American journal of cancer research最新文献

{"title":"Mechanism and intervention strategy of thymus atrophy in cancer immunotherapy.","authors":"Haohang Zhang, Fujie Zhang, Tiantian Li, Sheng Xu, Likun Cui","doi":"10.62347/FDZV7570","DOIUrl":"10.62347/FDZV7570","url":null,"abstract":"<p><p>Thymic atrophy is a major determinant of T-cell dysfunction and immunosenescence, as it restricts de novo T-cell generation, reduces the T-cell receptor (TCR) repertoire, hastens peripheral T-cell aging, and disrupts central immune tolerance. It presents an enormous barrier to antitumor immune surveillance as well as current cancer immunotherapies such as immune checkpoint inhibitors (ICIs) and chimeric antigen receptor T-cell (CAR-T) therapy. In this review, we discuss how age, metabolic disorders, psychological stress, cancer pathology, and cancer-directed therapies converge upon thymic epithelial cells, stromal organization, and hematopoietic progenitor trafficking leading to structural and functional thymic decline. We then describe how thymopoiesis impairment reshapes tumor immunity and therapeutic responsiveness, and summarize noninvasive imaging methods for assessment of thymic health, and highlight new strategies for thymic regeneration or functional replacement through pharmacologic agents, cytokine and endocrine modulation, mRNA-based trophic factor delivery, cell replacement, tissue engineering, and thymus-centered CAR-T platforms. Despite significant translational challenges, rapid advances in thymic regeneration biology suggest that restoration of thymic function may be a rational host-directed approach to enhance the depth, duration, and safety of cancer immunotherapy.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3710-3742"},"PeriodicalIF":3.1,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559303/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928632","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: DOT1L promotes cell proliferation and invasion by epigenetically regulating STAT5B in renal cell carcinoma.","authors":"Yanguang Hou, Shiyu Huang, Jiachen Liu, Lei Wang, Yan Yuan, Hao Liu, Xiaodong Weng, Zhiyuan Chen, Juncheng Hu, Xiuheng Liu","doi":"10.62347/AIYL3323","DOIUrl":"https://doi.org/10.62347/AIYL3323","url":null,"abstract":"<p><p>[This corrects the article on p. 276 in vol. 13, PMID: 36777512.].</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3746-3747"},"PeriodicalIF":3.1,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: CKAP2 promotes cervical cancer progression by modulating the tumor microenvironment via NF-κB signaling.","authors":"Luopei Guo, Chunbo Li, Jingjing Guo, Junjun Qiu, Keqin Hua","doi":"10.62347/RXFR3012","DOIUrl":"https://doi.org/10.62347/RXFR3012","url":null,"abstract":"<p><p>[This corrects the article on p. 2376 in vol. 13, PMID: 37424820.].</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3750-3752"},"PeriodicalIF":3.1,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Disulfiram combined with chemoimmunotherapy potentiates pancreatic cancer treatment efficacy through the activation of cGAS-STING signaling pathway via suppressing PARP1 expression.","authors":"Shenan Huang, Peiyi Xie, Xiaomei Huang, Zhimeng Chen, Jinhuan Yang, Jian Wang, Cong Liu, Hui Li, Binghai Zhou","doi":"10.62347/FSIN8036","DOIUrl":"https://doi.org/10.62347/FSIN8036","url":null,"abstract":"<p><p>[This corrects the article on p. 2055 in vol. 13, PMID: 37293156.].</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3748-3749"},"PeriodicalIF":3.1,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: <i>In vitro</i> and <i>in vivo</i> antiangiogenic activity of desacetylvinblastine monohydrazide through inhibition of VEGFR2 and Axl pathways.","authors":"Xueping Lei, Minfeng Chen, Qiulin Nie, Jianyang Hu, Zhenjian Zhuo, Anita Yiu, Heru Chen, Nanhui Xu, Maohua Huang, Kaihe Ye, Liangliang Bai, Wencai Ye, Dongmei Zhang","doi":"10.62347/LOLL8628","DOIUrl":"https://doi.org/10.62347/LOLL8628","url":null,"abstract":"<p><p>[This corrects the article on p. 843 in vol. 6, PMID: 27186435.].</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3743-3745"},"PeriodicalIF":3.1,"publicationDate":"2026-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559354/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathological role of deubiquitinating enzymes in lung cancer: recent insights and advances.","authors":"Qin Huang, Zhen Zhang, Ya-Ning Wang, Miao-Miao Li, Xin-Hao Han, Xiao-Jian Han, Qiu-Gen Li","doi":"10.62347/SYUJ9605","DOIUrl":"10.62347/SYUJ9605","url":null,"abstract":"<p><p>Lung cancer remains the leading cause of cancer-related death worldwide. Following extensive investigations into the mechanisms of lung cancer and targeted therapy, clinical treatment options are now more abundant than ever. However, the overall rates of treatment success and long-term survival remain low among patients with lung cancer, and the prognosis is even poorer for patients with metastatic disease. In this context, a more comprehensive