Recent patents on anti-cancer drug discovery最新文献

{"title":"Targeting Phosphatase and Tensin Homolog Deleted on Chromosome 10q23.3 (PTEN) as a Potential Theragnostic Biomarker in Tumors.","authors":"Ying Liu, Tian Li, Lifen Zhang, Shuhua He, Jialiang Hui","doi":"10.2174/0115748928370540250508101925","DOIUrl":"https://doi.org/10.2174/0115748928370540250508101925","url":null,"abstract":"<p><strong>Background: </strong>Immunotherapy and targeted therapy have been shown to be notably effective in tumor treatment; however, the mechanism of PTEN function in tumorigenesis, development, and immune response of tumors remains unclear.</p><p><strong>Methods: </strong>We show that PTEN expression varies significantly in many types of tumors and affects the prognosis of patients with cancer using pan-cancer analysis. Patents were reviewed using the World Intellectual Property Organisation database. We analyzed data from GTEx, CCLE, and TCGA to study the correlation between PTEN expression and prognosis, investigated the correlation between PTEN expression and tumor-infiltrating immune cells using TIMER, analyzed the mutation pattern of PTEN and its correlation with neoantigen expression, TMB, MSI, MMRs, and DNA methyltransferases in tumors, and conducted an enrichment analysis of PTEN in tumors using GSEA.</p><p><strong>Results: </strong>PTEN expression is related to the levels of infiltrating immune cells, such as B cells, CD4+ T cells, CD8+ T cells, neutrophils, macrophages, and dendritic cells. PTEN expression is closely related to neoantigen expression, tumor mutational burden, microsatellite instability, and mismatch repair. The results of a functional enrichment analysis of PTEN showed that PTEN has the potential as a biomarker for precision immunotherapy of tumors.</p><p><strong>Conclusion: </strong>This study suggests that PTEN may be involved in the recruitment and regulation of immune-infiltrating cells, tumor development, metastasis, prognosis, tumor immune escape, and immunotherapy, indicating its importance in tumor diagnosis and treatment.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"B-9-8, a Novel Harman Dimer, Reverses ABCG2-mediated Chemotherapeutic Drug Resistance.","authors":"Ruiqiang Zhao, Yan Wen, Chao-Yun Cai, Jing-Quan Wang, Pranav Gupta, Zi-Ning Lei, Dong-Hua Yang, Ri-Hui Cao, Zhe-Sheng Chen","doi":"10.2174/0115748928357067250512112852","DOIUrl":"https://doi.org/10.2174/0115748928357067250512112852","url":null,"abstract":"<p><strong>Background: </strong>Multidrug resistance (MDR) in cancer is a major obstacle to achieving success in clinical chemotherapy. It has been observed that overexpression of ATP-Binding Cassette (ABC) transporters plays a crucial role in MDR.</p><p><strong>Objective: </strong>This study aimed to find an effective resistance-reversed agent of ABC transporter. A series of new β-carboline derivatives have been synthesized and are being applied in various invention patents. One of these is B-9-8, a novel harman dimer, which was synthesized to conduct a series of experiments.</p><p><strong>Methods: </strong>In this study, we investigated whether B-9-8 could reverse ABCG2-mediated drug resistance by using MTT assay, [3H]-mitoxantrone accumulation/efflux assay, western blot analysis, immunofluorescence analysis, ATPase assay, and molecular modeling assay.</p><p><strong>Results: </strong>The results showed that B-9-8 could significantly increase the sensitivity of mitoxantrone, SN-38, and topotecan and effectively overcame drug resistance at non-toxic concentrations in ABCG2-overexpressing cells. Further studies showed that B-9-8 increased the intracellular accumulation of [3H]-mitoxantrone by suppressing the efflux function of ABCG2 in ABCG2-overexpressing cells. B-9-8 could down-regulate the ABCG2 protein expression but did not change the subcellular localization of ABCG2. ATPase analysis indicated that B-9-8 inhibited the ATPase activity of ABCG2 in a concentration-dependent manner. In the molecular docking analysis, B-9-8 demonstrated a strong interaction with the human ABCG2 transporter protein.</p><p><strong>Conclusion: </strong>Our findings indicated that B-9-8 could reverse ABCG2-mediated MDR as a potential and reversible modulator in combination with conventional chemotherapeutic drugs.