Radiation resistance is linked to immune escaping and radiation sensitivity. In this study, we found that the PD-L1 expressions of non-killed tumor cells in NSCLC were enhanced after radiotherapy, and dihydroartemisinin (DHA) could synergistically enhance the antitumor effect of radiotherapy in NSCLC. A total of 48 NSCLC patients with sufficient tumor tissues for further analyses were enrolled. The PD-L1 expressions of NSCLC were evaluated by immunohistochemistry. Cell apoptosis was measured by flow cytometry, and the relationship between the PD-L1 expression and radiation resistance was investigated in patient specimens, xenograft model, and cell lines. First, the results indicate that the PD-L1 expression of NSCLC was positively related with the radiation resistance. Second, we found that DHA could eliminate the radiation resistance and synergistically enhance the antitumor effect of radiotherapy in the NSCLC cells lines and xenograft model. Finally, mechanistically, DHA could inhibit the PD-L1 expression to avoid immune escaping by inhibiting TGF-β, PI3K/Akt, and STAT3 signaling pathways. In addition, DHA could activate TRIM21 and regulate the EMT-related proteins by inhibiting the PD-L1 so as to enhance the radiation sensitivity and eliminate radiation resistance to NSCLC. Collectively, this study established a basis for the rational design of integrated radiotherapy and DHA for the treatment of NSCLC. The incidence of colon cancer in young patients is on the rise, of which adenocarcinoma is the most common pathological type. However, a reliable nomogram for early onset colon adenocarcinoma (EOCA) to predict prognosis is currently lacking. This study aims to develop nomograms for predicting the overall survival (OS) and cancer-specific survival (CSS) of patients with EOCA. Patients diagnosed with EOCA from 2010 to 2015 were included and randomly assigned to training set and validation set. Cox regression models were used to evaluate prognosis and identify independent predictive factors, which were then utilized to establish the nomograms for predicting 3- and 5-year OS and CSS. The discrimination and calibration of nomograms were validated using the calibration plots, concordance index, receiver operating characteristics curve, and the decision curve analysis. A total of 2,348 patients were screened out, with 1,644 categorized into the training set and 704 into the validation set. Multivariate analysiA patients, which assisted clinicians to evaluate prognosis more accurately and optimize treatment strategies. To evaluate the impact of tonsillectomy on the detection of the primary tumor, based on p16 immunohistochemistry analysis, in patients with cervical unknown primary of squamous cell carcinoma (SCC-CUP). This was a retrospective study of 63 patients, included from January 2008 to December 2017 in a single institution. All patients had an initial assessment with physical examination, CT scan of the neck and chest, whole body FDG-PET CT, and endoscopy under general anesthesia, which failed to determine the primary tumor. Forty-seven out of the 63 patients had an ipsi- or bilateral tonsillectomy which revealed 12 tonsil cancers (26%). The tonsil primary was ipsilateral to positive nodes in 10 cases, contralateral in 1 case and, in 1 case, the patient had bilateral neck involvement. The analysis of the p16 status was carried out in 41/63 patients (65%). Among the 32 patients who had a p16 analysis and tonsillectomy, the rate of primary detection was 59% (10/17) for p16-postives and 0% (0/15) for p16-negatives (p < 0.001). These results suggest that an extended work-up should be systematically proposed including bilateral tonsillectomy (+/- mucosectomy of the base of tongue) in SCC-CUP p16-positive patients but not in p16-negatives.These results suggest that an extended work-up should be systematically proposed including bilateral tonsillectomy (+/- mucosectomy of the base of tongue) in SCC-CUP p16-positive patients but not in p16-negatives.The human TP53 locus, located on the short arm of chromosome 17, encodes a tumour suppressor protein which functions as a tetrameric transcription factor capable of regulating the expression of a plethora of target genes involved in cell cycle arrest, apoptosis, DNA repair, autophagy, and metabolism regulation. TP53 is the most commonly mutated gene in human cancer cells and TP53 germ-line mutations are responsible for the cancer-prone Li-Fraumeni syndrome. selleck inhibitor When mutated, the TP53 gene generally presents missense mutations, which can be distributed throughout the coding sequence, although they are found most frequently in the central DNA binding domain of the protein. TP53 mutations represent an important prognostic and predictive marker in cancer. The presence of a TP53 mutation does not necessarily imply a complete P53 inactivation; in fact, mutant P53 proteins are classified based on the effects on P53 protein function. Different models have been used to explore these never-ending facets of TP53 mutations, generating abundant experimental data on their functional impact. Here, we briefly review the studies analysing the consequences of TP53 mutations on P53 protein function and their possible implications for clinical outcome. The focus shall be on Chronic Lymphocytic Leukemia (CLL), which also has generated considerable discussion on the role of TP53 mutations for therapy decisions.Ovarian cancer is one of the most malignant gynecological cancers around the world. In spite of multiple treatment options, the five-year survival rate is still very low. Several metabolism alterations are described as a hallmark in cancers, but alterations of lipid metabolism in ovarian cancer have been paid less attention. To explore new markers/targets for accurate diagnosis, prognosis, and therapeutic treatments based on metabolic enzyme inhibitors, here, we reviewed available literature and summarized several key metabolic enzymes in lipid metabolism of ovarian cancer. In this review, the rate limiting enzymes associated with fatty acid synthesis (FASN, ACC, ACLY, SCD), the lipid degradation related enzymes (MAGL, CPT, 5-LO, COX2), and the receptors related to lipid uptake (FABP4, CD36, LDLR), which promote the development of ovarian cancer, were analyzed and evaluated. We also focused on the review of application of current metabolic enzyme inhibitors for the treatment of ovarian cancer through which the potential therapeutic agents may be developed for ovarian cancer therapy.