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  • REVIEW

    Zhi-Peng Wang, Ai-Qing Li, Dilinaer Wusiman, Rui-Cheng Wu, Ji-Min Zhu, Xin-Rui Li, Yuan-Ning Guo, Premkamon Chaipanichkul, Uzoamaka Adaobi Okoli, Siang Boon Koh, Jie Wang, Deng-Xiong Li, Xiao-Dong Jin, Da-Hong Zhang, Cheema Umber, Qi Zhang, De-Chao Feng

    Corrected Proof
    (2026) DOI: 10.1016/j.mmr.2026.100038
    Abstract：Radiopharmaceutical therapy (RPT) is a pivotal modality in cancer treatment, with its efficacy substantially modulated by the tumor microenvironment (TME). The TME regulates RPT penetration and influences therapeutic outcomes. Concurrently, RPT actively reconfigures the TME by enhancing immune activation and partially reversing immunosuppression. Specifically, RPT induces tumor cell senescence and immunogenic cell death, and catalyzes immune activation. RPT diminishes immunosuppressive elements, including regulatory T cells and tumor-associated macrophages, and augments populations of CD8+ T cells and natural killer cells, thereby fostering a more immunostimulatory TME. Additionally, RPT modulates critical cytokines and upregulates immune checkpoint molecules, bolstering anti-tumor immunity. Nevertheless, pathological features like hypoxia and extracellular matrix stiffness within the TME can hinder RPT biodistribution and therapeutic efficacy. Strategically targeting the TME through approaches, such as fibroblast depletion, hypoxia mitigation, metabolic reprogramming, nerve-immune-cancer interactions, or nanocarrier drug delivery, can amplify RPT effectiveness. Combination immunotherapies that integrate RPT with immune checkpoint inhibitors, chimeric antigen receptor (CAR)-T cells, or cancer vaccines have demonstrated enhanced anti-tumor responses and survival advantages in malignancies such as prostate cancer and neuroendocrine tumors. Given the complexity and heterogeneity of the TME, emerging strategies, including radiation-responsive nanocarriers, CAR-T cells engineered to secrete radiosensitizers, senolytic therapies, and artificial intelligence-driven multimodal data integration, are promising in addressing the challenges and refining precision cancer therapy. In summary, the TME serves as a critical bridge between RPT and immunotherapy; elucidating the interplay among these three elements is essential for advancing combination strategies.  
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  • RESEARCH

    Ling-Ling Yu, Fan-Shu Yan, Jin-Lei Qi, Li-Jun Wang, Mai-Geng Zhou, Peng Yin

    Corrected Proof
    (2026) DOI: 10.1016/j.mmr.2026.100041
    Abstract：BackgroundAs the world’s leading producer and consumer of tobacco, China bears a significant health burden attributable to tobacco. This study aims to provide a precise, updated analysis of the demographic, temporal, and spatial dimensions of the tobacco-attributable disease burden across China.MethodsUsing the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2023 comparative risk assessment framework and its hierarchical taxonomy, we analyzed tobacco use as a Level 2 (behavioral) risk. We estimated the national and provincial burdens of tobacco use in China from 1990 to 2023, quantifying deaths, years of life lost (YLLs), years lived with disability (YLDs), and disability-adjusted life years (DALYs) stratified by sex, age, cause, and the three Level 3 tobacco sub-categories: smoking, secondhand smoke (SHS), and chewing tobacco. Temporal trends were assessed via average annual percentage change (AAPC).ResultsIn 2023, tobacco use caused 2.38 million [95% uncertainty interval (UI) 2.02−2.83] deaths and 57.27 million (95% UI 48.28−60.82) DALYs, predominantly premature mortality [YLLs 49.45 million (95% UI 42.23−59.25)]. Direct smoking was the primary driver (2.01 million deaths), followed by SHS and chewing tobacco. A profound sex disparity existed in smoking burden, with the male (ASMR; 167.78/100,000) being 9.5-time higher than that of females, although females bore a greater SHS-attributable burden. From 1990 to 2023, absolute deaths and DALYs increased, but their age-standardized rates (ASRs) significantly declined (AAPC for mortality: −2.34%). The burden is concentrated in older adults, with the disease spectrum shifting from respiratory infections in youth to chronic diseases such as heart disease and lung cancer later in life. Geographically, northern provinces had the highest burden, whereas coastal areas had the lowest burden.ConclusionsDespite declining ASRs, China’s tobacco attributable burden is concentrated among males, older adults, and northern provinces. In the context of rapid aging and the long-term harmful effects of tobacco smoking, more stringent and targeted policies should be implemented to address the challenges associated with tobacco use in China.  
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  • RESEARCH

    Jing Feng, Yan-Hong Liu, Li-Ming Gong, Wen-Xuan Zhang, Chen-Fei Liu, Cong-Cong Xiao, Li-Qing Chen, Ming-Ji Jin, You-Yan Guan, Zhong-Gao Gao, Wei Huang

