Seminars in oncology最新文献

{"title":"Mapping the epidemiology of cancer-related anemia: A systematic scoping review of global prevalence and incidence","authors":"Dana Elkhalifa BSc, MSc ,&nbsp;Marjolijn N Lub-de Hooge PharmD, PhD ,&nbsp;Frank GA Jansman PharmD, PhD","doi":"10.1016/j.seminoncol.2025.152426","DOIUrl":"10.1016/j.seminoncol.2025.152426","url":null,"abstract":"<div><div>Cancer-related anemia (CRA) is a common and debilitating condition among oncology patients, driven by tumor burden, treatment toxicity, nutritional deficiencies, and systemic inflammation. This review aims to synthesize evidence on the global and geographical prevalence and incidence patterns of CRA. A systematic search of PubMed and Embase identified English-language studies on CRA published was performed between 2000 and November 30, 2024. Observational studies and clinical trials reporting CRA prevalence and/or incidence were included. Extracted data covered country, study design, patient demographics, cancer type, anemia classification, and CRA incidence/prevalence rates. The data were then charted by geographical locations. A total of 42 studies, encompassing 65,179 cancer patients across 5 continents and 40 countries, were included. CRA prevalence ranged from 12.8% to 100%, with the highest rates reported in lung (84.2%), pediatric cancers (80.9%), gynecological (62.99%), and gastrointestinal (57.4%) cancers. The composite prevalence of anemia across multiple cancer types and solid tumors was 64.99% and 25.68%, respectively. However, cancer-type-specific analyses often reported higher prevalence rates than composite outcomes, with variations largely influenced by geographical location. Chemotherapy and radiotherapy were consistently associated with increased incidence, with post-treatment anemia prevalence reaching 100% in some cohorts. Regional disparities were noted, particularly in Africa, South America, and the Middle East and North Africa (MENA) region. CRA is a globally prevalent condition, with rates influenced by cancer type, geographic region, and the initiation of chemotherapy or radiotherapy. Future research should prioritize standardized reporting and address regional data gaps.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 6","pages":"Article 152426"},"PeriodicalIF":2.5,"publicationDate":"2025-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145233537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering autophagy signaling in cancer: A paradigm shift from molecular classifications to clinical innovations.","authors":"Farag M A Altalbawy, Ehab Yassen Theab, Gaurav Sanghvi, R Roopashree, Aditya Kashyap, Hussein Riyadh Abdul Kareem Al-Hetty, S Gayathri, Rajashree Panigrahi, Yasser Fakri Mustafa, Hatif Abdulrazaq Yasin","doi":"10.1016/j.seminoncol.2025.152397","DOIUrl":"10.1016/j.seminoncol.2025.152397","url":null,"abstract":"<p><p>The intracellular breakdown process known as autophagy occurs when cells experience adverse conditions, such as organelle damage, the presence of abnormal proteins, hypoxia stress, low energy levels, or nutritional deprivation. The autophagic process begins by forming autophagosomes, which then merge with lysosomes to recycle degraded materials. Autophagy functions in multiple ways to affect cancer development and treatment outcomes. Tumor cells with low autophagy levels may exhibit anti-tumor effects during cancer initiation because their connection to malignant transformation is possible. The promotion of autophagy appears beneficial for cancer prevention in this context. The survival of cancer cells through increased autophagy enables tumor growth in existing tumors by allowing them to overcome metabolic and treatment-related challenges. Research indicates that blocking autophagy through the use of drugs or genetic methods makes cancer cells more susceptible to chemotherapy, radiation, and targeted therapies, suggesting that inhibiting the autophagic system may be a promising approach to enhance treatment. Excessive autophagy activation could be a therapeutic approach to manage cancer cells that resist cell death. The successful treatment of cancer requires an understanding of autophagy's dual nature. This review examines potential therapeutic strategies for tumors by analyzing autophagy-related signaling pathways and the essential factors that influence cancer development.</p>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 5","pages":"152397"},"PeriodicalIF":2.