Peripheral blood immuno-inflammatory biomarkers (IIBs) may help predict response to neoadjuvant chemotherapy (NAC) and prognosis in HER2-positive breast cancer. This study compared the predictive value of neutrophil-to-lymphocyte ratio (NLR), monocyte-to-lymphocyte ratio (MLR), platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) for pathological complete response (pCR) and disease-free survival (DFS).

A total of 224 female patients with HER2-positive invasive breast cancer who received NAC followed by surgery at two medical centers (2015-2023) were retrospectively analyzed. Baseline IIBs were calculated from complete blood counts. Receiver operating characteristic (ROC) curves identified optimal cut-offs. Logistic and Cox regression analyses combined with the least absolute shrinkage and selection operator (LASSO) method were used to determine factors associated with pCR and DFS. Subgroup analyses were performed to assess consistency across clinical and treatment variables.

SII demonstrated the highest discriminatory ability among tested IIBs for predicting pCR (AUC = 0.739) and was significantly associated with longer DFS (P < 0.001). Patients with low SII had higher pCR rates and improved DFS. These associations remained stable across prespecified subgroups. Other factors related to better response included lower CA15-3/CEA levels, ≥6 NAC cycles, receipt of HER2-targeted therapy, and breast-conserving surgery.

Among common inflammatory indices, SII demonstrated the strongest association with treatment response and prognosis in HER2-positive breast cancer. As an inexpensive, readily available biomarker, it may assist clinical risk stratification. However, given the retrospective design and substantial heterogeneity in treatment regimens, these findings should be interpreted cautiously and validated in prospective studies.

OX40 (CD134/TNFRSF4), a costimulatory receptor of the TNF receptor superfamily ((TNFRSF), has emerged as a compelling immuno-oncology target given its capacity to amplify T-cell activation, sustain effector and memory responses, and remodel the tumor microenvironment (TME). This review provides a comprehensive synthesis of OX40 biology from molecular architecture to pathway-specific signaling programs, emphasizing its distinct yet interconnected roles across CD4⁺ T-cell subsets, CD8⁺ T cells, T follicular helper cells, and regulatory T cells (Tregs). We further summarize the landscape of OX40 expression across major solid tumors, highlighting its heterogeneous prognostic significance and the immune-contextual factors that determine therapeutic responsiveness. Although early-phase clinical studies of OX40 agonists have demonstrated favorable tolerability and robust pharmacodynamic activation, their antitumor efficacy either as monotherapy or in combination with PD-1/PD-L1 or CTLA-4 inhibitors has remained modest. Mechanistic barriers such as transient OX40 expression kinetics, Treg counteractivation, metabolic suppression, and insufficient FcγR-mediated crosslinking likely underlie this translational gap. Emerging bispecific antibody platforms and OX40-integrated combinatorial regimens offer renewed opportunities to overcome these limitations by enabling spatially controlled receptor clustering, TME-selective activation, and multi-pathway synergy. Future translational success will require refined dosing strategies, optimized antibody engineering, biomarker-guided patient selection, and integrated approaches that align OX40 activation with favorable immune dynamics in the TME.

Endometrial cancer (EC) is a heterogeneous and increasingly prevalent malignancy characterized by distinct molecular subgroups that exhibit fundamentally different immune profiles. These immunologic differences shape tumor-immune interactions, influence responsiveness to immunotherapy, and underscore the importance of biologically informed treatment strategies. As the clinical application of immune checkpoint inhibitors expands, understanding the mechanistic and translational landscape of immunotherapy in EC has become essential for guiding precision oncology.

We systematically retrieved 836 immunotherapy-related publications on EC from the Web of Science Core Collection (1999-2024) and conducted a scientometric analysis using VOSviewer and CiteSpace. Analyses included publication trends, country and institutional collaborations, author networks, and keyword clustering. Furthermore, we screened 391 clinical trials from ClinicalTrials.gov and ICTRP databases to assess the clinical research landscape.

Publication output and clinical trials on EC immunotherapy have shown a continuous upward trend over the past two decades. The United States and China emerged as leading contributors in both publications and pivotal clinical trials. Among the most frequently co-cited references, clinical studies account for a significant proportion, particularly those published in the last five years. The landscape reflects a shift toward immune checkpoint blockade and combination therapy strategies, with some clinical trials demonstrating promising efficacy.

Our integrated scientometric and clinical trial analysis reveals a rapid evolution in EC immunotherapy research, highlighting checkpoint blockade as a central therapeutic approach. The trend toward combination regimens underscores the translational potential of immunotherapy in EC and points toward emerging directions for future research and clinical application.

Mismatch repair deficiency (dMMR) and microsatellite instability (MSI-H) cancers exhibit high immunogenicity and are highly responsive to immune checkpoint inhibitors. In patients with locally advanced dMMR/MSI-H colorectal cancer (CRC), neoadjuvant immunotherapy (NIT) has demonstrated unprecedented pathological complete response (pCR) rates, suggesting nonoperative management strategies may be possible. There remains a discrepancy between radiological assessment and pathological responses to NIT in CRC.

