early during radiotherapy, while inhibition of cell proliferation by tumoricidal effects mainly takes place gradually with the course of radiotherapy. 18F-FMISO and 18F-FLT PET/CT are sensitive and non-invasive tools for the monitoring of tumor reoxygenation and proliferation during radiotherapy.Purpose In this study, we developed and validated a radiomics nomogram by combining the radiomic features extracted from 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) images and clinicopathological factors to evaluate the overall survival (OS) of patients with non-small cell lung cancer (NSCLC).  https://www.selleckchem.com/products/gne-049.html  Patients and Methods A total of 315 consecutive patients with NSCLC (221 in the training cohort and 94 in the validation cohort) were enrolled in this study. A total of 840 radiomic features were extracted from the CT and PET images. Three radiomic scores (rad-scores) were calculated using the least absolute shrinkage and selection operator (LASSO) Cox regression based on subsets of CT, PET, and PET/CT radiomic features. A multivariate Cox regression analysis was performed for each rad-score combined with clinicopathological factors to determine the independent risk factors. The OS nomogram was constructed based on the PET/CT rad-score and independent clinicopathological factors. Validation and calibration were conducted to evaluate the performance of the model in the training and validation cohorts, respectively. Results A total of 144 (45.71%) women and 171 (54.29%) men with NSCLC were enrolled in this study. The PET/CT rad-score combined with the clinical model had the best C-index (0.776 and 0.789 for the training and validation cohorts, respectively). Distant metastasis, stage, carcinoembryonic antigen (CEA), and targeted therapy were independent risk factors for patients with NSCLC. The validation curve showed that the OS nomogram had a strong predictive power in patients' survival. The calibration curve showed that the predicted survival time was significantly close to the observed one. Conclusion A radiomic nomogram based on 18F-FDG PET/CT rad-score and clinicopathological factors had good predictive performance for the survival outcome, offering feasible, and practical guidance for individualized management of patients with NSCLC.ALDH is an enzyme involved in different cellular processes, including cancer. It has been shown that a cellular subpopulation with high ALDH activity (ALDHHIGH) within a tumor is related to functional capabilities such as stemness, chemoresistance, and tumorigenicity. However, few studies have focused on determining the mechanisms behind ALDH activity within the cells. Previously, our group reported that ALDHHIGH cells have higher tumorigenicity in Cervical Cancer (CC) cell lines. Based on this, we were interested to know the molecular mediators of the ALDHHIGH cells, specifically β-catenin, inasmuch as β-catenin is regulated through different pathways, such as Wnt signaling, and that it acts as a transcriptional co-activator involved in cancer progression. In this work, we show that the increase in ALDHHIGH cell percentage is reverted by β-catenin knockdown. Consistently, upon GSK3-β inactivation, a negative regulator of β-catenin, we observed an increase in ALDHHIGH cells. Additionally, we observed a low percentage of cells positive for Fzd receptor, suggesting that in our model there is a low capacity to respond to Wnt ligands. The analysis of ALDHHIGH cells in a sphere formation model demonstrated the active state of AKT. In accordance with this, impairment of AKT activity not only reduced β-catenin active state, but also the percentage of ALDHHIGH cells. This corroborates that AKT acts upstream of β-catenin, thus affecting the percentage of ALDHHIGH cells. In conclusion, our results show that ALDHHIGH cells are dependent on β-catenin, in spite of the Wnt pathway seems to be dispensable, while AKT emerges as central player supporting a mechanism in this important axis that is not yet well known but its analysis improves our understanding of ALDH activity on CC.Resveratrol is a natural polyphenolic compound with multiple biological effects, e.g., proliferation inhibition, anti-oxidation, and neuroprotection. Besides that, studies have shown that resveratrol inhibits tumor growth and migration, as well as epithelial-mesenchymal transition (EMT). However, its molecular mechanisms in tumor progression are not fully understood. Nutrient-deprivation autophagy factor-1 (NAF-1) is mainly found in the endoplasmic reticulum and mitochondrial outer membrane. It is an important genetic locus for regulating oxidative stress and autophagy. The molecular mechanism of NAF-1 in pancreatic cancer is currently unclear. The current study found that NAF-1 is expressed in pancreatic cancer tissue and correlated with the progression of pancreatic cancer. Furthermore, we found that NAF-1 inhibition significantly inhibits the stem cell characteristics and the invasion and migration abilities of pancreatic cancer cells. In a subcutaneous xenograft model of pancreatic cancer in nude mice, resveratrol inhibited the expression of NAF-1, thereby inhibiting tumor growth. Taken together, resveratrol could be an effective anti-tumor drug, and NAF-1 may be a rational therapeutic target.Colon cancer is one of the most prevalent malignancies that lead to high occurrence of cancer-related deaths. Currently, chemotherapies and radiotherapies remain the primary treatments for advanced colon cancer. Despite the initial effectiveness, a fraction of colon cancer patients developed cisplatin resistance, resulting in therapeutic failure. The long non-coding RNA differentiation antagonizing non-coding RNA (DANCR) has been shown to be upregulated in multiple cancers, indicating an oncogenic role of DANCR. This study aims to elucidate the roles of DANCR in regulating cisplatin (CDDP) resistance of colon cancer. We found DANCR was significantly upregulated in colon cancer tissues and cells compared with normal colon tissues and cells. DANCR was upregulated in cisplatin-resistant colon cancer cells. Moreover, overexpression of DANCR significantly desensitized colon cancer cells to cisplatin. On the other way, silencing DANCR dramatically overrode CDDP resistance of colon cancer cells. Bioinformatics prediction revealed DANCR could bind to seeding region of miR-125b-5p as a competitive endogenous RNA.