High-grade serous ovarian carcinoma (HGSC) demonstrates poor prognosis with approximately 80% recurrence rates and significant chemotherapy resistance. Conventional checkpoint inhibitors show limited efficacy (10-15%), necessitating alternative immunotherapeutic approaches. Engineered T lymphocytes, particularly CAR-T and TCR-T cells, have emerged as promising strategies for HGSC. This literature review examines the promising role of engineered T lymphocytes in immunotherapy for HGSC. A comprehensive literature search was conducted across PubMed, Scopus, and Cochrane Library databases for peer-reviewed studies published between 2015 and 2025. Search terms included "engineered T lymphocytes," "CAR-T cells," "TCR-T cells," "ovarian cancer immunotherapy". CAR-T cells demonstrate promising preclinical antitumor activity in HGSC, with high-avidity T-cell clones showing robust efficacy. Engineered T lymphocytes demonstrate promising approaches across disease contexts. In high-grade serous ovarian carcinoma, Engineered T lymphocytes orchestrate tumor cell apoptosis through coordinated granzyme/perforin and Fas/FasL signaling, enabling rapid cytotoxic elimination of multiple tumor targets.

Natural killer (NK) cells are vital for anti-tumor immunity, yet their effector functions are frequently constrained within the tumor microenvironment. Integrin β3 (ITGB3) has been implicated in breast cancer progression and stemness, but whether ITGB3 expression in malignant cells influences NK cell states and contributes to immune evasion remains unclear.

Single-cell RNA sequencing data were utilized to profile the transcriptomic and metabolic divergence of NK cells between ITGB3⁺ and ITGB3⁻ tumor microenvironments. Cell-cell communication and pseudotime trajectory analyses were performed to identify key signaling axes. The SCIPAC framework was employed to map single-cell subsets to the bulk TCGA-BRCA cohort for clinical correlation. The mechanistic findings were validated through in vitro co-culture assays and NKG2A blocking experiments using MDA-MB-231 and BT-474 cell lines.

NK cells associated with ITGB3⁺ tumor microenvironments displayed enhanced cytotoxic and inflammatory transcriptional programs, together with metabolic remodeling and stronger clinical associations with advanced TNM stages. Cell-cell communication analysis revealed intensified predicted interactions between ITGB3⁺ malignant cells and NK cells, with enrichment of MHC-I-related signaling and HLA-E-KLRC1/KLRC2 interactions. KLRC1 encodes the inhibitory receptor NKG2A, whereas KLRC2 encodes the activating receptor NKG2C. Therefore, these inferred interactions do not by themselves define the net functional direction of HLA-E signaling. Although KLRC2 was transcriptionally enriched in NK cells from the ITGB3⁺ tumor microenvironment, NKG2A blockade reversed ITGB3-associated suppression of NK-derived IFN-γ secretion, supporting a functional contribution of the inhibitory NKG2A branch.

ITGB3 expression in malignant cells is associated with a primed but functionally constrained NK cell state in breast cancer. Increased malignant-cell HLA-E expression and restoration of IFN-γ production following NKG2A blockade support a functional contribution of the inhibitory NKG2A branch, without excluding concurrent activating signaling through NKG2C.

Right-hemisphere gliomas have traditionally been regarded as less eloquent than left-sided lesions, influencing surgical decision-making and anesthetic approach. However, these tumors produce diverse non-motor manifestations affecting cognition, behavior, and socio-emotional functioning with important consequences for quality of life. This review aimed to characterize these manifestations and their implications for functional eloquence.

Following PRISMA guidelines, PubMed, Scopus, and Embase were searched using predefined terms for right-hemisphere gliomas and their manifestations. Eligible studies included patients with supratentorial right-hemisphere gliomas reporting motor and/or non-motor clinical manifestations. Studies were excluded if the clinical presentation was incompletely described or if glioma pathology lacked histopathological confirmation. Extracted data included tumor location, histopathology, clinical manifestations, neuropsychological assessments, and functional outcomes.

A total of 372 patients from 88 studies were included. Median age was 42 years (range, 11-87), with slight male predominance (49% vs. 48% female). Preoperative non-motor manifestations were common and heterogeneous, most frequently compromising cognition and executive performance (43%), followed by vision and visuospatial deficits (28.4%) and language deficits (24%). Postoperatively, the most common deficits involved language (46%), followed by vision and visuospatial deficits (40%), and cognition and executive dysfunction (23.1%). Analyses relating extent of resection to postoperative deficits were considered exploratory because reporting of extent of resection and postoperative outcome assessment were incomplete and heterogeneous.

