This study evaluated the diagnostic performance of CDO1 and ZSCAN12 methylation in paired endometrial (Em) and exfoliated cervical (Cx) samples for detecting endometrial cancer (EC) and endometrial atypical hyperplasia (EAH).

Diethylnitrosamine (DEN) is a potent environmental carcinogen commonly found in cigarette smoke and polluted air, which is strongly associated with the initiation and progression of lung cancer through oxidative stress, inflammation, and dysregulated cell signaling. Alloimperatorin, a bioactive furanocoumarin compound isolated from Angelica dahurica, has demonstrated anti-inflammatory, antioxidant, and anticancer potential. The current study was designed to explore the chemoprotective effect of alloimperatorin against DEN-induced lung cancer in rats and explore the underlying signaling pathways.

To evaluate the cytotoxic efficacy and interaction dynamics of curcumin, morin, and phyllanthin - individually and in dual (C + M) and triple (C + M + P) combinations - in estrogen receptor-positive (MCF-7) and triple-negative (MDA-MB-231) breast cancer cell lines.

Hepatocellular carcinoma (HCC) is an aggressive malignancy with frequent recurrence and strong immune evasion. Programmed death ligand-1 (PD-L1) facilitates immune evasion by suppressing T-cell activity. Andrographolide (AD), a natural diterpenoid with anti-inflammatory, antiviral, and immunomodulatory properties, has demonstrated antitumor potential.

Breast cancer remains one of the most serious malignancies threatening women's health. Quercetin, a major active component found in various Chinese herbal medicines, has shown antitumor potential; however, its specific role and underlying mechanisms in breast cancer require systematic investigation. This study demonstrated through MTT, colony formation, wound healing, and Transwell assays that quercetin significantly inhibits the viability, proliferation, and migration capabilities of breast cancer cells. Transcriptome sequencing combined with biochemical assays, qPCR, and Western blot further indicated that quercetin can induce ferroptosis, which is likely the key mechanism underlying its suppression of malignant progression in breast cancer cells. Mechanistically, by promoting the binding between the E3 ubiquitin ligase NEDD4L and SLC7A11, quercetin induces the ubiquitin-proteasome degradation of SLC7A11, ultimately leading to ferroptosis. Notably, quercetin maintained a significant inhibitory effect even during the malignant transformation of breast cancer cells induced by heavy metal lead (Pb) exposure. Collectively, these findings suggest a potential mechanism by which quercetin may inhibits breast cancer progression through ferroptosis activation via the NEDD4L/SLC7A11 axis, offering preliminary evidence that could support its possible therapeutic application in breast cancer.

Early diagnosis and effective treatment of pancreatic cancer remain major clinical challenges, one of the most aggressive and lethal tumors. The tumor microenvironment (TME) in pancreatic cancer exhibits unique features, including high interstitial fluid pressure (IFP), abnormal blood vessels, hypoxia, acidosis, and excess reactive oxygen species (ROS), all favoring tumor progression and immunosuppression, meanwhile offsetting diagnostic efficiency and treatment efficacy. Thus, the TME of pancreatic cancer is considered as a target of profound theranostic significance. Nanoparticles (NPs) have shown a high profile in bio-imaging and targeted drug delivery. Here, we depicted the TME of pancreatic cancer and reviewed the designs and performances of TME-transforming NPs in the diagnosis and treatment of pancreatic cancer, as well as the obstacles to be overcome before their clinical translation. This review is expected to provide sparks for the early diagnosis and personalized treatment for pancreatic cancer.

The ubiquitin-proteasome system (UPS) plays a central role in regulating protein homeostasis and degradation. Its dysregulation is closely associated with various diseases, including cancer. S-phase kinase-associated protein 2 (SKP2) is a key E3 ubiquitin ligase component of the UPS. It induces proteasome-mediated protein degradation or modulates substrate function by conjugating K48-linked or K63-linked ubiquitin chains to diverse target proteins. Recent studies have shown that the overexpression of SKP2 in several cancer types is correlated with poor clinical outcomes, underscoring its potential as a therapeutic target. Notably, emerging evidence has expanded the functional repertoire of SKP2 beyond cell cycle control to encompass metabolism, DNA repair, stemness, tumor microenvironment (TME) and immunotherapy response, positioning it as an increasingly attractive target for intervention. In this review, the oncogenic properties of SKP2 and its underlying mechanisms were elucidated in multiple cancer types. Moreover, we systematically summarized future directions for SKP2-targeted therapy.

