Oral cavity squamous cell carcinoma (OCSCC) represents the 16th most prevalent cancer worldwide accounting for greater than 389,000 cases annually. Most examples of OCSCC are preceded by a diverse group of lesions exhibiting variable risk of transformation to cancer, collectively termed oral potentially malignant disorders (OPMDs). The identification of salivary, serologic, and/or tumor tissue biomarkers holds substantial promise for improving detection, prognosis, and treatment of OPMDs and OCSCC. Although certain biomarkers have become standard of care in the management of patients, continued robust validation and stringent protocol standardization efforts are critical to ensure both diagnostic accuracy and widespread utilization.

Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome, is a common complex endocrinopathy affecting the reproductive, metabolic, and psychosocial health of females of reproductive age. A 26-year-old woman with PMOS and infertility (7-year duration) underwent multiple cycles of ovulation induction, intrauterine insemination, and in vitro fertilization. Following a 12-week structured yoga program (postures, breathwork, meditation), hormonal and metabolic parameters normalized and oxidative stress and inflammation decreased significantly. We saw significant improvement in mitochondrial integrity, reduced severity of comorbid depression, and improved quality of life. On follow-up, the participant was found to have conceived within 20 weeks of practice and delivered a healthy baby. This case highlights the role of yoga in the management of PMOS, adding evidence of yoga's benefit at the cellular and molecular level and clinical improvement. Regular yoga practice has the potential to serve as a holistic, nonpharmacological approach for managing PMOS and associated comorbidities.

The primary objective of this study was to evaluate the efficacy of oral nutritional supplements (ONS) on chemotherapy tolerance and long-term survival outcomes in postoperative colorectal cancer patients undergoing chemotherapy.

This study was a secondary analysis based on a randomized controlled trial, and patients undergoing chemotherapy after hospital discharge were included. Patients in the ONS group received dietary advice as well as ONS for three months, while the control group received only dietary advice. Clinical characteristics and nutritional indicators were collected at baseline and three months after hospital discharge to assess nutritional status. These included body weight, body mass index, skeletal muscle index, serum albumin, and hemoglobin levels. Chemotherapy modifications including dose reduction, delay, and discontinuation were recorded to represent chemotherapy tolerance. The survival information within 5 years was collected and analysed.

There were 157 patients included in this study, with 80 patients in the ONS group and 77 in the control group. At three months after hospital discharge, nutrition-related parameters showed no significant differences between the two groups. However, the ONS group demonstrated a significant improvement in chemotherapy tolerance comparing to the control group (17.5% vs. 35.1%, p = 0.01). Additionally, the ONS group exhibited a lower 5-year all-cause mortality rate and significantly improved survival outcomes compared to the control group (hazard ratio 0.58, 95%CI: 0.34-0.98, p = 0.04).

The administration of ONS after hospital discharge can improve chemotherapy tolerance and long-term survival rates in colorectal cancer patients under-going chemotherapy, highlighting the importance of nutritional support during postoperative chemotherapy. Further studies are warranted to validate the underlying mechanisms and other long-term effects.

Patients with malignancy often have a poor prognosis and dismal quality of life. This study aimed to evaluate whether a combined nutrition, exercise, and psychological intervention could improve these outcomes.

In an open-label, randomized controlled trial at the First Hospital of Hebei Medical University (Oct 2021-Jun 2022), 90 patients were assigned (1:1) to a treatment group receiving 6-month cyclic combined assessments and interventions, or a control group receiving assessments only. Body composition, hand grip strength (HGS), 6-minute walk test (6MWT), Hospital Anxiety and Depression Scale (HADS), Patient Health Questionnaire-9 (PHQ-9), and quality of life were compared at baseline and 6 months. Data were analyzed using SPSS 21.0, with p <0.05 considered significant.

90 people were enrolled, and 80 people have completed the study. Compared to controls, the intervention group showed significantly lower nutritional risk (10.0 % vs. 100 %, p <0.001) and malnutrition rates (22.5 % vs. 100 %, p <0.001). Significant improvements were observed in BMI, muscle mass, phase angle, HGS, and 6MWT distance (all p <0.001). HADS and PHQ-9 scores decreased (p <0.001). Quality-of-life scores (physical, role, emotional, social function, overall health) improved, while symptom scores (fatigue, pain, nausea/vomiting, etc.) decreased markedly (p <0.05). The control group exhibited opposite trends.

