Journal of the National Cancer Center最新文献

{"title":"Upper gastrointestinal cancers global burden profile, trends, contributors, and attributable change in life expectancy from 1990 to 2021","authors":"Yi Teng ,&nbsp;Haoyu Zhang ,&nbsp;Siyi He ,&nbsp;Mengdi Cao ,&nbsp;Qianru Li ,&nbsp;Nuopei Tan ,&nbsp;Jiachen Wang ,&nbsp;Yujie Wu ,&nbsp;Tianyi Li ,&nbsp;Yuanjie Zheng ,&nbsp;Changfa Xia ,&nbsp;Wanqing Chen","doi":"10.1016/j.jncc.2026.02.005","DOIUrl":"10.1016/j.jncc.2026.02.005","url":null,"abstract":"<div><h3>Background</h3><div>Upper gastrointestinal (GI) cancers, comprising esophageal cancer (EC) and gastric cancer (GC), remain a significant global health burden with disproportionate geographic distribution of incidence and mortality. A comprehensive assessment of global and regional patterns and trends of upper GI cancer burden is essential to inform targeted prevention strategies.</div></div><div><h3>Methods</h3><div>Data were sourced from the Global Burden of Disease (GBD) study 2021. We examined the incidence, mortality, and life expectancy (LE) impacts of upper GI cancers from 1990 to 2021 across 21 GBD world regions. Trends were assessed using age-standardized rates and average annual percentage change (AAPC). Non-modifiable demographic factors and modifiable risk-attributable burdens were analyzed. A three-step decomposition method was applied to quantify the contribution of upper GI cancer to changes in LE.</div></div><div><h3>Results</h3><div>In 2021, upper GI cancers accounted for 1.80 million new cases and 1.49 million deaths globally, with Asia contributing over 70% of the burden. Global age-standardized incidence and mortality rates for upper GI cancers declined from 1990 to 2021, with AAPC of -1.53% and -1.87%, respectively, although absolute incidence and deaths increased due to population growth and ageing, contributing to 1.13 million deaths for upper GI cancers. Population expansion and ageing drove increases in age-related deaths during the study period and were offset by reduced incidence and case fatality. Risk-attributable deaths declined for most modifiable factors, with tobacco remaining the leading risk, responsible for 21.9% of all deaths. A total of 0.24 year of LE gained was attributable to upper GI cancers from 1990 to 2021. Regionally, high-income Asia Pacific achieved the greatest gains in LE (0.67 years). GC predominantly contributed to the most gains, whereas EC mostly contributed to LE changes in Central and East Asia (0.27 years and 0.19 years, respectively).</div></div><div><h3>Conclusions</h3><div>Although the burden of upper GI cancers has declined, progress is uneven, and the absolute burden remains high in Asia. Continued region-specific prevention, risk factor control, and equitable access to early detection and treatment are essential to further reduce the disease burden and close global disparities.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 2","pages":"Pages 166-174"},"PeriodicalIF":9.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147652789","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":"Long-term outcomes and clinical features of stage III non-small-cell lung cancer harboring ALK rearrangements: a multicenter retrospective study of 176 patients","authors":"Fengwei Tan ,&nbsp;Ying Jiang ,&nbsp;Jianchun Duan ,&nbsp;Renda Li ,&nbsp;Jianzhong Cao ,&nbsp;Wei Jiang ,&nbsp;Qiang Li ,&nbsp;Guochao Zhang ,&nbsp;Jinghao Duan ,&nbsp;Yu Wang ,&nbsp;Zhijie Wang ,&nbsp;Weihua Li ,&nbsp;Jianming Ying ,&nbsp;Jie Wang ,&nbsp;Nan Bi ,&nbsp;Jie He","doi":"10.1016/j.jncc.2025.07.005","DOIUrl":"10.1016/j.jncc.2025.07.005","url":null,"abstract":"<div><h3>Background</h3><div>Stage III non-small-cell lung cancer (NSCLC) with anaplastic lymphoma kinase (<em>ALK</em>) gene rearrangements requires multimodal therapy. The ALINA trial demonstrated the efficacy of adjuvant <em>ALK</em> tyrosine kinase inhibitors (<em>ALK</em> TKIs) in early-stage <em>ALK</em>-positive NSCLC but provided limited long-term data for stage III patients. Real-world evidence is needed to validate and expand these findings.</div></div><div><h3>Methods</h3><div>This multicenter, real-world cohort study analyzed treatment patterns and clinical outcomes in 176 patients with stage III <em>ALK</em>-positive NSCLC. The prognosis of different <em>EML4-ALK</em> variants was evaluated. Inverse probability treatment weighting (IPTW) and sensitivity analyses were performed to adjust for the confounding factors.