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144103453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating the Therapeutic Potential and Molecular Mechanisms of Daphnetin: A Comprehensive Review.","authors":"Linyue Zhang, Jingwu Wu, Jinzhenwan Xue, Zhihong Jia, Xiaoni Zhou, Gang Hu","doi":"10.2174/0115748928371118250327084127","DOIUrl":"https://doi.org/10.2174/0115748928371118250327084127","url":null,"abstract":"<p><p>Coumarins, a ubiquitous class of aromatic compounds present in a broad spectrum of organisms, including bacteria, fungi, and over 150 plant species, have been extensively studied over the years. Researchers have isolated and characterized more than 1,300 natural coumarins, many of which exhibit promising biomedical properties. Among these, daphnetin has emerged as a distinctive coumarin derivative that is characterized by its unique structural features to impart special physicochemical attributes. Daphnetin is renowned for its diverse range of biological activities, encompassing anticancer, anti-inflammatory, and antiallergic effects. These activities can be attributed to its ability to regulate specific molecular pathways within the body, making it a highly attractive compound for pharmacological research. Consequently, daphnetin has garnered considerable attention within the scientific community, specifically prompting an extensive investigation into its therapeutic potential across diverse clinical conditions. In this comprehensive review, we delved into the structure and sources of daphnetin, with a focus on its unique characteristics that underscore its potential as a therapeutic agent. We further explored the therapeutic potential of daphnetin, highlighting its multifaceted biological activities and the underlying molecular mechanisms. In addition, we scrutinized the potentially toxic effects of daphnetin in light of the current research status and prospects in this direction. By emphasizing the clinical significance of daphnetin, we aim to contribute to the ongoing endeavors toward the development of innovative and efficacious therapeutic strategies for an array of diseases.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"How Oncovirus Affects Drug Resistance in Cancer Cells.","authors":"Yuping Yang, Yuwen Wang, Zhengdong Zhou, Junlong Zhuang, Wei Zhao","doi":"10.2174/0115748928324072250317050917","DOIUrl":"https://doi.org/10.2174/0115748928324072250317050917","url":null,"abstract":"<p><p>Cancer drug resistance has emerged as a formidable challenge in the field of clinical oncology, significantly hampering the success of treatment strategies and leading to suboptimal outcomes for patients. In a broad array of therapeutic settings, the emergence of resistance has become a primary source of concern, ranging from conventional chemotherapy to modern immunotherapy and targeted therapies. The complexity of cancer drug resistance is further exacerbated by the involvement of oncoviruses, such as human papillomavirus (HPV), Epstein-Barr virus (EBV), and hepatitis B virus (HBV), which play pivotal roles in the initiation, progression, and response to treatment of various cancers. The intricate interactions between these oncoviruses and cancer cells have been found to significantly influence drug efficacy. These viruses can alter critical cellular pathways, including drug metabolism, DNA repair mechanisms, and the tumor microenvironment, thus promoting drug resistance. A profound understanding of these virus-cancer-drug interactions is crucial for the development of novel treatment approaches that can effectively overcome drug resistance. This review aimed to contribute to a broader awareness of the multifaceted nature of cancer drug resistance, particularly in the context of oncovirus involvement. By highlighting the critical role of oncoviruses in cancer development and treatment response, this review hopes to stimulate further research and the development of novel treatment strategies that can effectively overcome drug resistance and ultimately improve patient outcomes. As we advance toward precision oncology, a more holistic understanding of the complex interplay among cancer, its associated viruses, and therapeutic drugs is crucial for achieving optimal therapeutic responses.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resibufogenin and Oxaliplatin Synergistically Inhibit Diffuse Gastric Cancer by Inactivating the FAK/AKT/GSK3β/β-Catenin Signaling Pathway.","authors":"Hui-Hui Hu, Hai-Li Shang, Yongjing Ren, Hui-Fang Lv, Shuiping Tu, Jian-Zheng Wang, Ya-Nan Gong, Zhi-Fei Li, He Zhang, Tiepeng Li, Yuhang Wang, Bei-Bei Chen, Sai-Qi Wang, Xiao-Bing Chen","doi":"10.2174/0115748928320605241112094549","DOIUrl":"https://doi.org/10.2174/0115748928320605241112094549","url":null,"abstract":"<p><strong>Background: </strong>Diffuse Gastric Cancer (DGC) is a highly aggressive form of gastric cancer with a poor prognosis. Oxaliplatin (OX) is one of the first-line chemotherapeutic agents for the treatment of gastric cancer. However, some patients with DGC do not benefit from OX therapy. Resibufogenin (RBF), one of the main active components of the Chinese medicine Huachansu, has demonstrated significant anti-cancer effects. Nevertheless, the potential of RBF to enhance the sensitivity of OX treatment in DGC and its underlying mechanisms have not been reported.</p><p><strong>Objective: </strong>The aim of this study is to investigate the sensitizing effect of RBF on OX therapy for DGC, as well as to elucidate the potential targets and mechanisms of action. This exploration is of significant importance for the development of sensitizers that can improve the therapeutic efficacy of OX and for the advancement of patentable innovations in this field.