By comparing deep learning and habitat analysis models based on contrast-enhanced CT (CECT), this study explores a novel approach to predict cervical lymph node metastasis and pathological subtypes in oral squamous cell cancer (OSCC).

This study aimed to explore the impact of dihydroartemisinin (DHA) on cell proliferation, migration, and invasion in oral squamous cell carcinoma (OSCC). Our findings offer a theoretical foundation for advancing the research and development of novel therapeutic agents for OSCC.

Metabolic reprogramming is a hallmark of cancer, with the Warburg effect-driven aerobic glycolysis leading to a substantial accumulation of lactate in the tumor microenvironment. For a long time, lactate was considered a mere metabolic end product; however, recent studies have found that it acts as an important signaling molecule, profoundly influencing tumor progression by inducing a novel post-translational modification - lactylation. Lactylation, driven by lactate, occurs on both histones and non-histone proteins and is finely regulated by the 'writer' 'eraser' and 'reader' mechanisms, thereby altering the function of target proteins and gene expression. This review systematically explores the bidirectional regulatory network between glycolytic reprogramming and lactylation: on one hand, key glycolytic regulators promote lactate production, thereby increasing lactylation levels; on the other hand, lactylation can feedback to regulate the activity and expression of key glycolytic enzymes, forming a pro-tumor positive feedback loop. This interaction plays a central role in tumor proliferation, metastasis, DNA damage repair, and immune evasion. Consequently, targeting lactate production, lactate transport, or the lactylation process itself has emerged as a highly promising anti-cancer strategy and shows potential synergy with existing therapies such as immune checkpoint inhibitors. In-depth analysis of the glycolysis-lactylation axis will provide a crucial theoretical basis for developing novel cancer treatment approaches.
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Global cancer statistics in 2022 ranked lung cancer as the leading cause of cancer incidence and mortality worldwide, with lymph node metastasis serving as a pivotal determinant of prognosis and treatment strategy. Extranodal extension (ENE) refers to the pathological phenomenon where tumor cells breach the lymph node capsule and invade surrounding tissues. In non-small cell lung cancer (NSCLC), although ENE has not yet been formally incorporated into the tumor-node-metastasis (TNM) staging system, its clinical value is gaining increasing attention. This review systematically summarizes the current research progress regarding the definition, diagnostic approaches, prognostic significance, and treatment implications of ENE in NSCLC, analyzes existing challenges, and proposes future directions. The goal of this paper is to provide insights for optimizing clinical practice and guiding subsequent research.
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First-line immunotherapy for advanced non-small cell lung cancer (NSCLC) shows significant survival benefits in patients without driver mutations, but the optimal duration of treatment remains controversial. Some studies support limiting immunotherapy to 2 years, arguing that longer treatment does not bring additional survival benefits; while other studies believe that treatment should continue until disease progression to maximize survival benefits. This article systematically reviews the current research progress on the duration of immunotherapy and discusses the potential predictive value of biomarkers such as circulating tumor DNA (ctDNA), the best efficacy response, and programmed cell death ligand 1 (PD-L1) expression levels in individualized treatment decisions. More prospective studies, especially biomarker-driven trials, are still needed to clarify the optimal duration of treatment and establish an individualized treatment strategy based on multidimensional indicators.
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Serous effusion is a common complication in patients with advanced lung cancer, which often indicates that the tumor has metastasized to the pleura or other serosal membranes. It is essential to achieve an accurate diagnosis and pathological classification of tumor cells in effusion to guide clinical treatment. However, there are limitations to relying solely on morphological diagnosis, especially in atypical cases where diagnostic uncertainty is common. The International System for Serous Fluid Cytopathology (TIS) proposes a standardized hierarchical diagnostic framework that integrates morphology and auxiliary techniques. Nevertheless, its clinical application value in the Chinese lung cancer population remains insufficiently validated. This study aimed to systematically evaluate the diagnostic performance of the TIS system in the assessment and classification of serous effusions based on a large sample of lung cancer cases.