</div></div><div><h3>Results</h3><div>At a median follow-up of 48.9 months, the 5-year overall survival (OS) and progression-free survival (PFS) rates were 71.9 % and 14.8 %, respectively, with a median PFS of 19.5 months. Among all 176 patients, 144 (81.8 %) received definitive local therapy, including 132 who underwent surgery and 12 who received definitive chemoradiotherapy (CRT); the remaining 32 patients (18.2 %) received systemic therapy alone. The most common <em>EML4</em>-<em>ALK</em> variants were v1 (25.3 % of patients, <em>n</em> = 23) and v3 (38.5 % of patients, <em>n</em> = 35). <em>EML4-ALK</em> v1 variants was associated with significantly better OS compared to other variants (<em>P</em> &lt; 0.05). A total of 126 (71.6 %) patients relapsed, and 97 (55.1 %) had distant metastasis. Local treatment (HR = 0.33, 95 % CI: 0.15–0.73; <em>P</em> = 0.007) and targeted therapy (HR = 0.34, 95 % CI: 0.17–0.69; <em>P</em> = 0.003) were significant independent prognostic factors for better OS. Patients receiving local therapy and adjuvant <em>ALK</em> TKIs achieved 100 % 5-year OS without progression. The sensitivity analysis yielded similar findings.</div></div><div><h3>Conclusions</h3><div>This study provided long-term follow-up data that validated the findings of the ALINA trial. Stage III <em>ALK</em>-positive NSCLC is prone to relapse but local therapy combined with adjuvant <em>ALK</em> TKIs offers a promising strategy. Patients with <em>EML4-ALK</em> v1 mutations may show improved outcomes.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 2","pages":"Pages 159-165"},"PeriodicalIF":9.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147652790","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":"Genetic and epigenetic mechanisms underlying treatment-induced neuroendocrine prostate cancer","authors":"Viriya Keo ,&nbsp;Xiaodong Lu ,&nbsp;Jonathan C. Zhao ,&nbsp;Jindan Yu","doi":"10.1016/j.jncc.2025.11.001","DOIUrl":"10.1016/j.jncc.2025.11.001","url":null,"abstract":"<div><div>Treatment-induced neuroendocrine prostate cancer (t-NEPC) is a lethal subtype of castration-resistant prostate cancer (CRPC) characterized by unique pathological features and molecular changes, including the loss of androgen receptor (AR) activities and the gain of neuroendocrine gene expression. The incidence of t-NEPC has increased substantially in the last decade, in up to 20 % of CRPC cases, largely due to intensive treatment of advanced prostate cancer (PCa) with AR pathway inhibitors (ARPi). While genomic alterations between CRPC and t-NEPC are largely conserved, their epigenetic programs are markedly distinct. The molecular mechanisms underlying the neuroendocrine transformation (NET) of PCa are rapidly emerging. Here, we first briefly summarize the genetic drivers of t-NEPC and then comprehensively review 2D and 3D chromatin alterations, including changes in DNA methylation, histone modifications, chromatin accessibility, and 3D chromatin organization, during NET of PCa. We then review key molecular regulators, including lineage-specific transcription factors and chromatin modifiers, of such epigenetic programs. Lastly, we discuss evidence that suggests a mixed model of clonal selection and transformation that underlies NEPC progression.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 88-97"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286448","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":"Temporal dynamics in cancer immunotherapy: the interplay between circadian rhythms, tumor microenvironment, and immune checkpoint blockade","authors":"Anqi Lin ,&nbsp;Xiuhui Fang ,&nbsp;Pengpeng Zhang ,&nbsp;Nan Zhang ,&nbsp;Zaoqu Liu ,&nbsp;Quan Cheng ,&nbsp;Jian Zhang ,&nbsp;Bufu Tang ,&nbsp;Peng Luo","doi":"10.1016/j.jncc.2025.09.007","DOIUrl":"10.1016/j.jncc.2025.09.007","url":null,"abstract":"<div><div>The tumor microenvironment (TME) is a highly intricate and dynamic system composed of various cellular and non-cellular components, which plays a crucial role in regulating key biological processes such as tumor initiation, progression, and therapeutic response. Recent studies have uncovered a complex regulatory network between the circadian rhythm system and TME, which significantly impacts the clinical efficacy of immune checkpoint inhibitors (ICIs). This review systematically delineates the multi-level regulatory mechanisms by which circadian rhythms influence key components within the TME, including tumor cell biological characteristics, immune cell functional states, angiogenesis processes, and cancer-associated fibroblast activity. It deeply analyzes the systemic impact of the TME on ICI treatment efficacy via immunosuppressive networks, immune checkpoint molecule expression, T cell functional states, and drug bioavailability. The review underscores the central role and clinical significance of circadian rhythms in regulating immune checkpoint molecule expression, immune cell function, ICI drug pharmacokinetics, and TME homeostasis. Based on these research advancements, this paper systematically presents ICI treatment optimization strategies grounded in circadian rhythm dynamics and TME characteristics, encompassing time-dependent dosing regimens, combination therapies targeting the TME, circadian rhythm modulation methods, and precision personalized treatment approaches. Additionally, it offers a systematic outlook on the research frontiers and clinical translation prospects in this field, encompassing multi-omics integrated analysis of circadian regulatory networks, artificial intelligence (AI)-based precision chronomedicine strategies, novel chronotherapeutic approaches, and standardized clinical translation systems. This review establishes a crucial theoretical foundation for understanding the circadian rhythm-TME-ICI interaction network and optimizing cancer immunotherapy strategies.