Right-hemisphere gliomas carry a substantial and under-recognized burden of non-motor manifestations that challenge conventional definitions of functional eloquence and support the expansion of functional assessment and surgical planning encompassing right-hemisphere cognitive and behavioral networks.

β-Lapachone exhibits potent anticancer activity although its clinical application remains limited by toxicity and mechanisms of resistance. Therefore, structural modifications have been explored to improve its pharmacological profile. This study evaluated the cytotoxic, genotoxic, and toxicological effects of the oxime derivative β-lapachone oxime (Oxβ-Lp), together with its predicted pharmacokinetic properties and potential molecular interactions. Oxβ-Lp displayed cytotoxic activity against all tested cancer cell lines (NCI-H460, PC9, K562, and HepG2) after 72 h of exposure, with the greatest potency and selectivity observed in NCI-H460 non-small cell lung cancer cells (IC₅₀ = 1.88 µM; SI = 13.1). Mechanistic analyses demonstrated reduced cell viability, mitochondrial membrane depolarization, DNA damage, and induction of apoptosis, without significant cell cycle arrest. In Allium cepa, Oxβ-Lp did not alter the mitotic index or induce micronucleus formation but promoted chromosomal aberrations and DNA strand breaks. The Artemia salina assay indicated high acute toxicity (LC₅₀ = 16.80 µg/mL). Molecular docking suggested a potential interaction between Oxβ-Lp and NQO1, with binding energies comparable to those of dicoumarol and similar interaction patterns within the catalytic site. Overall, these findings demonstrate that Oxβ-Lp exhibits selective cytotoxicity against NCI-H460 cells and promotes apoptosis associated with mitochondrial dysfunction and DNA damage. Although the molecular mechanisms underlying its biological activity require further investigation, Oxβ-Lp represents a promising scaffold for developing novel anticancer agents.

Colorectal cancer ranks among the most common malignancies worldwide. Rectal serrated lesions represent a significant precancerous condition, accounting for approximately 30% of sporadic colorectal carcinomas. Their flat morphology and indistinct borders often lead to missed detection during routine colonoscopy. In addition, the complex classification system and considerable molecular heterogeneity of these lesions create challenges for clinical management, including diagnostic accuracy, risk stratification, and treatment decisions. Research in recent years has progressively clarified the unique oncogenic pathway associated with serrated lesions-referred to as the serrated pathway. Characteristic molecular events include mutations in b-raf murine sarcoma viral oncogene homolog B (BRAF) or kirsten rat sarcoma viral proto-oncogene (KRAS) mutations, CpG island methylator phenotype (CIMP), and microsatellite instability (MSI). Among these, the BRAF V600E mutation serves as the core driver event. Combination therapy with encorafenib and cetuximab, which targets this mutation, has been shown to improve outcomes in patients with BRAF-mutated metastatic colorectal cancer. Furthermore, Microsatellite Instability-High (MSI-H) lesions exhibit sensitivity to immune checkpoint inhibitors, offering novel options for personalized treatment. Concurrently, the application of technologies such as artificial intelligence (AI)-assisted endoscopy, molecular imaging, and liquid biopsy holds promise for improving the detection of early-stage lesions. This systematic review examines the current research landscape regarding rectal serrated lesions, covering an evolution of classification systems, elucidation of molecular and cellular mechanism, advances in diagnostic technology, and optimized treatment strategies. We further discussed molecular differences between the serrated pathway and the classical adenoma-carcinoma sequence, epigenetic regulatory mechanisms, tumour microenvironment characteristics, and personalized management strategies based on molecular subtyping. By synthesizing existing evidence, this review aims to provide theoretical guidance for the clinical management of rectal serrated lesions and lay the groundwork for future research.