</p><p><strong>Methods: </strong>MTT assay, flow cytometry, Western blotting, and immunofluorescence assays were employed to assess the inhibitory effects of Resibufogenin (RBF) in combination with OX on DGC in vitro. Human DGC cell xenografts were established in a mouse model to evaluate the efficacy and safety of RBF and OX for treating DGC in vivo.</p><p><strong>Results: </strong>It was found that RBF inhibited the proliferation of DGC cells in a time- and dose-dependent manner. When RBF was used in combination with OX, the sensitivity of DGC cells to OX was improved. Significantly, the combination of OX and RBF acts synergistically to induce apoptosis and autophagy while inhibiting migration and invasion of DGC cells in vitro. In vivo, the combination of OX and RBF dramatically inhibited the progression of DGC in the subcutaneous xenograft model without observable toxicity. Mechanistically, RBF significantly inhibited the expression and activation of FAK. OX and RBF synergistically inhibited the phosphorylation of FAK, AKT, and GSK3β to abrogate the entry of β-catenin into the cell nucleus.</p><p><strong>Conclusion: </strong>RBF exhibits a pronounced suppressive effect on FAK, and its combination with OX synergistically blocks the FAK/AKT/GSK3β/β-catenin signaling cascade, thereby inhibiting the growth and metastasis of DGC. This study provides a novel avenue for future research and patent development of FAK inhibitors, with the potential to enhance the therapeutic efficacy of DGC treatment and overcome drug resistance.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143702608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitexin's Role in Colon Cancer Apoptosis: AMPK/mTOR Pathway Modulation Explored Through Experimental and Computational Approaches.","authors":"Mohammed Abdalla Hussein, Gamila A Farouk, Haneen Kh Abdelkader, Mina A Daniel, Mohamed A Youssef, Gaber E Eldesoky, Seikh Mafiz Alam, Mohammad Shahidul Islam, Yasser O Mosaad","doi":"10.2174/0115748928361989250226083146","DOIUrl":"https://doi.org/10.2174/0115748928361989250226083146","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer is a significant global public health challenge, contributing substantially to cancer-related mortality worldwide. Vitexin has been shown to promote the polarization of macrophages towards the M1 phenotype, a process dependent on the Vitamin D receptor. This polarization is crucial in the tumor microenvironment, as it helps mitigate the progression from chronic colitis to colorectal cancer. Despite its potential, the mechanisms of vitexin's action and its impact on colon cancer remain unclear.</p><p><strong>Objective: </strong>This study aims to evaluate the inhibitory effects of vitexin on cell proliferation and apoptosis in the Caco-2 colon cancer cell line, with a specific focus on its modulation of antioxidant enzyme activities, pro-apoptotic factors, and key signaling pathways involved in cell survival and proliferation.</p><p><strong>Methods: </strong>The IC50 of vitexin against Caco-2 cells was determined. Cell viability and necrosis rates were assessed after 48 hours of incubation with vitexin at concentrations of 19.01, 38.01, and 76.02 μg/mL. Additionally, levels of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), P53, Bax, TSC2, Sestrin 2, and PUMA, as well as the expression of AMPK, PI3K, Akt, and mTOR genes and proteins, were measured using q-PCR and Western blotting techniques in Caco-2 cells post-incubation.</p><p><strong>Results: </strong>Vitexin exhibited an IC50 of 38.01 ± 0.64 μg/mL against Caco-2 cells. Treatment with vitexin at the specified concentrations for 48 hours resulted in a significant decrease in cell viability by 28.40%, with inhibitory rates reaching 71.6%. Apoptosis rates increased to 93.81%, 171.41%, and 294.12%, respectively, with a corresponding rise in necrosis rates by 194.19%, 400.22%, and 811.44%. Pharmacological analysis revealed that vitexin significantly inhibited SOD and CAT activities while enhancing MDA production. Furthermore, vitexin treatment upregulated the expression of key apoptotic markers (P53, Bax, TSC2, Sestrin 2, and PUMA) and the expression of AMPK, PI3K, and Akt, while downregulating mTOR genes and proteins, implicating various signaling pathways.</p><p><strong>Conclusion: </strong>This study demonstrates that vitexin induces apoptosis in Caco-2 colon cancer cells through multiple mechanisms, including modulation of antioxidant enzymes, upregulation of pro-apoptotic factors, and regulation of key signaling pathways involved in cell survival and proliferation. These findings suggest that vitexin's mechanisms of action involve complex interactions with various cellular pathways, making it a promising candidate for further research and potential therapeutic applications in colorectal cancer.