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Epidemiology and prevention of gastric cancer: A comprehensive review\" [Seminars in Oncology Volume 52 (2025) 152341].","authors":"Smruti Priyambada Pradhan, Ayushman Gadnayak, Sukanta Kumar Pradhan, Venkatarao Epari","doi":"10.1016/j.seminoncol.2025.152424","DOIUrl":"https://doi.org/10.1016/j.seminoncol.2025.152424","url":null,"abstract":"","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":" ","pages":"152424"},"PeriodicalIF":2.5,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145207486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ubiquitin-specific proteases in pancreatic cancer: Molecular regulators of tumor progression and therapy resistance","authors":"Jitendra Gupta ,&nbsp;Furqan N. Al-Khateeb ,&nbsp;Ahmad Zwenal ,&nbsp;Ali G. Alkhathami ,&nbsp;Malathi H ,&nbsp;Mayank Kundlas ,&nbsp;Laxmidhar Maharana ,&nbsp;Ashish Singh Chauhan ,&nbsp;Yasser Fakri Mustafa ,&nbsp;Mohammed Jawad Alnajar","doi":"10.1016/j.seminoncol.2025.152410","DOIUrl":"10.1016/j.seminoncol.2025.152410","url":null,"abstract":"<div><div>Pancreatic cancer is caused by a complicated set of molecular changes that include genetic mutations and aberrant signaling pathways, which result in tumor growth, metastatic spread, and resistance to therapeutics. Of the various molecular changes, standard modifying processes, such as ubiquitination and deubiquitination, influence protein levels, cellular localization, and protein function. In this context, ubiquitin-specific proteases (USPs), a primary class of deubiquitinases (DUBs), play a crucial role in regulating the ubiquitin-proteasome system, which controls protein degradation and activity in cells. These USPs can cause the removal of ubiquitin from target proteins, thereby reversing the ubiquitination process. They are key for maintaining cellular homeostasis by regulating the turnover of proteins, including those responsible for signal transduction, cellular processes (such as the cell cycle), and the response to stress events. At the same time, USPs (including USP21, USP13, USP51, and USP22) also affect multiple signaling pathways, including the Wnt, NF-κB, and TGF-β pathways, all of which are involved in the biology of pancreatic cancer. USPs will promote or inhibit cancer-associated pathways that drive proliferation, metastasis, immune evasion, and therapy resistance by stabilizing or destabilizing specific signaling molecules. This review will examine the mechanistic roles of USPs in pancreatic cancer, as well as the tumor behavior and therapeutic resistance that may result from the dysregulation of these proteins. Ultimately, by presenting an opportunity to develop targeted therapies against specific USPs, we hope to emphasize new therapeutic strategies that could positively impact the lives of patients suffering from this aggressive disease.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 6","pages":"Article 152410"},"PeriodicalIF":2.5,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145081472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolism at the core of melanoma: From bioenergetics to immune escape and beyond","authors":"Chou-Yi Hsu ,&nbsp;Yasmeen Kateb Ahmed ,&nbsp;Shaker mohammed ,&nbsp;Mohammad A. Alghamdi ,&nbsp;Hasan S. AL-Ghamdi ,&nbsp;Jaafaru Sani Mohammed ,&nbsp;Mohammed Abed Jawad ,&nbsp;Salim B. Alsaadi","doi":"10.1016/j.seminoncol.2025.152413","DOIUrl":"10.1016/j.seminoncol.2025.152413","url":null,"abstract":"<div><div>Melanoma is a particularly aggressive type of skin cancer due to its rapid growth and capacity to metastasize. There is substantial metabolic reprogramming in melanoma that is linked to its malignant characteristics, including therapeutic resistance. This review intended to provide a detailed overview of the central metabolic pathways reprogrammed in melanoma, including the Warburg effect and the complex interactions between glycolysis and oxidative phosphorylation, which ultimately influence energy production, biosynthesis, and adaptation to the tumor microenvironment. We also discuss the molecular pathways that regulate these metabolic pathways and the effect these metabolic processes have on crucial elements of melanoma progression, including invasion, metastasis, and survival during nutrient deprivation and hypoxia. Furthermore, we discuss the importance of metabolism beyond glucose, including glutamine metabolism, changes in lipid metabolism, and alterations in one-carbon and nucleotide biosynthesis, as well as mechanisms critical for the proliferation and survival of melanoma cells. An emphasis is placed on the active metabolic crosstalk between melanoma cells and the immune system within the tumor microenvironment, where melanoma cells utilize nutrient competition and the production of immunosuppressive metabolites to alter and block the function of anti-tumor immune cells, thereby facilitating immune evasion and therapy resistance. Lastly, we critically assess developments targeting melanoma metabolism, including pharmacological inhibition of key metabolic enzymes and pathways, as well as metabolic modulation to enhance the efficacy of conventional and immunotherapies. Although promising, this area is complex and subject to contextual effects and metabolic heterogeneity, indicating that we still have a way to go in annotating robust and clinically relevant metabolic targets. We sought to consolidate current knowledge about melanoma metabolism and highlight the challenges, future directions, and complexity of a potential therapeutic vulnerability in the rapidly evolving field of cancer research.