Pancreatic ductal adenocarcinoma, which accounts for more than 90% of pancreatic cancer cases, remains one of the deadliest malignancies worldwide, with a poor 5-year survival rate of approximately 10-13% despite advances in diagnosis and treatment. Its poor prognosis is attributed to aggressive biological behavior, extensive desmoplastic stroma, profound metabolic reprogramming, and resistance to conventional therapeutic interventions. Among the hallmark metabolic alterations in PDAC, the Warburg effect enables tumor cells to sustain rapid proliferation under hypoxic and nutrient-deprived conditions. Excessive lactate accumulation within the tumor microenvironment promotes extracellular acidification, suppresses cytotoxic T-cell activity, enhances regulatory T-cell expansion, and stimulates cancer-associated fibroblast signaling, thereby facilitating immune evasion and tumour progression. Key mediators of this metabolic rewiring include glucose transporters, lactate dehydrogenase A, and monocarboxylate transporters. Consequently, integrating immunometabolic insights into therapeutic strategies has emerged as a promising approach for PDAC management. Natural compounds such as quercetin, resveratrol, curcumin, anthraquinones, and camphene have shown potential to modulate glycolytic enzymes, inhibit lactate transport, and attenuate TME-associated immunosuppression. These bioactive molecules, therefore, represent promising candidates for combination-based therapeutic interventions in PDAC. This review summarizes the molecular mechanisms underlying glucose metabolic rewiring, lactate-mediated immune evasion, and the translational potential of natural compounds as immunometabolic modulators. By highlighting the intricate interplay among glucose metabolism, lactate-driven immunosuppression, and tumor microenvironment remodeling, this review provides a mechanistic framework for the development of natural compound-based therapeutic strategies. It identifies promising directions for future preclinical and clinical investigations in PDAC.

The laminin α3 chain, encoded by LAMA3, constitutes a principal component of laminin-332 (LN-332), an essential extracellular matrix (ECM) glycoprotein governing cell adhesion, proliferation, and tissue homeostasis. This systematic review consolidates current evidence on the molecular features and regulatory mechanisms of LAMA3, including its roles in PI3K/Akt, epithelial-mesenchymal transition (EMT), and Hippo-YAP signaling, as well as epigenetic and post-transcriptional modulation. Its context-dependent functions across distinct pathological states are delineated. In malignancies, including colorectal and ovarian cancers, LAMA3 functions as an oncogenic determinant that enhances invasion, metastatic dissemination, and chemotherapeutic resistance. In contrast, in hereditary diseases such as junctional epidermolysis bullosa (JEB) and chronic disorders such as idiopathic pulmonary fibrosis (IPF), LAMA3 deficiency or dysfunction constitutes a structural basis of tissue pathology. From a translational standpoint, elevated LAMA3 expression has been recognized as an independent prognostic indicator in pancreatic ductal adenocarcinoma, whereas LAMA3 promoter methylation is a candidate biomarker for platinum resistance in ovarian cancer. LAMA3-directed gene therapy for JEB has progressed to clinical evaluation. Current limitations in the field are critically examined, and emerging therapeutic approaches, including proteolysis-targeting chimeras (PROTACs), are discussed. Collectively, an integrated framework that connects LAMA3 biology with clinical applications is presented to inform future investigations and precision therapeutic strategies targeting this multifunctional molecule.

To investigate the mechanism of artemisinin liposomes regulating breast cancer metastasis and apoptosis through TIGIT/CD155 signal axis. Artemisinin liposomes were synthesized by thin film dispersion method and characterized in morphology, zeta potential, hydrodynamic size, entrapment efficiency as well as thermal stability. Furthermore, the cytotoxic effects of artemisinin liposomes on HC11 and 4T1 cell was evaluated by the MTS test. Scratch, transwell and colony formation experiment were conducted to assess the effect of artemisinin liposomes on cell metastasis. Apoptosis, cell cycle arrest were measured using flowcytometry. Meanwhile, bioinformatics analysis was used to investigate the relationship between TIGIT as a drug target for breast cancer and artemisinin liposomes, TIGIT/CD155 signal axis. Additionally, the mouse tumor model(group(saline, artemisinin, liposomes, artemisinin liposomes), dose(100 mg/kg/d)) was employed to detect the tumor-suppressive efficacy. Finally, the expression levels of Src, Akt, Mtor and Stat3 was further explored by Western Blot and RT-PCR to elucidate the regulatory mechanism of artemisinin liposomes on the TIGIT/CD155 signaling axis. The liposomes and artemisinin liposomes had average sizes of approximately 80 nm and 130 nm respectively, with a polydispersity index (PDI) of 0.225, 0.287. Artemisinin was effectively encapsulated within liposomes, as shown by the high encapsulation efficiency of 90.11% ± 0.88, with a cumulative release rate of 32.8% at pH = 5.5. In vitro studies demonstrated that artemisinin liposomes possessed significantly greater cytotoxicity against 4T1 cells, the IC₅₀ values were approximately 480 µM. In contrast to artemisinin alone, artemisinin liposomes can effectively inhibit 4T1 cell metastasis, with an inhibition rate of 93.02% at 20 µM, and also promote cell apoptosis, with an apoptosis rate of 14.17% at 20 µM. Bioinformatic analysis demonstrated that TIGIT/CD155 signal axis was highly expressed in breast cancer and had poor prognosis. In vivo results revealed that artemisinin liposomes alone produced an anti-tumor effect comparable to the combination of TIGIT/CD155 and IL-15. Ultimately, artemisinin liposomes can regulate breast cancer progression by modulating the TIGIT/CD155 signaling axis and critical factors in the SRC pathway, specifically SRC, AKT, STAT3, and mTOR. The clinical treatment of breast cancer does not rely on the use of chemotherapy drugs alone, but selects the effective ingredients of Chinese medicine with higher safety.