We conducted a systematic review and meta-analysis of studies published between February 2015 and February 2025 to determine if radiological and pathological assessments following neoadjuvant immune checkpoint inhibitor therapy (NIT) were consistent in patients with non-metastatic dMMR/MSI-H CRC. Using PubMed, Embase, and Web of Science, the literature was retrieved, with inclusion criteria focusing on studies that reported both imaging data and pathological results. A random-effects model was used to calculate pooled odds ratios (ORs) and 95% confidence intervals (CIs). Subgroup analyses were conducted based on tumor location (colon versus rectum) and type of response (cCR versus pCR).

In 12 studies, 396 patients were included. A total rate of 59.6% discordance was found between radiological and pathological responses. Compared to rectal cancer patients (34.9%), colon cancer patients exhibited a significantly higher rate of discordance (64.2%). A total of 238 patients with confirmed pCR were incorrectly diagnosed as having residual disease on radiological assessment (OR = 61.41; 95% CI: 10.05-375.27;P < 0.00001). A high level of heterogeneity was observed across studies (I2 = 85%), but no publication bias was observed.

In dMMR/MSI-H CRC, radiologic assessment alone cannot reliably assess the efficacy of NIT, particularly in colon cancer. It should be integrated with additional modalities-such as endoscopic evaluation and biomarker analysis-to ensure an accurate appraisal of treatment efficacy.

Paragangliomas are rare neuroendocrine tumors arising from extra-adrenal paraganglionic cells, with an estimated annual incidence of 2-8 cases per million. Primary pulmonary paragangliomas are exceptionally uncommon and are frequently mistaken for more prevalent pulmonary diseases, leading to diagnostic delays and management challenges. We report the case of a 60-year-old woman who presented with diffuse, non-radiating left-sided chest pain, progressive dyspnea transitioning from Modified Medical Research Council (mMRC) grades 0 to I, and unintentional weight loss over a two-year period. Laboratory investigations were unremarkable. Imaging demonstrated a well-defined mass in the left upper zone on chest radiograph, and contrast-enhanced computed tomography (CT) revealed a smoothly marginated, heterogeneously enhancing soft tissue lesion in the left upper lobe. Bronchoscopic biopsy initially suggested a clear cell neoplasm; however, immunohistochemical analysis demonstrated findings consistent with paraganglioma. The absence of clinical features suggestive of hereditary syndromes supported the diagnosis of a sporadic, non-functional pulmonary paraganglioma. This case underscores the importance of considering paraganglioma in the differential diagnosis of pulmonary masses and highlights the critical diagnostic role of immunohistochemistry in distinguishing this rare entity from morphologically similar tumors.

Pulmonary pneumocytoma is a rare benign tumor most often detected incidentally as a solitary pulmonary nodule. Although its radiological appearance is nonspecific, its histological complexity can mimic several malignant neoplasms, leading to potential overtreatment. We report a case of a 40-year-old female with a suspicious pulmonary lesion discovered during the evaluation of an unrelated oropharyngeal carcinoma. Surgical resection and histopathological analysis confirmed the diagnosis of pneumocytoma. This case highlights the importance of considering pneumocytoma in the differential diagnosis of solitary pulmonary nodules, particularly in middle-aged female patients. Early multidisciplinary evaluation is essential to avoid unnecessary radical treatment.

Introduction Accurate differentiation of benign and malignant thyroid nodules is critical for appropriate management. Fine-needle aspiration cytology (FNAC), although valuable, has limitations, especially in follicular-patterned neoplasms. Galectin-3, a beta-galactoside-binding lectin involved in cell proliferation and apoptosis, has been proposed as a diagnostic immunohistochemical marker. This study evaluates the utility of galectin-3 in distinguishing malignant from non-malignant nodular thyroid lesions. Methods A prospective observational study was conducted on 56 female patients undergoing thyroidectomy. Histopathological evaluation categorized cases into the benign (n=25), borderline (n=6), and malignant (n=25) groups. Immunohistochemical staining for galectin-3 was performed on paraffin-embedded tissue sections. Positivity was defined by cytoplasmic and/or nuclear staining. Results Galectin-3 expression was observed in 66.7% (14/21) of malignant lesions, predominantly in classic papillary thyroid carcinoma. None of the benign or borderline cases exhibited galectin-3 positivity. Notably, other papillary carcinoma variants were also negative. Statistical analysis showed a significant correlation between galectin-3 expression and malignancy (p < 0.001). Conclusion Galectin-3 is a highly specific immunohistochemical marker for malignant thyroid lesions, particularly classic papillary thyroid carcinoma. Its absence in benign and borderline lesions highlights its diagnostic value. Incorporating galectin-3 into routine histopathological evaluation can improve diagnostic accuracy, especially in indeterminate or follicular-patterned thyroid neoplasms.

