To investigate the effects of Trifolium repens extract on proliferation, apoptosis, invasion and NLRP3/PRKD3 protein levels of oral squamous cell carcinoma cell line OSC-4.

Objective:Intermuscular lipoma（IL） is a rare type of deep-seated benign lipoma, accounting for approximately 0.3% of all lipomas. Its occurrence in the temporal region is particularly uncommon, and giant lesions are even rarer. We report the case of an 84-year-old male patient with a giant intermuscular lipoma in the temporal region, who had undergone two surgical excisions at an outside hospital, both followed by recurrence. The patient underwent another surgery at our hospital, during which the mass was completely excised. Postoperative histopathology confirmed the diagnosis of intermuscular lipoma, and no recurrence was observed during a 1-year follow-up. Based on the clinical presentation and treatment course of this case, combined with a review of relevant literature, the authors analyze the etiology, diagnosis and treatment, recurrence factors, and prognosis of giant intermuscular lipomas in the temporal region, aiming to improve awareness of this rare disease, emphasize intraoperative management, and reduce postoperative recurrence rates.

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.

Small cell lung cancer (SCLC) is a highly aggressive neuroendocrine tumor. Although it accounts for only about 13% of all lung cancers, its rapid proliferation, early metastasis, and very poor prognosis result in an extremely low five-year survival rate. In recent years, immune checkpoint inhibitors have improved outcomes in a subset of patients; however, the proportion of patients who derive meaningful benefit remains limited. For patients with limited-stage SCLC (LS-SCLC) undergoing chemoradiotherapy (CRT), standardized serum biomarkers suitable for routine monitoring of treatment response and early detection of relapse have yet to be established. Progastrin-releasing peptide (ProGRP) is generally more specific than neuron-specific enolase (NSE) for SCLC, yet neither marker is diagnostic when used alone. This review summarizes the roles of ProGRP and NSE in LS-SCLC during chemoradiotherapy (CRT), with an emphasis on differential diagnosis (particularly when pleural effusion cytology suggests adenocarcinoma but ProGRP is markedly elevated-raising the possibility of SCLC, mixed histology, or transformation and underscoring the need for tissue confirmation), longitudinal monitoring, and prognostic implications. Notably, universally accepted cut-off values for survival prediction are lacking; therefore, clinical interpretation should focus on within-assay dynamic trends and incorporate potential interfering factors, including renal dysfunction and hemolysis.

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 systematically summarize the research progress of clinical trials on breast cancer drugs in China from 2011 to 2022, as well as provide an overview of the marketed drugs. The goal is to offer data and decision-making evidence for relevant departments. Methods: Based on the registration database of the China National Medical Products Administration's Clinical Trial Registration and Information Disclosure Platform, as well as data from the domestic and imported drug query systems, an analysis was conducted on clinical trials of breast cancer drugs, including information on investigational drugs and marketed drugs from January 1, 2011, to December 31, 2022. The study compared differences between Chinese and foreign enterprises in terms of trial scope, trial phases, number of treatment lines, drug types, and mechanisms of action. Results: From 2011 to 2022, a total of 401 clinical trials for breast cancer were registered in China, accounting for 8.0% of the country's overall anti-tumor clinical trials (401/5 011), with 304 trials (75.8%) initiated by domestic enterprises. Over the past decade, clinical trials for breast cancer showed fluctuating growth, reaching a peak of 84 trials in 2020. These trials involved 254 drugs, with 156 (61.4%) being original drugs and 174 (68.5%) being targeted therapies. The most focused targets included human epidermal growth factor receptor 2 (HER-2), cyclin-dependent kinases 4/6 (CDK4/6), and estrogen receptors (ER). There are 50 drugs targeting HER-2 (28.7%), 35 targeting CDK4/6 (20.1%), and 31 targeting ER (17.8%). During the period from 2011 to 2022, a total of 15 drugs for treating breast cancer were approved and launched in China, covering 19 indications. Among these, 7 indications are for adjuvant or neoadjuvant therapy of early-stage breast cancer, and 12 indications are for advanced breast cancer. Conclusions: Substantial achievements have been made in the development of new breast cancer drugs in China from 2011 to 2022. However, there remains a significant gap in the innovation capabilities of domestic pharmaceutical companies compared to international counterparts in the field of breast cancer. Future efforts should be directed towards strengthening research and development in breast cancer, exploring new target points, and investigating combination therapy mechanisms.