review of the targeted regulatory mechanisms involved in the occurrence and progression of lung cancer could expand the population of patients benefiting from existing clinical treatments and ultimately improve the prognosis of this malignancy. Deubiquitinating enzymes (DUBs) are a specialized class of cellular proteases. These enzymes cleave ubiquitin moieties from substrate proteins or ubiquitin chains, thereby modulating ubiquitination dynamics. Through this catalytic process, DUBs maintain the dynamic balance of ubiquitination within cells. In recent years, accumulating evidence has demonstrated that DUBs serve diverse regulatory functions in multiple molecular events associated with tumorigenesis and malignant progression. Rather than acting through a single mechanism, DUBs participate in tumor progression through multifaceted pathways. In this comprehensive review, we systematically summarize the recent advances in our understanding of the biological functions of DUBs during the pathogenesis and progression of lung cancer. We highlight the mechanistic roles of various DUBs in tumor initiation, development, and metastasis. The topics covered include the regulation of cancer-associated signaling pathways by DUBs, their role in metabolic reprogramming, the DUB-induced modulation of tumor immune responses, the control of cell cycle progression and proliferation by DUBs, as well as other fundamental cellular processes modulated by these enzymes. In addition, we clarify the pathological mechanisms linking DUBs with lung cancer, including upstream regulators and the corresponding downstream molecular signals. Furthermore, we assess the therapeutic potential of these DUBs as candidate therapeutic targets and mediators of drug resistance. This synthesis of the literature provides a strategic framework for identifying clinically relevant DUB targets in lung cancer.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3254-3293"},"PeriodicalIF":3.1,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of differential miRNAs in serum exosomes and development of an integrated diagnostic model for early gastric cancer.","authors":"Jianming Wei, Puyu Luo, Wen Yao, Dawei Di, Junfu Wang","doi":"10.62347/AOPT3512","DOIUrl":"10.62347/AOPT3512","url":null,"abstract":"<p><p>Early detection of gastric cancer (GC) improves patient outcomes. However, conventional serum biomarkers show limited sensitivity in early disease stages. Circulating microRNAs (miRNAs) are remarkably stable in body fluids. These molecules have emerged as promising noninvasive biomarkers. In this study, we isolated serum-derived exosomes from healthy controls and GC patients. Transmission electron microscopy, nanoparticle tracking analysis, and Western blotting confirmed exosomal characteristics. Small RNA sequencing then established miRNA expression profiles to identify progression-associated molecules. We conducted bioinformatics analyses to explore their biological roles and validated candidate miRNAs using quantitative real-time PCR. Notably, miR-17-3p levels declined progressively during disease development. This expression level correlated significantly with tumor differentiation (P = 0.0324), TNM stage (P = 0.0100), and neural invasion (P = 0.0100). Combining miR-17-3p with conventional markers increased the area under the curve (AUC) from 0.7847 to 0.8472 for staging. These findings demonstrate that serum exosomal miR-17-3p is a promising biomarker for GC diagnosis and evaluation.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3359-3376"},"PeriodicalIF":3.1,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic reprogramming in diabetes and cancer: the role of PI3K/AKT/mTOR and beyond.","authors":"Nahed S Alharthi","doi":"10.62347/OGYT1108","DOIUrl":"10.62347/OGYT1108","url":null,"abstract":"<p><p>Diabetes mellitus and cancer are among the most prevalent chronic diseases worldwide, and accumulating evidence suggests a significant association between these conditions. The metabolic disturbances characteristic of diabetes, including hyperglycemia, hyperinsulinemia, insulin resistance, and chronic inflammation, create a favorable environment for tumor initiation and progression. These alterations contribute to cellular metabolic reprogramming, enhanced proliferative signaling, and resistance to apoptosis. Key molecular pathways such as PI3K/AKT/mTOR, along with dysregulated glucose, lipid, and amino acid metabolism, play central roles in linking diabetic and oncogenic processes. In addition to metabolic alterations, genetic and epigenetic modifications, including mutations in oncogenes and tumor suppressor genes, as well as the involvement of non-coding RNAs, further strengthen this association. Emerging evidence also highlights the gut microbiome's role in modulating inflammation, metabolic homeostasis, and cancer susceptibility in diabetic conditions. Therapeutically, antidiabetic agents such as metformin, GLP-1 receptor agonists, and SGLT2 inhibitors have shown potential in modulating cancer-related pathways, although clinical evidence remains variable and requires further validation. This review provides a comprehensive overview of the shared metabolic and molecular mechanisms underlying the diabetes-cancer link, emphasizing the interplay between metabolic dysregulation, genetic alterations, and microbiome dynamics. A better understanding of these interconnected pathways may support the development of targeted therapeutic strategies and improve clinical outcomes. However, further well-designed studies are necessary to establish causal relationships and translate these findings into effective clinical interventions.