Non-small cell lung cancer (NSCLC) is one of the leading causes of cancer-related deaths worldwide, and its occurrence and development are closely related to complex molecular mechanisms. Alternative splicing of precursor mRNA is a key step in gene expression regulation, and its dysregulation is common in tumors. The serine/arginine-rich splicing factor (SRSF) family, a core protein family in splicing regulation, has been confirmed to play oncogenic roles in various cancers. However, systematic research on the SRSF family in NSCLC remains insufficient. This study aims to systematically analyze the specific expression patterns, clinical prognostic value, collaborative mechanisms and potential biological functions of SRSF individual members in NSCLC by the combination of bioinformatics analysis and experimental verification.

The prognosis for non-small cell lung cancer (NSCLC) with leptomeningeal metastasis (LM) is extremely poor. However, in oncogene addicted patients, the emergence of targeted therapies with high central nervous system (CNS) penetration is significantly reshaping the treatment landscape. Existing guidelines, which often favor conservative strategies, are no longer sufficient to meet the demands of precision medicine. To address this challenge, the Metastasis Lung Cancer Collaboration Group, Youth Specialists Committee of Beijing Medical Reward Foundation convened multidisciplinary experts from Medical Oncology, Radiology, Pathology, Radiotherapy, and Neurosurgery. Based on evidence-based medicine from the past decade and clinical practice experience, they have developed the Chinese expert consensus on clinical management of oncogene addicted NSCLC with leptomeningeal metastasis (2026 edition). This consensus emphasizes that the diagnosis of LM should be based on a comprehensive assessment of clinical symptoms, magnetic resonance imaging (MRI), and cerebrospinal fluid (CSF) cytology. It also highlights the critical role of CSF molecular liquid biopsy in clarifying driver gene status and assessing treatment efficacy. In terms of treatment, this consensus advocates for a fundamental paradigm shift: therapy should be led by a multidisciplinary team (MDT), with high-CNS-penetration targeted therapies as the first-line intervention, while local treatments (such as intrathecal injection and radiotherapy) are positioned as supplementary measures. The consensus provides a series of expert recommendations on key aspects, including the selection of high-CNS-penetration tyrosine kinase inhibitors (TKIs), the application of intrathecal chemotherapy, the timing of radiotherapy, and palliative surgery. It aims to establish proactive, individualized treatment standards for patients with NSCLC LM in China, based on molecular subtyping and MDT collaboration, thereby improving patient survival outcomes.
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To investigate the expression of Golgi membrane protein 1 (GOLM1) in oral squamous cell carcinoma (OSCC) and its effects on proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) in OSCC cells and the underlying mechanisms.

The patient was a 7-year-old boy admitted with facial edema. Ultrasound indicated moderate pericardial effusion and pleural effusion. Contrast-enhanced chest computed tomography showed indistinct mediastinal structures with mild-to-moderate enhancement, suggestive of a mediastinal space-occupying lesion. Further evaluation with whole-body PET-CT, pathological biopsy of the mediastinal lesion, cytological examination of pleural and pericardial effusions, and immunohistochemistry led to the final diagnosis of isolated myeloid sarcoma. Pathological examination is the gold standard for clinical diagnosis; however, limited sampling sites can result in missed or incorrect diagnoses. Multiple and multi-site sampling should be undertaken according to the clinical context, combined with flow cytometry and immunohistochemistry to assist diagnosis and reduce missed diagnoses and misdiagnoses.

To investigate the regulatory mechanism of Yiqi Jiedu Formula on immune microenvironment of hepatocellular carcinoma (HCC) in mice.

To explore the molecular mechanism by which selenocystine (SeC) inhibits colon cancer cell growth in vitro.

To explore the effect of Shengmai San (SMS) for improving osimertinib resistance in non-small cell lung cancer cells and the underlying mechanism.

To determine whether dentin sialophosphoprotein (DSPP) modulates oxaliplatin efficacy for colorectal cancer (CRC) and explore the underlying integrin αvβ3-dependent mechanism.