Objective: To investigate the preoperative diagnostic value of ultrasound-guided fine-needle aspiration biopsy wash-out fluid (FNA-CT) in medullary thyroid carcinoma (MTC) with mildly elevated serum calcitonin levels. Methods: 267 patients with MTC diagnosed in Tianjin Cancer Hospital between Jan 2015 and Jan 2024 were enrolled in the study. Based on serum calcitonin, patients were divided into two groups:＞100 ng/L and 10-100 ng/L. Sonographic features, clinicopathological characteristics and prognostic outcomes were evaluated between the two groups. The diagnostic efficacy of serum calcitonin and FNA-CT in MTC and non-medullary thyroid carcinoma with slightly high serum calcitonin were evaluated. The best cutoff values of serum calcitonin and FNA-CT were calculated by subject operating characteristic curve (ROC). The diagnostic efficacy was analyzed for MTC with mildly elevated serum calcitonin according the best cut off points. Results: Compared to the >100 ng/L group, MTC patients with serum calcitonin 10-100 ng/L exhibited distinct ultrasonographic features: taller-than-wide shape, non-adjacent to thyroid capsule, less vascularity, and CACA-TIRADS 4 (all P＜0.05). Clinicopathologically, the serum calcitonin 10-100 ng/L group demonstrated single focus rather than multifocality, smaller tumor size, higher prevalence of microcarcinoma, a lower degree of local invasion, earlier tumor stages (T stage, N stage, TNM stage), smaller extent of thyroidectomy and lymphadenectomy and lower diagnostic accuracy of FNA (all P＜0.05). The group also showed higher biochemical cure rate (90.0% and 54.2%)and lower rates of biochemical recurrence (5.5% and 23.1%) and tumor recurrence (3.6% and 22.6%, P＜0.001). Among MTC with serum calcitonin 10-100 ng/L, the median of serum calcitonin levels were 40.0 ng/L (19.5, 65.8 ng/L) for MTC vs. 16.6 ng/L (13.2, 20.8 ng/L, P＜0.001) for non-medullary thyroid carcinoma. The median of FNA-CT were 2 000.0 ng/L (1 334.0, 2 000.0 ng/L) vs. 0.8 ng/L (0.5, 2.0 ng/L, P＜0.001). The best cutoff points were 22.9 ng/L for serum calcitonin and 58.7 ng/L for FNA-CT. The sensitivity, specificity, negative predictive value, positive predictive value and the area under curve (AUC) were 67.3%, 82.9%, 65.4%, 61.2% and 0.829 (95% CI: 0.731-0.903) at the best cutoff point of 22.9 ng/L for serum calcitonin. The sensitivity, specificity, negative predictive value, positive predictive value and AUC were 98.2%, 97.6%, 97.61%, 98.1% and 0.998 (95% CI: 0.989-0.998) at the best cutoff point of 58.7 ng/L for FNA-CT. Conclusions: MTC with slightly elevated serum calcitonin commonly correlates with an early-stage disease. FNA-CT has demonstrated near-perfect diagnostic performance and improved the early detection in this population.

Objective: To exploit the elevated glutathione (GSH) levels in the tumor microenvironment and investigate the therapeutic efficacy of a novel glutathione-responsive apurinic/apyrimidinic (AP) site captor, Probe-NEt, against anaplastic thyroid cancer (ATC). Methods: Fluorescence imaging compared Probe-NEt uptake and activation in normal thyroid (Nthy ori 3-1), ATC (THJ-16T, CAL-62), and lung cancer (H1299) cells. Half maximal inhibitory concentration (IC50) values were determined by cytotoxicity assays; DNA damage was evaluated using appropriate assays. Flow cytometry analyzed cell cycle distribution and apoptosis following treatment with low (5 μmol/L) or high (20 μmol/L) Probe-NEt concentrations. BALB/c nude mice bearing subcutaneous ATC xenografts received low (0.025 mg) or high (0.05 mg) dose injections. Tumor volumes were monitored; HE staining assessed biosafety in major organs; immunohistochemistry detected apoptosis-related protein expression. Results: ATC cells demonstrated significantly higher Probe-NEt activation than normal thyroid cells. Probe-NEt exhibited selective cytotoxicity (higher IC50 in normal vs. ATC cells; all P＜0.01) with time-dependent characteristics; the selectivity ratio increased from 1.7 at 24 h (62.4 vs. 37.7 μmol/L) to 2.4 at 48 h (32.7 vs. 13.5 μmol/L). Probe-NEt induced DNA damage, G2/M arrest (THJ-16T: from 5% to 43%; CAL-62: from 19% to 37%), and dose-dependent late apoptosis. In THJ-16T cells, late apoptotic rates rose from 5.49% (control) to 13.95% (low-dose) and 63.43% (high-dose), with viable cells decreasing accordingly (89.42%, 76.01%, 20.45%). CAL-62 cells showed similar trends (16.72%, 40.19%, 69.88%). In vivo, Probe-NEt significantly suppressed tumor growth without hepatorenal toxicity (all P＞0.167). Immunohistochemistry revealed upregulated pro-apoptotic proteins, downregulated anti-apoptotic proteins, and decreased Ki-67 expression. Conclusion: The glutathione-responsive AP site captor Probe-NEt significantly inhibits ATC cell growth, induces G2/M phase cell cycle arrest, promotes late apoptosis, and exhibits high selectivity and favorable biosafety profiles.