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143702610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioinformatics Analysis of Key Genes Associated with Resistance to the Combination of Bevacizumab and Pemetrexed Chemotherapy in Non-small Cell Lung Cancer.","authors":"Chenling Hu, Shenjie Xu, Siwen Chen, Qian Sun, Xudong Pan","doi":"10.2174/0115748928376905250210055408","DOIUrl":"https://doi.org/10.2174/0115748928376905250210055408","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to identify key genes linked to resistance to a combination treatment regimen of bevacizumab and pemetrexed in non-small cell lung cancer (NSCLC) through bioinformatics analysis and analysis of their associated pathways.</p><p><strong>Methods: </strong>Expression data from the Gene Expression Omnibus (GEO) database (GSE154286) were analyzed. The differentially expressed genes (DEGs) between tissues sensitive and resistant to combined bevacizumab and pemetrexed treatment in NSCLC were identified. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment was investigated, and protein-protein interaction (PPI) networks, as well as transcription factor (TFs)- DEGs-miRNA networks, were created using the STRING tool. Key genes were identified with the help of the MCODE plugin. Additionally, gene set enrichment analysis (GSEA) was utilized to identify pathways linked to the key genes. A retrospective analysis was conducted on clinical data from 80 NSCLC patients. Patients were categorized into drug-resistant and non-resistant groups based on RECIST1.1 criteria. The expression of the key gene TNFSF4 was analyzed using quantitative real-time PCR (qRT-PCR).</p><p><strong>Results: </strong>In the GSE154286 dataset, 35 downregulated DEGs were discovered. KEGG pathway enrichment analysis revealed that these DEGs were primarily associated with immunity and inflammation-related pathways. The PPI network construction highlighted a significant module and led to the identification of 8 candidate genes: TNFRSF18, TNFSF4, LGALS9, FAS, LAG3, CD86, CD80, and FOXP3. The TFs-DEGs-miRNA network analysis pinpointed TNFSF4 as a key gene, potentially regulated by 7 transcription factors and interacting with 9 miRNAs. GSEA analysis suggested that TNFSF4 may influence NSCLC's pathological processes through involvement in pathways involved in chemokine, JAK/STAT, NOD-like receptor, T cell receptor, toll-like receptor, and PPAR signaling. qRT-PCR detection displayed significantly lower expression of TNFSF4 in the peripheral blood of the patients in the resistant group relative to the non-resistant group (p < 0.0001). Logistic regression analysis showed that low TNFSF4 levels were independently linked to a raised risk of resistance to bevacizumab combined with pemetrexed therapy in lung adenocarcinoma patients.</p><p><strong>Conclusion: </strong>The identification of key genes, such as TNFSF4, and resistance-related signaling pathways through bioinformatics analysis offers valuable insights into potential mechanisms of chemotherapy resistance in NSCLC when treated with the combination of bevacizumab and pemetrexed. These findings provide a theoretical foundation for advancing clinical research on diagnosis and treatment.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The ER Stress-related Gene Prognostic Signature for Predicting Chemosensitivity and Prognosis in AML.","authors":"Jie Guo, Hongwei Peng, Luyao Long, Li Sun, Lin Yang, Simei Ren","doi":"10.2174/0115748928349165250202172440","DOIUrl":"https://doi.org/10.2174/0115748928349165250202172440","url":null,"abstract":"<p><strong>Introduction: </strong>Acute myeloid leukemia is characterized by high heterogeneity, and the current European Leukemia Net (ELN) risk stratification system is not universally applicable to all AML patients, requiring approximately three weeks for testing.</p><p><strong>Aim: </strong>This study aimed to develop an applicable prognostic tool capable of addressing the limitations of current methods. We selected AML patients from the clinic and TCGA database to explore the role of ER stress in response to chemotherapy.</p><p><strong>Methods: </strong>Patients from the TCGA database were employed as the training cohort, and two GEO datasets were used as external validation cohorts. Univariate/multivariate COX and LASSO regression were exemplified to establish the prognostic model. Kaplan-Meier and timedependent ROC were used to assess and compare the efficiency of the model with ELN stratification and other models. In the training cohort, we selected 5 ER stress-related genes to predict chemosensitivity and establish the ERS-5 prognostic model.</p><p><strong>Results: </strong>The model successfully predicted the overall survival of patients (p < 0.0001, HR = 4.86 (2.79-8.44); AUC = 0.83). It was verified in validation cohorts and could further stratify the risk of various AML subgroups. It also enhanced the ability of ELN to predict the response of patients with AML to main chemotherapeutic drugs. Finally, an \"ERS-5\" risk score was constructed by the nomogram based on the ERS-5 model and age.</p><p><strong>Conclusion: </strong>Consequently, in this study, the ERS-5 model was constructed, which allowed more rapid (about 3 hours) and accurate risk stratification and complemented the ability of ELN to assess chemosensitivity.