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 6","pages":"Article 152413"},"PeriodicalIF":2.5,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145046405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of single-layer continuous duct-to-mucosa pancreaticojejunostomy in oncologic pancreaticoduodenectomy","authors":"Qun Chen ,&nbsp;Fengyuan Liu ,&nbsp;Lingtao Yan ,&nbsp;Xumin Huang ,&nbsp;Jishu Wei ,&nbsp;Feng Guo ,&nbsp;Jianmin Chen ,&nbsp;Zipeng Lu ,&nbsp;Junli Wu ,&nbsp;Jie Yin ,&nbsp;Pengfei Wu ,&nbsp;Kuirong Jiang","doi":"10.1016/j.seminoncol.2025.152415","DOIUrl":"10.1016/j.seminoncol.2025.152415","url":null,"abstract":"<div><div>Pancreaticojejunostomy is a critical step in pancreaticoduodenectomy, and its failure often results in pancreatic fistula. Clinically relevant pancreatic fistula (CRPF) can cause severe complications. This study evaluates the safety and feasibility of single-layer continuous duct-to-mucosa (SCD) pancreaticojejunostomy in preventing CRPF. We prospectively collected baseline characteristics and perioperative data from patients who underwent SCD pancreaticojejunostomy at our center between January and December 2020. A total of 156 patients were included in this study. The mean pancreaticojejunostomy time was 6.5 min, and the mean operation time was 247.6 min. CRPF occurred in 31 patients (19.9%), severe complications (Clavien-Dindo classification ≥III) occurred in 27 patients (17.3%), the mean length of hospitalization was 17.2 days, and the 90-days mortality was 0.0%. SCD pancreaticojejunostomy is an efficient and straightforward technique. It is applicable to various pancreatic conditions and demonstrates favorable clinical outcomes.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 6","pages":"Article 152415"},"PeriodicalIF":2.5,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145046406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor tough, therapy smarter: Rethinking CAR-T for pancreatic cancer","authors":"Daniel A. Guirguis ,&nbsp;Fariha Hasan ,&nbsp;Natalie Morris ,&nbsp;Andrew Alabd ,&nbsp;Paula Mortada Shehata Tawfik ,&nbsp;Kartick Pramanik ,&nbsp;Manoj K Pandey","doi":"10.1016/j.seminoncol.2025.152411","DOIUrl":"10.1016/j.seminoncol.2025.152411","url":null,"abstract":"<div><div>Chimeric antigen receptor (CAR) T-cell therapy has changed how we treat blood cancers but hasn't worked as well for solid tumors like pancreatic ductal adenocarcinoma (PDAC), mainly because these tumors are very aggressive and resistant to regular treatments. This review critically examines peer-reviewed studies to chart the evolution of immunotherapy in PDAC, emphasizing the unique barriers to effective CAR T-cell treatment and emerging strategies to overcome them. CAR T-cells that focus on tumor-related markers like mesothelin, HER2, and MUC1 have shown promise in early research models. However, clinical translation is hampered by obstacles such as a dense desmoplastic stroma that restricts T-cell infiltration, antigenic heterogeneity that promotes immune escape, and adverse effects including cytokine release syndrome. Recent innovations include dual-antigen targeting CARs (eg, CEA/MSLN), metabolic reprogramming to enhance T-cell function in nutrient-deprived tumor microenvironments, and stromal-targeting approaches such as fibroblast activation protein (FAP)-specific CARs and heparanase overexpression. Safety enhancements - such as reversible CAR inhibition using Dasatinib and GM-CSF neutralization - are also being explored to mitigate toxicity. Collectively, these advances represent promising strides toward enhancing the efficacy and safety of CAR T-cell therapy for pancreatic cancer. Ongoing research continues to identify new strategies to further refine these therapies, including the exploration of combination treatments with checkpoint inhibitors and novel immunomodulatory agents. As our understanding of the tumor microenvironment deepens, the potential for personalized approaches to CAR T-cell therapy may unlock even greater therapeutic benefits for patients.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 6","pages":"Article 152411"},"PeriodicalIF":2.5,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144997589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-differential responses to immune checkpoint inhibitors across the disease continuum unified by tumor mutational burden","authors":"Ming Zheng MD, PhD","doi":"10.1016/j.seminoncol.2025.152414","DOIUrl":"10.1016/j.seminoncol.2025.152414","url":null,"abstract":"<div><div>While the efficacy of immune checkpoint inhibitors (ICIs) in advanced non–small-cell lung cancer (NSCLC) is well-established, sex-based differences in treatment responses remain insufficiently explored. This study examines how sex disparities impact ICI treatment outcomes in advanced-stage NSCLC, focusing on the role of tumor mutational burden (TMB) in these differences. This study analyzed data from 174 advanced-stage, chemotherapy-naïve, NSCLC patients treated with ICIs, including PD-1/PD-L1 and CTLA-4 inhibitors, to assess sex differences in treatment response and survival