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 98-115"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286464","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":"Experimental approaches to the function of tumor-associated lymphatic vessels","authors":"Yubo Liang ,&nbsp;Xingming Chen ,&nbsp;Jin Li ,&nbsp;Jinxiang Zuo ,&nbsp;Jianbiao Zhang ,&nbsp;Shuangxi Li ,&nbsp;Yang Ke","doi":"10.1016/j.jncc.2025.10.002","DOIUrl":"10.1016/j.jncc.2025.10.002","url":null,"abstract":"","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 3-4"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286419","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":"Transcriptional and epigenetic reprogramming, lineage plasticity and therapy resistance in prostate cancer","authors":"Yujun Shuai ,&nbsp;Haojie Huang","doi":"10.1016/j.jncc.2025.06.001","DOIUrl":"10.1016/j.jncc.2025.06.001","url":null,"abstract":"<div><div>Prostate cancer is the most commonly diagnosed and the second-leading cause of cancer-related mortality in men worldwide, especially in Western counties. Therapeutic resistance of prostate cancer remains a major challenge in modern oncology, necessitating new scientific understanding of the disease and devising new targeting strategies. This review examines the intricate relationship between transcriptional and epigenetic reprogramming, lineage plasticity, and therapeutic resistance in prostate cancer. Prostate cancer cells can adapt and resist various treatment modalities, including androgen deprivation therapy (ADT) and next-generation androgen receptor (AR) signaling inhibitors (ARSI), through transcriptional reprogramming and epigenetic modifications. Lineage plasticity, the ability of cells to alter their cellular identities, further drives treatment resistance. Moreover, cancer cells can adjust their gene expression profiles to evade therapy by activating key transcription factors and epigenetic regulatory mechanisms such as DNA methylation, histone modification, and non-coding RNA expression. The article concludes by discussing new therapeutic strategies targeting these reprogramming and plasticity mechanisms, emphasizing the importance of combination therapy and precision medicine in developing more effective treatments for advanced prostate cancer.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 73-87"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286288","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":"Clinicopathologic, genetic and immune cell infiltration analysis of colorectal signet ring cell carcinoma with comparison to conventional adenocarcinoma","authors":"Yang An ,&nbsp;Jiaolin Zhou ,&nbsp;Lan Su ,&nbsp;Lin Cong ,&nbsp;Xinxin Mao ,&nbsp;Bo Chen ,&nbsp;Yuhua Gong ,&nbsp;Yaping Xu ,&nbsp;Han Chen ,&nbsp;Chentong Wang ,&nbsp;Guole Lin ,&nbsp;Huanwen Wu","doi":"10.1016/j.jncc.2025.06.006","DOIUrl":"10.1016/j.jncc.2025.06.006","url":null,"abstract":"<div><h3>Objective</h3><div>We sought to characterize the genomic and immune landscape of signet ring cell carcinoma (SRCC), a rare and aggressive subtype of colorectal cancer (CRC).</div></div><div><h3>Methods</h3><div>Tissue samples and clinicopathological data were retrospectively analyzed from 37 SRCC and 172 conventional adenocarcinomas (AC) of rectum and sigmoid colon. The genetic and immune profiles were assessed using DNA next-generation sequencing (NGS) and multiplex immunohistochemistry.</div></div><div><h3>Results</h3><div>Compared to AC, SRCC patients were younger, had higher tumor, node, metastasis (TNM) stages and tumor grades (all <em>P</em> &lt; 0.05), and exhibited significantly worse 3-year disease-free survival (DFS) and overall survival (OS) (both <em>P</em> &lt; 0.0001). SRCC exhibited fewer somatic mutations in well-known CRC driver genes including <em>APC</em> (32 % vs. 74 %), <em>KRAS</em> (16 % vs. 42 %), and <em>FBXW7</em> (0 vs. 20 %), but showed higher frequencies of genetic alterations in <em>SMAD4, RNF43, BCL2L11</em> (present only in SRCC), <em>MYC</em>, and <em>ARID2</em> (all <em>P</em> &lt; 0.05). SRCC showed significantly higher levels of CD8⁺ tumor-infiltrating lymphocytes (TILs), but lower PD-1⁺CD8⁺ TILs in both stroma and intratumoral regions (all <em>P</em> &lt; 0.05). Interestingly, high PD-1⁺CD8⁺ TILs in intratumoral regions significantly predicted longer DFS and OS in all SRCC and stage II-III SRCC patients (all <em>P</em> &lt; 0.05), while CD3⁺ or CD8⁺ TILs did not. Moreover, the characteristic immune cell infiltration correlated with specific genetic alterations in SRCC.