Objective:To determine the performance of FDG-PET/CT in the detection of relevant colorectal neoplasms (adenomas ≥10 mm, with high-grade dysplasia, cancer) in relation to CT dose and contrast administration and to find a PET cut-off.Methods:84 patients, who underwent PET/CT and colonoscopy (n = 79)/sigmoidoscopy (n = 5) for colonic segments, were included in a retrospective study. The accuracy of low-dose PET/CT in detecting mass-positive segments was evaluated by ROC analysis by two blinded independent reviewers relative to contrast-enhanced PET/CT. On a per-lesion basis characteristic PET values were tested as cut-offs.Results:Low-dose PET/CT and contrast-enhanced PET/CT provide similar accuracies (area under the curve for the average ROC ratings 0.925 vs. 0.929, respectively). PET demonstrated all carcinomas (n = 23) and 83% (30/36) of relevant adenomas. In all carcinomas and adenomas with high-grade dysplasia (n = 10) the SUVmax was ≥5. This cut-off resulted in a better per-segment sensitivity and negative predictive value (NPV) than the average PET/CT reviews (sensitivity: 89% vs. 82%; NPV: 99% vs. 98%). All other tested cut-offs were inferior to the SUVmax.Conclusion:FDG-PET/CT provides promising accuracy for colorectal mass detection. Low dose and lack of iodine contrast in the CT component do not impact the accuracy. The PET cut-off SUVmax ≥ 5 improves the accuracy.
Crocin, a bioactive molecule of saffron, inhibited proliferation of both HCT116 wild-type and HCT116 p53−/− cell lines at a concentration of 10 mM. Flow cytometric analysis of cell cycle distribution revealed that there was an accumulation of HCT116 wild-type cells in G1 (55.9%, 56.1%) compared to the control (30.4%) after 24 and 48 h of crocin treatment, respectively. However, crocin induced only mild G2 arrest in HCT116 p53−/− after 24 h. Crocin induced inefficient autophagy in HCT116 p53−/− cells, where crocin induced the formation of LC3-II, which was combined with a decrease in the protein levels of Beclin 1 and Atg7 and no clear p62 degradation. Autophagosome formation was not detected in HCT116 p53−/− after crocin treatment predicting a nonfunctional autophagosome formation. There was a significant increase of p62 after treating the cells with Bafilomycin A1 (Baf) and crocin compared to crocin exposure alone. Annexin V staining showed that Baf-pretreatment enhanced the induction of apoptosis in HCT116 wild-type cells. Baf-exposed HCT116 p53−/− cells did not, however, show any enhancement of apoptosis induction despite an increase in the DNA damage-sensor accumulation, γH2AX indicating that crocin induced an autophagy-independent classical programmed cell death.
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