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143416404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Prognostic Role of Interferon Gamma-inducible Protein 30 in Clear Cell Renal Cell Carcinoma with Immune Infiltrates.","authors":"Wu Xu, Taihong Wu, Yufeng Liu, Yang Luo, Dawei Liu, Lingfei Yan, Qing Li, Tao Wang","doi":"10.2174/0115748928367598250124123411","DOIUrl":"https://doi.org/10.2174/0115748928367598250124123411","url":null,"abstract":"<p><strong>Background: </strong>Recent research has demonstrated the significance of Interferon Gamma- Inducible Protein 30 (IFI30), an interferon gamma-induced protein, in the immune response to cancerous growths. However, the relationship between IFI30 expression levels, patient prognosis, and tumor-infiltrating lymphocytes in clear cell renal cell carcinoma (ccRCC) remains inadequately defined.</p><p><strong>Methods: </strong>To ascertain the potential link between IFI30 expression, clinical data, and overall survival (OS) in ccRCC patients, we employed diverse databases, which include TCGA, Gene Expression Profiling Interaction Analysis (GEPIA), and UALCAN. Furthermore, an in-depth analysis of the link between tumor-infiltrating immune cells (TIIC) and IFI30 was carried out using the TIMER, GEPIA, and TISIDB databases. Immunohistochemistry (IHC) was utilized to identify the IFI30 and PD-1 expression levels in a tissue microarray. Patents about molecular classification and drugs in ccRCC were reviewed through Worldwide Espacenet®.</p><p><strong>Results: </strong>The expression of IFI30 demonstrated a strong association with sample type, lymph node stage, tumor grade, and cancer stage. Elevated IFI30 expression was linked to unfavorable Disease- Specific Survival (DSS) and Overall Survival (OS) outcomes (p <0.01). Furthermore, overexpression of IFI30 was strongly linked to immunomodulatory molecules, chemokines, and increased infiltration of regulatory T cells (Tregs), natural killer (NK) CD56 cells, T helper 1 (Th1) cells, cytotoxic T cells, and T helper cells. IHC analysis confirmed a robust correlation between IFI30 and PD-1 expression.</p><p><strong>Conclusion: </strong>IFI30 is a prognostic biomarker for ccRCC patients. Targeting IFI30 may provide new strategies for cancer therapy and improve the prognosis of ccRCC patients.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143401122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Present State and Potential Applications of Artificial Intelligence in Cancer Diagnosis and Treatment.","authors":"Anuja Mishra, Srishti Sharma, Swaroop Kumar Pandey","doi":"10.2174/0115748928361472250123105507","DOIUrl":"https://doi.org/10.2174/0115748928361472250123105507","url":null,"abstract":"<p><p>An aberrant increase in cancer incidences has demanded extreme attention globally despite advancements in diagnostic and management strategies. The high mortality rate is concerning, and tumour heterogeneity at the genetic, phenotypic, and pathological levels exacerbates the problem. In this context, lack of early diagnostic techniques and therapeutic resistance to drugs, sole awareness among the public, coupled with the unavailability of these modern technologies in developing and low-income countries, negatively impact cancer management. One of the prime necessities of the world today is the enhancement of early detection of cancers. Several independent studies have shown that screening individuals for cancer can improve patient survival but are bogged down by risk classification and major problems in patient selection. Artificial intelligence (AI) has significantly advanced the field of oncology, addressing various medical challenges, particularly in cancer management. Leveraging extensive medical datasets and innovative computational technologies, AI, especially through deep learning (DL), has found applications across multiple facets of oncology research. These applications range from early cancer detection, diagnosis, classification, and grading, molecular characterization of tumours, prediction of patient outcomes and treatment responses, personalized treatment, and novel anti-cancer drug discovery. Over the past decade, AI/ML has emerged as a valuable tool in cancer prognosis, risk assessment, and treatment selection for cancer patients. Several patents have been and are being filed and granted. Some of those inventions were explored and are being explored in clinical settings as well. In this review, we will discuss the current status, recent advancements, clinical trials, challenges, and opportunities associated with AI/ML applications in cancer detection and management. We are optimistic about the potential of AI/ML in improving outcomes for cancer and the need for further research and development in this field.</p>","PeriodicalId":94186,"journal":{"name":"Recent patents on anti-cancer drug discovery","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143124249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}