Objective: To analyze platelet (PLT) characteristics and mitochondrial features in patients with multiple myeloma (MM) , and to investigate the impact of PLT mitochondrial respiration on MM cell proliferation, metabolism, and mitochondrial dynamics. Methods: Peripheral blood was collected from healthy volunteers and newly diagnosed MM (NDMM) patients at Sichuan Provincial People's Hospital between January 2020 and December 2023, and PLTs were isolated. PLT activation and mitochondrial reactive oxygen species (ROS) levels were assessed by scanning and transmission electron microscopy and flow cytometry. Serum levels of PLT-related factors were measured by enzyme-linked immunosorbent assay (ELISA) . MM cell lines (RPMI 8226 and U266) were co-cultured with untreated PLTs from healthy volunteers or with PLTs pretreated with rotenone or oligomycin. MM cell proliferation was assessed by the CCK-8 assay. mRNA expression of metabolism- and mitochondrial dynamics-related genes in MM cells was quantified by real-time quantitative PCR (qPCR) . Drp1 and phosphorylated Drp1 were analyzed by Western blot. Results: Compared with healthy volunteers, MM patients showed increased expression of the PLT activation marker CD41/CD61 [ (2.10 ± 1.15) % vs (0.22 ± 0.19) % , P=0.048], decreased CD42b expression [ (52.80 ± 8.73) % vs (74.58 ± 5.11) % , P=0.020], and elevated mitochondrial ROS levels in PLTs (150.50 ± 17.79 vs 62.45 ± 21.34, P=0.001) . Serum factor analysis showed reduced levels of interleukin-34 (IL-34) and platelet factor 4 (PF4) and increased levels of basic fibroblast growth factor (bFGF) , insulin-like growth factor 1 (IGF-1) , IL-6, P-selectin, platelet-derived growth factor (PDGF) , and transforming growth factor β1 (TGF-β1) in MM patients (all P<0.05) , whereas vascular endothelial growth factor (VEGF) levels did not differ significantly (P=0.086) . In vitro co-culture experiments showed that co-culture with PLTs for 48 h promoted MM cell proliferation, whereas PLTs pretreated with rotenone or oligomycin lost this pro-proliferative effect (all P<0.001) . qPCR showed that co-culture increased mRNA expression of the metabolism-related genes citrate synthase (CS) and lactate dehydrogenase A (LDHA) and the mitochondrial dynamics related genes dynamin-1-like protein (DNM1L) and mitochondrial fission 1 (FIS1) in MM cells (all P<0.05) . Pretreatment with the Drp1 inhibitor Mdivi-1 inhibited DNM1L mRNA expression in MM cells (0.75 ± 0.16 vs 1.00 ± 0.09, P=0.002) ; this inhibition was reversed by subsequent co-culture with PLTs (1.02 ± 0.13 vs 0.75 ± 0.16, P=0.007) . Western blot analysis showed that co-culture with PLTs increased p-Drp1 (Ser616) protein levels in U266 cells (P<0.05) . Conclusion: In vitro experiments suggest that PLTs and their mitochondrial respiratory function may be involved in regulating MM cell proliferation, metabolic reprogramming, and mitochondrial dynamics. However, their relevance and applicability in vivo and in clinical practice require further validation in additional preclinical and clinical studies.

To investigate the association between the expression levels of galectin-9 and sonic hedgehog (SHH) and the risk of occurrence and prognosis in patients with colorectal cancer (CRC).

Neuroendocrine tumors are rare, low-grade malignant tumors with a gradually increasing incidence rate in recent years, with gastroenteropancreatic neuroendocrine tumors being the most common among them. The majority of gastropancreatic neuroendocrine tumors have already metastasized to the liver at the time of initial diagnosis; therefore, treatment targeting liver metastases is crucial. The most effective treatment for hepatic metastases of gastropancreatic neuroendocrine tumors is surgical resection. However, 60%-70% of patients are ineligible for radical resection due to diffuse liver involvement. Thus, an alternative treatment option offered for these patients is liver transplantation. Liver transplantation is considered an indication for well-differentiated, unresectable hepatic metastases of gastropancreatic neuroendocrine tumors because of the tumor's low invasiveness, slow growth, and the fact that the liver is often the only distant metastasis site. This article reviews the research progress of liver transplantation therapy for hepatic metastases in gastropancreatic neuroendocrine tumors.

