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Recent Patents on Anti-Cancer Drug Discovery - Online First
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Selinexor as a Therapeutic Target: Advances in Non-small Cell and Small Cell Lung Cancer Treatment Strategies
Authors: Bosheng Zheng, Wenqi Zhang, Shaonan Xie, Yaqing Han, Guangjie Liu, Yanjie Liu, Maogang Gao, Shize Wang and Qingyi LiuAvailable online: 29 October 2024More LessSelinexor treats lung cancer, particularly non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). This review summarizes the prevalence and types of lung cancer and emphasizes the challenges associated with current treatments like resistance and limited effectiveness. Selinexor is a selective inhibitor of nuclear export (SINE) that has emerged as a potential therapy that targets the nuclear export of tumor suppressor proteins. The mechanisms of selinexor, its potential in combination therapies, and challenges like side effects and drug resistance are explained in this review. Key findings highlight the effectiveness of selinexor in preclinical studies, particularly against KRAS-mutant NSCLC and in combination with chemotherapy for SCLC. The review concludes with a discussion of future directions and underscores the potential of selinexor to improve the treatment strategies for lung cancer.
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Comprehensive Analysis of Prognostic Alternative Splicing Signatures in Tumor Immune Infiltration in Bladder Cancer
Authors: Gao-Lei Liu, Hao Luo, Dan-Dan Liang, Li Zhong, Nan Dai and Wei-Hua LanAvailable online: 29 October 2024More LessBackgroundBladder cancer exhibits substantial heterogeneity encompassing genetic expressions and histological features. This heterogeneity is predominantly attributed to alternative splicing (AS) and AS-regulated splicing factors (SFs), which, in turn, influence bladder cancer development, progression, and response to treatment.
ObjectiveThis study aimed to explore the immune landscape of aberrant AS in bladder cancer and establish the prognostic signatures for survival prediction.
MethodsBladder cancer-related RNA-Seq, transcriptome, and corresponding clinical information were downloaded from The Cancer Genome Atlas (TCGA). Gene set enrichment analysis (GSEA) was used to identify significantly enriched pathways of cancer-related AS events. The underlying interactions among differentially expressed genes (DEGs) and cancer-related AS events were assessed by a protein-protein interaction network. Univariate and multivariate Cox regression analyses were performed to identify crucial prognostic DEGs that co-occurred with cancer-related AS events (DEGAS) for overall survival. The area under the curve (AUC) of receiver operating characteristic (ROC) curves was used to assess the efficiency of the prognostic signatures. The CIBERSORT algorithm was used to explore the abundance of immune infiltrating cells.
ResultsA total of 3755 cancer-related AS events and 3110 DEGs in bladder cancer were identified. Among them, 379 DEGs co-occurred with cancer-related AS events (DEGAS), of which 102 DEGAS were associated with 14 dysregulated SFs. GSEA and KEGG analysis showed that cancer-related AS events were predominantly enriched in pathways related to immunity, tumorigenesis, and treatment difficulties of bladder cancer. Multivariate Cox regression analysis identified 8 DEGAS (CABP1, KCNN2, TNFRSF13B, PCDH7, SNRPA1, APOLD1, CX3CL1, and DENND5A) significantly associated with OS, and they were further integrated into the prediction model with good AUCs at 3-year, 5-year and 7-year ROC curves (all>0.7). Immune infiltration analysis revealed the significant enrichment of three immune cell types (B cells naïve, dendritic cells resting, and dendritic cell activated) in high-risk bladder cancer patients.
ConclusionThis study not only unveiled comprehensive prognostic signatures of AS events in bladder cancer but also established a robust prognostic model based on survival-related DEGAS. These aberrant AS events, dysregulated SFs, and the identified 8 DEGAS may have significant clinical potential as therapeutic targets for bladder cancer.
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West African Medicinal Plant Substances and Molecules Activities Against Viral Hepatitis B and Hepatocellular Carcinoma
Authors: Pengdwendé Fabienne Ingrid Zongo, Bagora Bayala and Jacques SimporeAvailable online: 21 October 2024More LessBackgroundChronic hepatitis B virus (HBV) infection remains a major global public health problem with devastating consequences, such as hepatocellular carcinoma. Currently, approved treatments are limited to interferon and nucleoside/nucleotide analogues for chronic hepatitis B and chemotherapy, radiotherapy, and surgery for cancer. Both treatments have their limitations, making complete cure an elusive goal. Therefore, the identification of new therapeutic targets using medicinal plants and the development of new antiviral and anticancer strategies are of utmost importance.
ObjectiveThe aim of this review is to identify from the literature the substances and molecules of West African flora involved in the fight against chronic hepatitis B and liver cancer and to provide a summary of their mechanisms of action.
MethodsPubmed, HAL open science, and Google Scholar literature search engines were used to identify medicinal plants and molecules from the West African flora.
ResultsAmong West African countries, Gambia and Niger had the highest prevalence of hepatitis B virus infection, and 09 West African countries had high rates of liver cancer. A number of studies carried out in Mali, Benin, Senegal, and Burkina Faso enabled us to list anti-HBV and anticancer plants, as well as a number of molecules isolated from plants found in West African regions.
ConclusionBy offering a glimpse into the world of anti-HBV and anticancer molecules from West Africa, this review provides valuable information to support the future development of herbal antiviral and anticancer drugs.
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Quercetin Promotes the M1-to-M2 Macrophage Phenotypic Switch During Liver Fibrosis Treatment by Modulating the JAK2/STAT3 Signaling Pathway
Authors: Dongqi Sun, Xiaoling Zhou, Teng Wu, Zepeng Li, Shigao Huang and Zheng PengAvailable online: 02 October 2024More LessObjectiveTo investigate the underlying mechanism by which quercetin (Que) regulates macrophage polarization and its subsequent therapeutic effect on liver fibrosis, an important pathological precondition for hepatocellular carcinoma (HCC).
MethodsIn vitro experiments were performed on the RAW264.7 mouse macrophage line. After the induction of M1-type macrophages with LPS, the effects of Que on cell morphology, M1/M2 surface marker expression, cytokine expression, and JAK2/STAT3 expression were analyzed. In vivo, male SD rats were used as a model of CCL4-induced hepatic fibrosis, and the effects of Que on serum aminotransferase levels, the histopathological structure of liver tissues, and macrophage-associated protein expression in liver tissues were analyzed.
ResultsIn vitro experiments revealed that Que can suppress the activation of the JAK2/STAT3 signaling pathway, leading to decreases in the expression of M1 macrophage surface markers and cytokines. Additionally, Que was found to increase the expression of M2 macrophage surface markers and cytokines. In vivo, assays demonstrated that Que significantly ameliorated the development of inflammation and fibrosis in a rat liver fibrosis model.
ConclusionQue can inhibit hepatic fibrosis by promoting M1 to M2 macrophage polarization, which could be associated with its ability to suppress the JAK2/STAT3 signaling pathway in macrophages.
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