surgeons to implement personalized prevention strategies, thereby improving patient outcomes.

The crosstalk between glucose metabolism and telomerase regulation in cancer.

Accumulated alterations in metabolic control provide energy and anabolic demands for enhanced cancer cell proliferation. Exemplified by the Warburg effect, changes in glucose metabolism during cancer progression are widely recognized as a characteristic of metabolic disorders. Since telomerases are a vital factor in maintaining DNA integrity and stability, any damage threatening telomerases could have a severe impact on DNA and, subsequently, whole-cell homeostasis. However, it remains unclear whether the regulation of glucose metabolism in cancer is connected to the regulation of telomerase. In this review, we present the latest insights into the crosstalk between telomerase function and glucose metabolism in cancer cells. However, at this moment this subject is not well investigated that the association is mostly indirectly regulations and few explicit regulating pathways were identified between telomerase and glucose metabolism. Therefore, the information presented in this review can provide a scientific basis for further research on the detail mechanism and the clinical application of cancer therapy, which could be valuable in improving the effectiveness of chemotherapy.