Combined nutrition, exercise, and psychological interventions effectively improve nutritional status, physical and psychological well-being, and quality of life in patients with malignancy, potentially enhancing treatment tolerance and promoting rehabilitation.

Herbal medicine has emerged as an important area of investigation in gastrointestinal cancers owing to its multitarget therapeutic potential and growing integration with modern oncology. However, the rapid expansion of the literature has resulted in a fragmented understanding of the field's knowledge structure, research evolution, and emerging directions.

A bibliometric analysis was performed using publications retrieved from the Web of Science Core Collection between 2016 and 2025. Bibliometrix, VOSviewer, and CiteSpace were employed to evaluate publication trends, collaboration networks, thematic evolution, and knowledge foundations. To further assess the biological relevance of major research themes, representative molecular markers associated with apoptosis, cell-cycle regulation, and epithelial biology were examined using transcriptomic data integrated from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) project through the Gene Expression Profiling Interactive Analysis (GEPIA) platform.

A total of 1,985 publications were included. Research activity increased substantially over the study period, particularly after 2020. Bibliometric analyses revealed a progressive transition from traditional investigations of apoptosis, proliferation, and metastasis toward emerging themes involving tumor microenvironment regulation, ferroptosis, gut microbiota interactions, network pharmacology, and molecular docking. Knowledge structure analyses demonstrated increasing integration of experimental oncology, bioinformatics, and traditional Chinese medicine research. China dominated global publication output, while the United States exhibited the strongest international collaborative profile. Exploratory transcriptomic validation showed that representative molecular markers (BCL2, CCND1, and CDH1) exhibited differential expression patterns across multiple gastrointestinal malignancies, supporting the biological relevance of the dominant research themes identified through bibliometric analyses.

Research on herbal medicine for gastrointestinal cancers is transitioning from descriptive pharmacological investigations toward mechanism-oriented, data-driven, and translational research. By integrating bibliometric visualization with exploratory pan-gastrointestinal-cancer transcriptomic validation, this study provides a comprehensive overview of the field's evolution and offers a complementary framework linking knowledge mapping with molecular-level evidence. These findings provide biological context for emerging research priorities and may facilitate future biomarker discovery and precision-oriented herbal medicine research for gastrointestinal cancers.

Ulcerative colitis (UC) is associated with an increased risk of colitis-associated colorectal cancer (CAC), which develops through inflammation-driven carcinogenesis distinct from sporadic colorectal cancer (CRC). Reliable molecular markers to differentiate CAC from CRC remain limited. This study aimed to identify genes preferentially expressed in CAC and to evaluate their potential diagnostic relevance.

Surgically resected specimens from 42 patients with UC were reviewed. RNA sequencing was performed using normal mucosa, inflamed mucosa, and cancer tissue from three patients with CAC, and compared with tissue from one patient with sporadic CRC. Candidate genes were validated at the protein level using immunohistochemistry.

Transcriptomic analysis identified three genes - MUC5AC, CEACAM7, and DUOX2 - that were expressed at higher levels in CAC than in sporadic cancer. Immunohistochemical staining confirmed protein expression of all three markers in CAC tissues. In contrast, CEACAM7 and MUC5AC expression levels were lower in sporadic CRC. These findings indicate that the expression patterns of these genes differ between CAC and CRC.

MUC5AC, CEACAM7, and DUOX2 exhibit expression profiles in CAC distinct from those observed in sporadic CRC. Combined evaluation of these markers may assist in the differential diagnosis between CAC and CRC.

Kisspeptin signaling is recognized as a metastasis-suppressive pathway, but its role in oncogenic HRAS-driven tumor progression remains incompletely understood. This study investigated whether kisspeptin signaling suppresses HRAS^G12V-induced tumorigenic and metastatic phenotypes in NIH3T3 cells and examined the involvement of SP1-dependent transcription of N-cadherin.

NIH3T3 cells expressing HRAS^G12V, KISS1, and KISS1R were analyzed for proliferation, migration, invasion, luciferase reporter activity, anchorage-independent growth, and in vivo tumor growth and pulmonary metastasis. N-cadherin expression was examined by RT-PCR and immunoblotting. N-cadherin promoter regulation was analyzed using luciferase reporter and chromatin immunoprecipitation assays.