This study aimed to assess the efficacy and safety of integrating programmed death-1 (PD-1) inhibitors with chemoradiotherapy (CRT) in the treatment of locally advanced nasopharyngeal carcinoma (LA-NPC), explore the optimal sequencing of immunotherapy, and to compare the short-term efficacy of different combination regimens during the induction phase.

The aim of this study was to compare the efficiency of 2017 ACR-TIRADS and contrast-enhanced ultrasound (CEUS) in diagnosing malignant thyroid nodules, and propose a new classification system based on CEUS and 2017 ACR-TIRADS.

Triple-negative breast cancer (TNBC) is a highly aggressive subtype characterized by significant inter- and intra-tumoral heterogeneity. Its varied response to radiotherapy limits clinical outcomes, yet the underlying molecular determinants remain poorly understood.

Delta-like ligand 3 (DLL3) is the first tumor cell surface antigen in small cell lung cancer (SCLC) to support an approved T-cell-redirecting therapy with demonstrated survival benefit, namely the DLL3×CD3 bispecific T-cell engager tarlatamab. DLL3-directed agents are usually surveyed by platform. Here, we argue instead that DLL3 is best understood not as a static surface target but as the surface readout of a plastic, ASCL1-associated neuroendocrine lineage state. DLL3-directed immune redirection works by holding two intrinsically unstable systems in transient alignment: a lineage-defined antigen state on the tumor side and an activatable but exhaustible T cell effector system on the host side. This framework helps explain why the same antigen has produced different clinical outcomes across therapeutic platforms. The failure of rovalpituzumab tesirine does not establish that DLL3 is intrinsically unsuitable for payload delivery; rather, it highlights the construct-specific challenge of achieving a sufficient therapeutic index with a PBD-based antibody-drug conjugate. Tarlatamab clinically validates a distinct use of DLL3-as a surface recognition tag for T-cell redirection-while leaving open the possibility that redesigned DLL3-directed antibody-drug conjugates may succeed. That recruitment makes therapeutic success contingent on a host effector system the drug does not fully control, and resistance correspondingly emerges along two axes. In antigen-side escape, therapeutic pressure may select for, or in some contexts drive, a DLL3-low or non-neuroendocrine state. In execution-side escape, pre-existing T-cell dysfunction may limit primary efficacy, whereas repeated redirected activation may deepen exhaustion within a suppressive niche. The lineage-defined vulnerability that the therapy exploits can thus double as the route of escape. We propose that next-generation strategies should be organized by the axis they are designed to preserve, and that the operative clinical question should shift from baseline DLL3 positivity toward the durability of antigen availability and effector function.

A new type of regulated cell death known as Necrosis by Sodium Overload (NECSO) has been discovered recently. There is growing evidence indicating that NECSO is essential in both anti-tumor immune responses and the proliferation of cancer cells. Nonetheless, the underlying mechanisms and clinical relevance of NECSO are still not well understood, especially regarding its prognostic significance in kidney renal clear cell carcinoma (KIRC).

Radiotherapy r5emains a cornerstone of treatment for localized and locally advanced prostate cancer, yet substantial heterogeneity persists in oncological outcomes and treatment-related toxicity. Increasing evidence suggests that systemic inflammation, immune microenvironment characteristics, and tumor-specific molecular features contribute to these variations and may provide clinically relevant biomarkers. This narrative review summarizes current evidence regarding immunological and inflammatory biomarkers in prostate cancer treated with radiotherapy, focusing on their biological rationale, prognostic significance, predictive potential, and clinical applicability. Circulating biomarkers, including neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, C-reactive protein, fibrinogen, and cytokines such as IL-6 and TGF-β1, have been associated with oncological outcomes and toxicity in several studies. However, their interpretation remains limited by biological nonspecificity, methodological heterogeneity, variable cutoff definitions, and lack of prospective validation. Within the tumor microenvironment, immune cell populations, including CD8+ tumor-infiltrating lymphocytes, regulatory T cells, CD163+ macrophages, and immune checkpoint molecules, provide insights into tumor-immune interactions and radiotherapy-induced immune modulation. Emerging biomarkers such as extracellular vesicles, circulating tumor DNA, circulating tumor cells, and microRNAs offer promising opportunities for disease monitoring and treatment adaptation, although most evidence remains preliminary, particularly in localized disease. In contrast, genomic classifiers such as Decipher, Prolaris, and OncotypeDX currently represent the most clinically mature biomarker platforms for risk stratification and treatment decision support. Although several biomarkers demonstrate biological plausibility and prognostic value, few have sufficient clinical validation to guide routine radiotherapy decision-making. Future multicenter prospective studies, standardized biomarker assessment protocols, and integrated approaches combining clinical, imaging, molecular, and immune data are required to enable clinically actionable precision radiotherapy strategies.