This paper discusses an EWSR1-SMAD3-rearranged fibroblastic tumor (ESFT) occurring in the wrist of a 5-year-old child and summarizes its clinicopathological features, immunohistochemical phenotype, and molecular characteristics to improve the accuracy of clinical diagnosis. A retrospective analysis was performed on the clinical manifestations, histopathology, immunohistochemical phenotype, and molecular characteristics of a 5-year-old patient with recurrent ESFT. Additionally, this paper presents a literature review of relevant studies on ESFT. Among the 21 cases of ESFT, including the present case, the disease primarily affects young and middle-aged adult females, with most tumors measuring 1-2 cm in diameter. It preferentially occurs in the soft tissues of the distal extremities-particularly the foot-and exhibits low-grade invasiveness. Histomorphologically, the tumor is composed of uniform spindle-shaped fibroblasts arranged in fascicular and interlacing patterns, with no prominent nucleoli or mitotic figures. A zonation pattern, focal microcalcification, and interstitial myxoid change are observed in some cases. Immunohistochemistry reveals diffuse, strong ERG expression in tumor cells; FISH molecular detection shows EWSR1 break-apart; and NGS results confirm EWSR1-SMAD3 rearrangement. ESFT is a benign neoplasm with a risk of local recurrence. It exhibits complex histomorphological features but demonstrates diffuse, strong immunoreactivity for ERG on immunohistochemistry and harbors characteristic genetic alterations.

Volatile organic compounds (VOCs) in human biofluids are promising non-invasive cancer biomarkers. However, their potential in urological cancers, including prostate, bladder, and kidney cancers is less explored, and the relationships between urinary and cellular VOC profiles across these cancer types remain unclear.

This systematic review aimed to evaluate gas chromatography-mass spectrometry (GC-MS)-based untargeted volatolomics studies in urological cancers to investigate cancer-specific, cross-cancer, and cross-matrix (urine vs. cell culture media) VOC biomarkers, while assessing methodological factors influencing biomarker discovery.

Published urinary and cellular VOC studies in prostate, bladder, and kidney cancers were systematically reviewed. VOC biomarkers, direction of change, diagnostic performance, sampling methods, analytical platforms, compound-identification strategies, and statistical approaches were extracted and compared across cancer types and sample matrices.

A total of 12 urinary prostate, 9 urinary bladder, 5 urinary renal, and 3 cellular VOC studies were identified. Prostate cancer profiles were mainly characterized by decreased organic acids and alcohols, whereas bladder and renal cancers more frequently showed elevated ketones and aldehydes. Several VOCs, including 2-butanone, 2-heptanone, hexanal and phenol, were identified across multiple cancer types. Cellular studies showed consistent directional changes for six VOCs, and cross-matrix analysis identified 28 shared VOCs, seven of which showed aligned trends in urine and cell models. These findings suggest that VOCs reflect both unique and shared metabolic alterations in urological cancers and may serve as useful diagnostic biomarker candidates.

This review integrates urinary and cellular VOC data across major urological cancers and identifies unique, recurrent, and cross-matrix VOCs that warrant further mechanistic and clinical validation. Although methodological heterogeneity remains a challenge, VOC-based approaches have generally shown good sensitivity and specificity for distinguishing malignant from healthy controls. With improved and standardized analytical methods, VOC volatolomics may support the future development of non-invasive and accurate diagnostics for urological cancers.