This study aimed to identify important genes associated with melanoma to further develop new target gene therapies and analyze their significance concerning prognosis. Gene expression data for melanoma and normal tissue were downloaded from three databases. Differentially co-expressed genes were identified by WGCNA and DEGs analysis. These genes were subjected to GO, and KEGG enrichment analysis and construction of the PPI visualized with Cytoscape and screened for the top 10 Hub genes using CytoHubba. We validated the Hub gene's protein levels with an immunohistochemical assay to confirm the accuracy of our analysis. A total of 435 differentially co-expressed genes were obtained. Survival curves showed that high expression of FOXM1,\ EXO1, KIF20A, TPX2, and CDC20 in melanoma patients with 5 of the top 10 hub genes was associated with reduced overall survival (OS). Immunohistochemistry showed that all five genes were expressed at higher protein levels in melanoma than in paracancerous tissues. FOXM1, EXO1, KIF20A, TPX2, and CDC20 are prognosis-associated core genes of melanoma, and their high expression correlates with the low prognosis of melanoma patients and can be used as biomarkers for melanoma diagnosis, treatment, and prognosis prediction. FOXM1, EXO1, KIF20A, TPX2, and CDC20 are prognosis-associated core genes of melanoma, and their high expression correlates with the low prognosis of melanoma patients and can be used as biomarkers for melanoma diagnosis, treatment, and prognosis prediction.Mesenchymal stromal cells (MSCs) comprise a heterogeneous population of multipotent stromal cells that have gained attention for the treatment of irradiation-induced normal tissue toxicities due to their regenerative abilities. As the vast majority of studies focused on the effects of MSCs for photon irradiation-induced toxicities, little is known about the regenerative abilities of MSCs for particle irradiation-induced tissue damage or the effects of particle irradiation on the stem cell characteristics of MSCs themselves. MSC-based therapies may help treat particle irradiation-related tissue lesions in the context of cancer radiotherapy. As the number of clinical proton therapy centers is increasing, there is a need to decidedly investigate MSC-based treatments for particle irradiation-induced sequelae. Furthermore, therapies with MSCs or MSC-derived exosomes may also become a useful tool for manned space exploration or after radiation accidents and nuclear terrorism. However, such treatments require an in-depth knowledge about the effects of particle radiation on MSCs and the effects of MSCs on particle radiation-injured tissues. Here, the existing body of evidence regarding the particle radiobiology of MSCs as well as regarding MSC-based treatments for some typical particle irradiation-induced toxicities is presented and critically discussed. The prognostic role of age among patients affected by Oral Tongue Squamous Cell Carcinoma (OTSCC) is a topic of debate. Recent cohort studies have found that patients diagnosed at 40 years of age or younger have a better prognosis. The aim of this cohort study was to clarify whether age is an independent prognostic factor and discuss heterogeneity of outcomes by stage and treatments in different age groups. We performed a study on 577 consecutive patients affected by primary tongue cancer and treated with surgery and adjuvant therapy according to stage, at European Institute of Oncology, IRCCS. Patients with age at diagnosis below 40 years totaled 109 (19%). Overall survival (OS), disease-free survival (DFS), tongue specific free survival (TSFS) and cause-specific survival (CSS) were compared by age groups. Multivariate Cox proportional hazards models were used to assess the independent role of age. The median follow-up time was 5.01 years (range 0-18.68) years with follow-up recorded up to February 202ewer younger people than older people died from tongue cancer in advanced stages. Young age at diagnosis is associated with a better overall survival. Fewer younger people than older people died from tongue cancer in advanced stages. Our study aimed to validate pathologic findings of ground-glass nodules (GGOs) of different consolidation tumor ratios (CTRs), and to explore whether GGOs could be stratified according to CTR with an increment of 0.25 based on its prognostic role. We retrospectively evaluated patients with clinical stage IA GGOs who underwent curative resection between 2011 and 2016. The patients were divided into 4 groups according to CTR step by 0.25. Cumulative survival rates were calculated by the Kaplan-Meier method. Univariate and multivariate Cox regression analyses were conducted to obtain the risk factors on relapse-free survival (RFS). The surv_function of the R package survminer was used to determine the optimal cutoff value. Receiver operating characteristic (ROC) analysis was generated to validate optimal cutoff points of factors. A total of 862 patients (608 women; median age, 59y) were included, with 442 patients in group A (CTR ≤ 0.25), 210 patients in group B (0.25<CTR ≤ 0.5), 173 patients in group Cere able to subdivide patients with different prognosis. CTR is an independent prognostic factor for clinical stage IA lung adenocarcinoma manifesting as GGO in CT scan. Radiologic cutoffs of CTR 0.50 and 0.75 were able to subdivide patients with different prognosis. Overexpression of breast cancer (BCa) resistance protein (BCRP) is detected in approximately 30% of BCa cases. BCRP indicates a poor response to chemotherapy, and it has become a classic target to overcome drug-resistant tumor cells. In this study, we aimed to explore the mechanism of BCRP overexpression and a strategy to reverse this overexpression in invasive BCa. BCRP expression in BCa tissues was determined by immunohistochemistry. https://www.selleckchem.com/products/cmc-na.html GSE25066 was downloaded from the NCBI GEO database. Western blot was used to determine the expression of key molecules . Cell counting kit-8 assays were used to assess the drug response of BCa cells. Our results suggested that BCRP is an independent risk factor for BCa. We further established that upon 17α-PG binding, membrane progesterone receptor α (mPRα) promoted BCRP expression the PI3K/Akt/mTOR signaling pathway. mPRα physically interacted with p-Akt1 S473. Moreover, rapamycin, an inhibitor of mTOR complex 1 (mTORC1), downregulated BCRP expression and enhanced the effects of particular drugs, including doxorubicin and paclitaxel.