Pulmonary alveolar proteinosis (PAP) is a rare condition characterised by impaired alveolar macrophage-mediated surfactant clearance, resulting in the accumulation of lipoproteinaceous material within the alveoli. Secondary PAP has been associated with certain medications. Ruxolitinib, a Janus kinase 1/2 inhibitor has recently been implicated in rare cases of PAP.We report the case of a woman in her early 60s treated with ruxolitinib for chronic pulmonary graft-versus-host disease following an allogeneic haematopoietic stem cell transplant for acute lymphoblastic leukaemia, who developed progressive exertional dyspnoea. High-resolution CT demonstrated a 'crazy paving' pattern, and bronchoalveolar lavage revealed periodic acid-Schiff positive granular material consistent with PAP. Microbiological studies were negative. Ruxolitinib was discontinued with subsequent symptomatic, radiological and lung function improvement.This case highlights ruxolitinib as a potential cause of secondary PAP and emphasises the importance of considering this rare complication in patients who develop new respiratory symptoms while receiving ruxolitinib.

Chimeric antigen receptor (CAR) macrophage therapy shows significant potential for solid tumors owing to the intrinsic tumor infiltration and phagocytic capacity of macrophages. However, its clinical translation is limited by macrophage phenotypic plasticity within the immunosuppressive tumor microenvironment and the complexity of ex vivo cell manufacturing. It is essential to develop techniques that enable macrophages to be activated specifically by antigens while sustaining their proinflammatory activity in vivo.

Here, we report a mannose-modified lipid nanoparticle (LNP) platform for the co-delivery of CAR-encoding messenger RNA (mRNA) and the Toll-like receptor (TLR) 7/8 agonist resiquimod (R848), enabling in situ generation of proinflammatory CAR macrophages. In vitro, we assessed macrophage-preferential uptake, CAR expression efficiency, TLR7/8 agonist-mediated macrophage polarization, and immune activation. In vivo efficacy was assessed in syngeneic and humanized mouse models of triple-negative breast cancer, including postoperative recurrence and lung metastasis models.

Systemic administration of M-LNP/CAR+R848 induced robust CAR expression in tumor-associated macrophages and promoted sustained M1 polarization. Engineered macrophages exhibited enhanced antigen-specific phagocytic activity and tumor cell clearance, and promoted CD8+ T cell proliferation and NK cell infiltration, thus coordinating innate and adaptive immune responses. Functional macrophage depletion experiments demonstrated that tumor control was dependent on macrophages. In vivo treatment significantly reduced the growth of primary tumors, prevented postoperative recurrence, and prolonged survival in mice with lung metastases in both syngeneic and humanized models.

Our findings demonstrate that M-LNPs enabling co-delivery of mRNA and an innate immune agonist enable in situ generation of proinflammatory CAR macrophages and induce durable antitumor immunity. This controllable and non-integrative strategy allows tunable immune activation, provides a flexible platform for CAR macrophage-based immunotherapy in triple-negative breast cancer.

The peritumoral microenvironment has emerged as a key role in affecting tumor invasion and immunotherapy responses. In adipose-enriched tumors, such as breast cancer (BC), peritumoral adipose tissue (PA) harbors unconventional immune populations, yet its immunological functions remain poorly understood. In particular, how adipocyte regulate innate-like lymphocytes, such as γδ T cells, remains unclear.

We performed single-cell RNA sequencing and spatial profiling of paired specimens from patients with BC. Integrated multi-omics analyses, immunofluorescence staining, human γδ T-cell expansion assays, functional assays, and in vivo models were used to define the immune cell states and evaluate the impact of lipid mediator leukotriene B4 (LTB4) on γδ T-cell activation and signaling. Clinical correlations were assessed using our cohort and patient datasets.

We identified a previously unrecognized population of NKG2A⁺γδ T cells with predominant Vδ2 usage that preferentially accumulated in PA, particularly at the adipose-tumor interface. Multi-omics analyses revealed that they exhibited potent cytotoxic activity and extensive interactions with dendritic cells, coordinating a local immune surveillance network. Mechanistically, peritumoral adipocytes showed enhanced activation of the 5-lipoxygenase pathway and secreted the lipid mediator LTB4, which selectively combined to LTB4 receptors, thereby activating STAT1 signaling in γδ T cells and upregulating NKG2A expression. NKG2A⁺γδ T cells were preferentially enriched in ductal carcinoma in situ and early-stage BC. These cells were also associated with favorable clinical outcomes across multiple adipose-enriched tumors. Assays using human specimens confirmed that LTB4 potentiated γδ T cell-mediated antitumor responses. Importantly, LTB4-programmed γδ T cells displayed superior killing capacity using in vitro and in vivo assays.

These findings redefine PA as an active immunological niche that programs γδ T-cell immunity through adipocyte-derived LTB4 signaling. Our study identifies NKG2A⁺γδ T cells as cytotoxic sentinels at the adipose-tumor interface during early tumor development, providing a rationale for leveraging LTB4-mediated γδ T-cell programming in translational cancer immunotherapy.

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.