    Corrected Proof
    (2026) DOI: 10.1016/j.mmr.2026.100036
    Abstract：BackgroundEmerging evidence indicates that diverse bacteria colonize tumors and facilitate oncogenesis through multifaceted mechanisms, predominantly through immunosuppression of the tumor microenvironment (TME). Fusobacterium nucleatum (F.n) exemplifies this phenomenon in colorectal cancer (CRC), where it mediates immune evasion via tumor cell autophagy and upregulation of programmed death-ligand 1 (PD-L1). Effective strategies for combining precise elimination of intratumoral F.n with chemotherapy remain lacking.MethodsA targeted multimodal nano-based chemoimmunotherapy was engineered by co-loading hyaluronic acid (HA)-coated silver nanoparticles (Ag NPs) and paclitaxel (PTX) into tumor-targeting cationic liposomes (Cls). The combination was mechanistically evaluated for F.n eradication capacity, antitumor effects, and remodeling of the tumor immune microenvironment. Antitumor efficacy and safety were also evaluated in vivo using a tumor-bearing mouse model.ResultsIntratumoral F.n subverted antitumor immunity through a dual mechanism, coupling major histocompatibility complex class I (MHC-I) degradation with PD-L1 upregulation. HA@Ag NPs/PTX Cls exerted synergistic antitumor effects through multimodal mechanisms. HA@Ag NPs/PTX Cls eliminated intratumoral bacteria, restoring microbial homeostasis, enhancing MHC-I antigen presentation, increasing production of tumor necrosis factor (TNF) and interferon (IFN), and downregulating PD-L1 to promote tumor immunorecognition. Combined with PTX-induced apoptosis, the nanotherapy inhibited both primary and metastatic tumors. Notably, bacterial clearance-triggered immune activation established long-term immunological memory, providing durable protection against tumor recurrence. These results highlighted the dual benefit of liposomes in addressing microbial dysbiosis and immune evasion in CRC.ConclusionThis innovative liposomal strategy disrupts the immunosuppressive TME and synergizes with a small-molecule chemotherapeutic agent to induce tumor cell apoptosis, representing a novel approach to potentiate cancer immunotherapy.  
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  • REVIEW

    Qiu-Yu Xu, Jie Zhang, Xin-Jian Wan, Ling Wu, Ji-Chun Yang, Yan Lu

    Corrected Proof
    (2026) DOI: 10.1016/j.mmr.2026.100037
    Abstract：Glucocorticoids (GCs), steroid hormones synthesized and secreted by the adrenal cortex, have been the subject of intensive scientific investigation for over eight decades due to their critical roles in physiological and pathological processes. The systemic secretion, bioavailability, and tissue-specific concentrations of GCs are strictly orchestrated by the hypothalamic-pituitary-adrenal axis, serum corticosteroid-binding globulin levels, and the enzymatic activation of 11β-hydroxysteroid dehydrogenase type 1 and 2 (11β-HSD1 and 11β-HSD2). As pivotal metabolic messengers, GCs signal through binding to glucocorticoid receptors (GR) to maintain metabolic homeostasis by modulating the transcriptional landscape of genes central to glucose and lipid metabolism. Any imbalance in GC levels, whether excess or deficiency, leads to the development of diverse metabolic disorders. Elucidating the underlying mechanisms of this metabolic regulation remains a primary objective of contemporary research. This review summarizes landmark discoveries and focuses on the metabolic impact and dysfunction of glucocorticoids, aiming to establish a robust foundation for the development of optimized therapeutic interventions for patients with metabolic diseases.  
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  • REVIEW

    Circadian clock and cancer AI Introduction

    Zhi-Hao Wei, Zi-Rui Dong, An-Shu Li, Qing-Yi Li, Jian Shi, Ke-Shan Wang, Xiao-Ping Zhang

    Corrected Proof
    (2026) DOI: 10.1016/j.mmr.2026.100025
    Abstract：Circadian rhythms play a critical role in regulating physiological and behavioral processes, such as the sleep-wake cycle, hormone secretion, and metabolism. These rhythms are controlled by endogenous biological clocks, which are synchronized with environmental cues, primarily the light-dark cycle. Notably, disruption or reprogramming of circadian rhythms is closely associated with cancer initiation, progression, and treatment response. At the molecular level, the dysregulation of core clock genes can disturb normal cellular rhythms, leading to aberrant cell proliferation, impaired DNA repair, altered metabolism, and disrupted immune responses. This review systematically summarizes the pivotal roles and molecular mechanisms of circadian rhythms in tumor development, with a particular focus on strategies to modulate clock genes through behavioral interventions, pharmacological approaches, and gene-editing techniques, highlighting their potential as novel therapeutic strategies and clinical applications in cancer management.  
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  • LETTER TO THE EDITOR

    Li Li, Qi Han, Hao-Lei Bai, Qin Xiao, Xie He, Jia-Fei Chen, Zhi-Ming Zhen, Xue-Qin Luo, Yuan-Jing Zhang, Min-Min Lu, Xiao Wang, Shi-Yin Li, Jia-Xiang Xiong, Yun Wang, Zhi-An Hu, Xiao-Long Zhang, Yong Liu, Chao He

    Corrected Proof
    (2026) DOI: 10.1016/j.mmr.2026.100035
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