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3294-3318"},"PeriodicalIF":3.1,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aryl hydrocarbon receptor-dependent lipid droplet accumulation supports redox homeostasis in hypoxia-induced PCa cells.","authors":"Yuan Yao, Shanshan Liang, Tianji He, Chenjun Ma, Guotong Gong, Xiang Chen, Jingsong Yu","doi":"10.62347/HYGZ1071","DOIUrl":"10.62347/HYGZ1071","url":null,"abstract":"<p><p>Tumor cells in hypoxic environments generate large amounts of reactive oxygen species (ROS), and lipid droplets (LDs) play an essential role in maintaining redox homeostasis under these harsh conditions. The aryl hydrocarbon receptor (AhR) is a member of the basic helix-loop-helix (bHLH) transcription factor superfamily that is closely associated with malignant tumor phenotypes. AhR has been shown to drive prostate cancer (PCa) cell growth, but the specific mechanistic basis for this effect remains unclear. In this study, we used a hypoxia-induced PC-3M cell model to explore the molecular pathways through which AhR promotes PCa progression. Significant LD accumulation was observed in hypoxia-induced PC-3M cells, and AhR knockdown inhibited LD formation, supporting a potential role for AhR in this process. AhR-dependent LD formation enhanced the ability of PC-3M cells to adapt to oxidative stress, as evidenced by reduced ROS production and a decreased NADP/NADPH ratio. AhR-dependent LD formation also alleviated mitochondrial dysfunction, as evidenced by increased membrane potential, reduced cell apoptosis, and decreased levels of active caspase-3. Treatment with the LD inhibitor PF-06424439 reversed these protective effects, as did DGAT2 knockdown. Mechanistically, AhR was found to activate the PI3K/AKT pathway through RAB3D, thereby promoting LD formation. Co-immunoprecipitation (Co-IP) experiments demonstrated that CYLD inhibits AhR activity by eliminating the K63-linked ubiquitination of AhR. In summary, under hypoxic conditions, these results indicate that AhR protects PCa cells from ROS-associated toxicity through the induction of LD formation.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3433-3444"},"PeriodicalIF":3.1,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HMTA, a natural alkylphenol from <i>Ardisia virens</i> Kurz, obstructs autophagic flux to exert anti-pancreatic cancer activity.","authors":"Yu-Fang Chuang, Ying-Ray Lee, Wan-Chi Tsai","doi":"10.62347/TVYX8770","DOIUrl":"10.62347/TVYX8770","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal malignancies worldwide due to its aggressive nature and limited therapeutic options. HMTA (4-hydroxy-2-methoxy-6-tridecylphenyl acetate), a natural alkylphenol derived from <i>Ardisia virens</i> Kurz, has previously demonstrated anti-tumor potential as a tubulin polymerization inhibitor. However, its impact on the autophagic machinery in pancreatic cancer remains to be elucidated. In this study, we investigated the anti-cancer effects of HMTA across four human pancreatic cancer cell lines (PANC-1, BxPC-3, MIA PaCa-2, and AsPC-1) with varying KRAS mutation statuses. HMTA significantly inhibited cell viability in a dose-dependent manner. Mechanistically, HMTA treatment led to a substantial accumulation of LC3-II and p62/SQSTM1 proteins. Notably, the expression of upstream autophagy-initiating markers, such as ATG5 and Beclin-1, remained unchanged, suggesting a defect in autophagic clearance rather than induction. Using a tandem mRFP-EGFP-LC3 fluorescence reporter assay, we found that HMTA obstructs autophagic flux by preventing the fusion of autophagosomes with lysosomes. Furthermore, the combination of HMTA with the autophagy inhibitor chloroquine resulted in enhanced cytotoxicity, whereas the early-stage inhibitor 3-MA partially rescued HMTA-induced cell death. Our findings demonstrate that HMTA exerts its anti-pancreatic cancer activity mainly through the blockade of autophagic flux, regardless of KRAS background. These results position HMTA as a promising therapeutic candidate for the treatment of PDAC.</p>","PeriodicalId":7437,"journal":{"name":"American journal of cancer research","volume":"16 8","pages":"3422-3432"},"PeriodicalIF":3.1,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13559389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148928604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}