Previous studies have shown that locoregional therapy combined with systemic treatment provides survival benefits with manageable safety in patients with intermediate-to-advanced large hepatocellular carcinoma (HCC). However, the optimal treatment strategy for HCC beyond the up-to-7 criteria remains unclear because of the high tumor burden and recurrence risk. This study aimed to evaluate the efficacy and safety of transarterial chemoembolization (TACE) plus microwave ablation (MWA) followed by targeted immunotherapy in patients with HCC beyond the up-to-7 criteria.

The study aimed to evaluate the efficacy and safety of intensity-modulated radiotherapy (IMRT) combined with immunotherapy and targeted therapy (IT) in hepatocellular carcinoma (HCC) patients with portal vein tumor thrombus (PVTT) classification I-IV.

This study aimed to evaluate the efficacy of a single-test, targeted DNA next-generation sequencing (NGS) panel in classifying endometrial carcinoma (EC) into molecular subtypes and to compare its performance with that of the established Sanger sequencing + immunohistochemistry (Sanger + IHC) molecular classification.

The contribution of the microbiome to sporadic colorectal cancer (CRC) has traditionally been interpreted through the detection of individual tumor-enriched taxa or isolated virulence factors. However, accumulating evidence indicates that CRC-associated microorganisms often act as structured polymicrobial consortia rather than as independent agents. This review proposes an expanded ecological framework for understanding the role of oral taxa in colorectal carcinogenesis. Oral bacteria, including genera Fusobacterium, Parvimonas, Peptostreptococcus, Porphyromonas, Prevotella, Streptococcus, and related taxa, may translocate to the colorectal niche through enteral or hematogenous routes and establish tumor-associated communities that partially recapitulate the structural organization and succession patterns of oral biofilms. Within these communities, Fusobacterium nucleatum serves as the primary bridging organism, facilitating interspecies adhesion and spatial organization. Parvimonas micra, Porphyromonas gingivalis, and Candida albicans display potential bridging structural and functional properties, with their roles in cooperative pathogenicity and tumor progression supported by substantial experimental evidence. We integrate three complementary conceptual frameworks: oral microbial complexes (gut co-abundance groups), bridging organisms and the extended driver-passenger model of CRC. This synthesis supports a shift from taxonomy-centered interpretation toward a functional virulome-based view, in which the role of a taxon is defined by its ecological position, interaction network, and virulence determinants. Key oral virulence factors contribute to biofilm formation, epithelial adhesion and invasion, barrier disruption, immune evasion, inflammatory modulation, metabolic remodeling of the tumor microenvironment, and metastatic potential. Because the composition of translocated oral consortia changes gradually within the colorectal niche, successive consortium members and their associated virulence determinants may serve as indirect microbial signatures of CRC progression. Recognizing CRC-associated oral communities as structured, interactive ecosystems has important diagnostic and therapeutic implications. Simultaneous detection of pathobionts, their cooperative clusters, and functionally relevant virulence determinants may improve microbiome-based risk stratification. Moreover, targeted disruption of bridging functions, interspecies interactions, or virulence factor activity may offer a precision strategy to weaken carcinogenic consortia without broad, dysbiosis-promoting antimicrobial pressure.

In this study, we used Mendelian randomization analysis to explore the causal relationships between drug targets and cutaneous melanoma (CM) and subsequently screened for new drug targets for CM. In addition, we verified whether targeted drugs could inhibit the development of CM in CM cells by suppressing the expression of target genes.

This study aims to elucidate the mechanism through which prostate cancer-associated transcript 6 (PCAT6) modulates immune escape in triple-negative breast cancer (TNBC), focusing on its interaction with IGF2BP1 and PD-L1.

To analyze epidemiological trends and diagnostic approaches for parotid gland tumors (PGTs) from 2010 to 2024 and predict future trends.