Tumor-associated macrophages (TAMs) are abundant immune cell content in the tumor microenvironment of hepatocellular carcinoma and are associated with tumor progression and therapeutic resistance. This article describes novel TAM subpopulations and potential targets in hepatocellular carcinoma that have been identified based on single-cell and spatial omics technologies. Additionally, it proposes TAMs' classification according to their functions into immunosuppressive, lipid-metabolizing, angiogenic, liver-resident, and immune-stimulating types and summarizes four major therapeutic strategies targeting TAMs, providing a reference for novel TAM-targeted therapies.

Epithelioid inflammatory myofibroblastic sarcoma (EIMS) is a rare and highly aggressive mesenchymal neoplasm that is frequently associated with anaplastic lymphoma kinase (ALK) gene fusion. Surgical resection remains the cornerstone of treatment for patients with early- and intermediate-stage EIMS; however, a standardized therapeutic approach for advanced-stage EIMS has yet to be established. Primary pulmonary EIMS is exceedingly rare, with only a limited number of cases reported in the literature. While treatment with ALK-tyrosine kinase inhibitors (TKIs) is considered a viable therapeutic option, and clinical outcomes with monotherapy using ALK-TKIs have frequently been suboptimal. This study presents a case of advanced primary pulmonary EIMS with a TPM3-ALK fusion. The patient received first-line targeted therapy with the second-generation ALK-TKI Ensartinib, in conjunction with radiotherapy for residual and metastatic lesions. This treatment regimen resulted in significant tumor reduction and sustained disease control. The progression-free survival (PFS) exceeded 32 months, with no significant treatment-related adverse events observed. This study investigates the feasibility of combining targeted therapy with local radiotherapy, guided by genetic testing, to offer novel treatment strategies for patients with advanced primary pulmonary EIMS.
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Tumor metastasis is the leading cause of cancer-related mortality. Disseminated tumor cells (DTCs), serving as the critical 'seeds' in the metastatic cascade, hold the key to determining the success or failure of metastasis. Following dissemination from the primary tumor and colonization of distant organs, DTCs often enter a prolonged state of dormancy. Their subsequent escape from immune surveillance through sophisticated mechanisms enables them to transition from this dormant state to a proliferative one, ultimately culminating in clinically detectable metastatic lesions. A profound understanding of DTCs immune evasion is therefore essential for unraveling the fundamental biology of metastasis and developing effective anti-metastatic strategies. This article systematically reviewed the latest advances in the mechanisms underlying DTCs immune evasion, focusing on three core aspects: defects in antigen presentation, formation of an immunosuppressive microenvironment, and metabolism reprogramming-mediated immunosuppression. Specifically, DTCs achieve 'immune invisibility' by downregulating major histocompatibility complex class-I (MHC-I) molecule expression; they actively construct a local 'protective shield' by recruiting immunosuppressive cells such as regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs); and they impair effector immune cell function at the energetic and metabolic levels by remodeling glucose, amino acid, and lipid metabolism. Building upon this, we innovatively integrate the traditional Chinese medicine (TCM) theories of 'hidden toxicity due to vital qi deficiency' and the 'metastatic state' to elucidate the dynamic pathogenic relationship between the body's systemic 'Zhengqi' (vital energy) status and the dormancy-awakening switch of DTCs, offering a novel holistic perspective for comprehending the metastatic process. Finally, we discussed the prospects of multi-target combination therapeutic strategies against DTCs immune evasion and highlight the potential of emerging technologies, such as single-cell sequencing and spatial transcriptomics, aiming to provide valuable insights for future in-depth research and clinical translation in the field of anti-metastasis therapy.
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