</div></div><div><h3>Conclusions</h3><div>Colorectal SRCC is a clinically and molecularly distinct and highly malignant subtype compared to AC. It exhibits a “pseudo-T cell-inflamed” tumor microenvironment with increased total CD8⁺ TILs but reduced PD-1⁺CD8⁺ TIL infiltration. Notably, PD-1⁺CD8⁺ TIL infiltration is associated with favorable prognosis. These findings provide new insights into tumor-immune interactions in SRCC, with potential implications for prognostic stratification and the development of personalized immunotherapeutic strategies.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 30-39"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286453","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":"Emerging therapies to overcome antiandrogen resistance and beyond in lethal prostate cancer","authors":"Furong Huang ,&nbsp;Kexin Li ,&nbsp;Jeffrey W. Shevach ,&nbsp;Qianben Wang","doi":"10.1016/j.jncc.2025.04.004","DOIUrl":"10.1016/j.jncc.2025.04.004","url":null,"abstract":"<div><div>Prostate cancer remains the second most common malignancy among men worldwide, with treatment paradigms evolving dramatically over the last two decades. Despite the longstanding efficacy of androgen deprivation therapy (ADT) and its combination with next-generation androgen receptor (AR) signaling inhibitors or chemotherapy in metastatic hormone-sensitive settings, most tumors ultimately develop resistance and progress to lethal castration-resistant prostate cancer (CRPC). This resistance often stems from a range of molecular alterations, including AR mutations, amplifications, splice variants, and tumor suppressor gene lesions (e.g., <em>TP53, RB1</em>). Recent advances in genomic and translational research underscore the importance of biomarker-guided patient stratification to optimize therapeutic choices. Novel strategies to circumvent resistance include non–ligand-binding-domain AR inhibitors, potent AR degraders (e.g., proteolysis-targeting chimeras [PROTACs]), bipolar androgen therapy, and combination regimens incorporating PARP inhibitors or immunotherapies for selected subsets of patients. Additionally, gene-editing approaches targeting “undruggable” genetic lesions offer promise in preclinical models. Moving forward, clinical development of these emerging agents and personalized treatment approaches, supported by robust genomic profiling, is poised to enhance tumor control, extend survival, and improve quality of life for patients with advanced prostate cancer.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 42-57"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286451","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":"Alterations in AR-FOXA1 signaling in prostate cancer progression and therapeutic resistance","authors":"Shuai Gao ,&nbsp;Nolan D. Patten ,&nbsp;Changmeng Cai","doi":"10.1016/j.jncc.2025.05.003","DOIUrl":"10.1016/j.jncc.2025.05.003","url":null,"abstract":"<div><div>The androgen receptor (AR) is instrumental in the onset and progression of prostate cancer (PCa), establishing androgen deprivation therapy (ADT) as the first-line treatment for metastatic disease. However, the effectiveness of ADT is commonly short-lived. Many patients eventually relapse and develop castration-resistant prostate cancer (CRPC), commonly marked by reactivated AR signaling. Although next-generation AR signaling inhibitors (ARSi) provide temporary control, resistance inevitably emerges. While a small subset of CRPC cases may evolve through AR-independent pathways, most regain partial AR function through multiple mechanisms. A key regulator of AR activity is the pioneer transcription factor FOXA1, which governs AR binding to chromatin. The AR-FOXA1 axis is essential for prostate luminal epithelial cell lineage determination and drives the development of prostate adenocarcinoma. Emerging evidence shows profound alterations in this axis in CRPC and in tumors resistant to ARSi therapies. In this review, we highlight the genetic, epigenetic, transcriptional, and posttranscriptional changes within the AR-FOXA1 axis in PCa following ADT and ARSi treatments.</div></div>","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 58-72"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286502","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 vicious cycle of circadian disruption and obstructive sleep apnea: implications for cancer risk","authors":"Allan Saj Porcacchia ,&nbsp;David Gozal ,&nbsp;Sergio Tufik ,&nbsp;Monica L. Andersen","doi":"10.1016/j.jncc.2025.10.004","DOIUrl":"10.1016/j.jncc.2025.10.004","url":null,"abstract":"","PeriodicalId":73987,"journal":{"name":"Journal of the National Cancer Center","volume":"6 1","pages":"Pages 1-2"},"PeriodicalIF":9.4,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147286021","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}