outcomes. Male patients with low TMB (&lt;10 mut/Mb) had worse treatment responses compared to female patients. In contrast, no sex differences were observed in patients with high TMB, where both sexes exhibited similar therapeutic responses. These results suggest that high TMB may reduce the impact of sex on ICI efficacy, with male and female patients showing comparable outcomes. Furthermore, sex disparities in disease progression and overall survival were more evident in low-TMB patients, emphasizing the role of TMB in modulating sex-related differences in immunotherapy outcomes. This study highlights the importance of incorporating both sex and TMB into precision oncology. High TMB appears to equalize treatment responses between sexes, while low TMB may necessitate more personalized treatment strategies, particularly for male patients. Further research into the biological mechanisms underlying these differences is essential to optimize ICI therapies and enhance patient outcomes. Integrating both sex and TMB into clinical decision-making will help to develop more tailored and effective cancer immunotherapy.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 6","pages":"Article 152414"},"PeriodicalIF":2.5,"publicationDate":"2025-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144933863","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Purine metabolism in tumorigenesis and its clinical implications","authors":"Zerui Lu ,&nbsp;Jiayi Li ,&nbsp;Ying Liu ,&nbsp;Hui Li ,&nbsp;Ying Sun ,&nbsp;Rui Geng ,&nbsp;Jiahang Song ,&nbsp;Jinhui Liu","doi":"10.1016/j.seminoncol.2025.152409","DOIUrl":"10.1016/j.seminoncol.2025.152409","url":null,"abstract":"<div><div>Metabolic reprogramming constitutes a hallmark of malignant neoplasms. Purine metabolism emerges as a pivotal regulator in cellular metabolic networks through multiple mechanisms, including dysregulation of de novo biosynthesis/salvage pathway coordination, adenosine-mediated immunosuppressive microenvironment formation, and collective contributions to tumorigenesis and malignant progression. During metastatic progression, purine metabolism reinforces tumor cell plasticity through mitochondrial energy regulation and modulation of cell cycle checkpoints (eg, G1/S transition). These mechanistic revelations have positioned purine metabolism-targeting strategies as promising oncotherapeutic candidates. This review methodically analyzes (1) purine metabolic pathways and their regulatory dynamics, (2) adenosine-mediated pathophysiological interactions, and (3) the synergistic impacts of these pathways in malignant transformation. We propose a unified mechanistic framework that clarifies oncogenic purine metabolic rewiring while evaluating translational potential through three clinical dimensions: pathogenesis elucidation, diagnostic biomarker discovery, and targeted therapeutic development. This comprehensive synthesis aims to advance precision oncology through mechanistic insights and therapeutic innovation.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 6","pages":"Article 152409"},"PeriodicalIF":2.5,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144926758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling the role of RAI14 in cancer: Biological significance and translational perspectives","authors":"Zhi-Xiong Chong","doi":"10.1016/j.seminoncol.2025.152412","DOIUrl":"10.1016/j.seminoncol.2025.152412","url":null,"abstract":"<div><div>Retinoic acid-induced protein 14 (RAI14) is an actin-binding protein that regulates actin dynamics, cell adhesion, and migration. RAI14 dysregulation has been reported to facilitate the development of at least 10 tumor types based on the findings from over 20 original research articles. This review article aims to fill in the gap in the literature by providing a comprehensive summary of the putative tumor-regulatory roles of RAI14 in different cancers. Overall, RAI14 can affect protein kinase B (AKT), mammalian target of rapamycin, yes-associated protein/Hippo, apoptosis, and epithelial-to-mesenchymal transition activities to promote tumorigenesis. Several noncoding RNAs like miR-23b-3p and AFAP1-AS1 can directly or indirectly affect RAI14 expression to control its tumor-modulatory function epigenetically. Additionally, RAI14 tissue or serum level are overexpressed in at least seven human tumors, including breast, gastrointestinal, genitourinary, and brain cancers. This gives RAI14 the translational potential as a diagnostic or prognostic biomarker. Targeting RAI14 as a cancer antigen can also potentially help halt tumor progression. Future large-scale trials are needed to confirm the tumor-regulatory role of RAI14 in human cancer and to evaluate the sensitivity, reliability, and accuracy of using this target as a biomarker or therapeutic target.</div></div>","PeriodicalId":21750,"journal":{"name":"Seminars in oncology","volume":"52 6","pages":"Article 152412"},"PeriodicalIF":2.5,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144926759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}