Kisspeptin signaling reduced NIH3T3 cell proliferation, migration, and invasion and activated SRF reporter activity through the KISS1R-Gaq/11-p63RhoGEF-RhoA pathway. In HRAS^G12V-expressing NIH3T3 cells, KISS1 reduced N-cadherin expression and suppressed anchorage-independent colony formation. HRAS^G12V increased N-cadherin promoter activity, whereas KISS1 reduced both basal and HRAS^G12V-induced promoter activation. Deletion of the SP1-responsive region abolished these effects, and chromatin immunoprecipitation showed reduced SP1 binding to the N-cadherin promoter. In vivo, KISS1 suppressed HRAS^G12V-induced tumor growth and pulmonary metastasis, and N-cadherin expression reversed these effects.

Kisspeptin signaling suppresses HRAS^G12V-induced tumor growth and metastasis in NIH3T3 cells by inhibiting SP1-dependent transcription of N-cadherin.

SUMOylation is implicated in the regulation of multiple malignancies. However, its potential roles in head and neck squamous cell carcinoma (HNSCC) remain insufficiently characterised. By integrating bulk RNA-seq, scRNA-seq and stRNA-seq datasets, we systematically interrogated the biological relevance of SUMOylation in HNSCC. Key markers from the signature were further validated using in vitro functional assays. A recognition model was established and validated using 692 HNSCC and 178 non-HNSCC samples. SROC analysis demonstrated robust performance across eight datasets (AUC = 0.92). Functional enrichment and scRNA-seq analyses indicated that SUMOylation may exert its effects in HNSCC primarily through cell-cycle regulation. Among the model features, SAE1 was markedly overexpressed in HNSCC (SMD = 1.07, 95% CI 0.56-1.59, p < 0.05). In vitro assays further confirmed that SAE1 enhanced proliferation, colony formation and migration in SAS and SCC-9 cells and validated its role in regulating cell cycle progression and apoptosis. We established a SUMOylation-related recognition model for HNSCC with consistently strong performance in multiple external validation cohorts. SAE1 emerges as a candidate molecular biomarker for HNSCC.

SWI/SNF chromatin remodelers are represented by three biochemically distinct subcomplexes, the abundant cBAF and the less abundant PBAF and GBAF. Genetics have identified important roles for PBAF in development and disease; however, relating PBAF-mediated phenotypes to biochemical function in chromatin regulation and gene activation has been challenging. Here, we show that the PBRM1 subunit of PBAF is critical for the completion of TGFβ1-mediated epithelial-mesenchymal transition (EMT) of mammary cells in vitro as well as the metastasis of murine breast cancers in vivo. Using epigenomics to profile different stages of EMT, we find that PBRM1 is necessary for targeting PBAF to inducible promoters marked by H3K14ac. We further find that PBRM1 facilitates DNA accessibility at sites bound by TGFβ1-inducible transcription factors, such as Atf3, for the induction of genes involved in migration, cell survival, and inflammation, providing evidence that PBAF is a vulnerability in late-stage metastatic cancers.

Growing evidence indicates that nuclear architecture is severely altered in many pathological contexts, primarily in cancer, with major implications for chromatin arrangement and, consequently, gene expression. Actin microfilaments located in the perinuclear region at the apical surface of cells, collectively known as the "perinuclear actin cap", integrate mechanical and biochemical cues from the cell membrane and translate them into compressive forces acting on the nuclear envelope, thereby modulating nuclear shape and size. In concert with well-established mechanotransduction paradigms, these highly dynamic and finely tuned stress fibers are emerging as key players in several biological processes - from cell migration to sensing of the surrounding microenvironment - with significant implications for development, genetic disorders and tumor progression. However, how classic pathogenetic mechanisms intersect with perinuclear actin remodeling remains mostly unknown. In this review, we will describe in detail the unique functional and structural features of perinuclear actin stress fibers and recapitulate current knowledge on their upstream regulation by membrane receptors signaling. Finally, we will explore how alterations of the perinuclear actin cap may contribute to different pathogenetic processes, with a particular focus on cancer progression and metastasis.