Melanoma is a highly metastatic skin cancer with occult early symptoms, making sensitive diagnostic tools essential for early intervention. Tyrosinase (TYR), a key enzyme in melanogenesis, is aberrantly secreted into the bloodstream by melanoma cells and thus serves as a promising biomarker for melanoma. However, the ultralow concentration of TYR in serum (0.066-0.636 U/L) poses a significant challenge to conventional detection methods, highlighting the need for more sensitive detection strategies.

An electrochemical biosensor was engineered using a screen-printed electrode (SPE) as the base. The SPE was modified with a nanocomposite consisting of tyramine-functionalized carboxylated multi-walled carbon nanotubes (MWCNTs-tyr), gold nanoparticles (Au NPs), and poly(3,4-ethylenedioxythiophene) (PEDOT). To validate the sensor's performance, differential pulse voltammetry (DPV) was employed, with tests conducted in phosphate-buffered saline (PBS, pH 7.0) and murine serum samples.

The MWCNTs-tyr/Au NPs/PEDOT nanocomposite synergistically enhanced the sensor's conductivity, catalytic activity, and TYR-specific binding capacity. The sensor exhibited a wide linear detection range for TYR (0.05~0.9 U/L, R² = 0.9914), and a low detection limit of 0.0091 U/L. Additionally, it showed excellent reproducibility (5 consistent measurements at a TYR concentration of 0.1 U/L) and high specificity against common serum interferents. In tumor-bearing mice, TYR serum levels were found to correlate with tumor progression: TYR concentration was 0.084 ± 0.009 U/L when tumor volume was 68 ± 5.25 mm³, and increased to 0.653 ± 0.028 U/L when tumor volume reached 1280 ± 89.22 mm³.

This study presents a proof-of-concept for a MWCNTs-tyr/Au/PEDOT/SPE biosensor. The platform enables rapid and sensitive detection of TYR in small-volume samples and effectively monitors tumor burden in a murine model, demonstrating its potential as a research tool for melanoma biomarker investigation.

Cancer therapy has long been constrained by challenges such as high recurrence rates, high metastasis rates, and damage to normal tissues, and conventional therapeutic approaches struggle to achieve a precise balance between efficacy and safety. The innovation of nanotechnology has brought breakthroughs to this field. As a typical class of zero-dimensional carbon-based nanomaterials, carbon dots (CDs) generally exhibit a size of less than 10 nm. Owing to their favorable biocompatibility and abundant surface functional groups, CDs offer a novel avenue for tumor therapy. This review systematically summarizes the various application strategies, mechanisms of action, and research progress of CDs in cancer therapy. First, it introduces two critical functions of CDs in tumor therapy: drug delivery and targeting. Subsequently, we delve into the applications of CDs in a series of anticancer strategies, including photodynamic therapy (PDT), photothermal therapy (PTT), chemodynamic therapy (CDT), sonodynamic therapy (SDT), gas therapy (GT), immunotherapy, gene therapy, and nanozyme-based therapy. Finally, the challenges faced by CDs in cancer therapy are summarized, and their future development directions are prospected, providing theoretical references and research ideas for the clinical translation of CD-based tumor therapeutic systems.

Consensus Molecular Subtype (CMS) 4 and BRAF mutations are poor prognostic indicators for colon adenocarcinoma (COAD). Although the prevalence of BRAF-mutated COAD is higher in the CMS1 subtype, we have identified certain cases of CMS4 subtypes in patients with BRAF mutations. However, there is currently a lack of research exploring whether this particular type of COAD exhibits a worse prognosis and unraveling its underlying mechanism.

This retrospective study analyzed the transcriptome profiles and clinical parameters of COAD patients from six public datasets. Kaplan-Meier plots and bioinformatics methods predicted the correlation between ATP23 expression and patient survival. We compared enriched pathways, genomic mutations, immune cell infiltration, copy number alterations, cell-cell communication, and TIDE scores between ATP23-high and ATP23-low groups. Furthermore, in vitro experiments verified the potential roles of ATP23 in COAD.

The expression of ATP23 was significantly lower in tumor tissues, particularly in the CMS4 subtype. No significant correlation was observed between ATP23 expression and clinical characteristics or molecular mutations in COAD. Higher ATP23 levels were associated with improved survival rates in COAD patients. In vitro experiments indicated that ATP23 inhibits the proliferation, migration, and invasion capabilities of COAD cells. Moreover, decreased ATP23 expression may impair oxidative phosphorylation in T cells, contributing to the formation of an immune-evasive microenvironment, and potentially leading to reduced efficacy of both immunotherapy and conventional chemotherapy.

ATP23 is a potential prognostic marker for COAD patients. Reduced ATP23 expression may inhibit oxidative phosphorylation in T cells and contribute to the formation of an immunosuppressive microenvironment.