Therapeutic antibodies are widely used in cancer biotherapy due to their target specificity, mediating tumor cell inhibition, angiogenesis suppression, and immune modulation. However, systemic administration often leads to off-target effects, as many antibody targets are also expressed in normal tissues, limiting intratumoral drug concentration and causing adverse events. Oncolytic viruses (OVs), which selectively infect and lyse tumor cells while activating host anti-tumor immunity, offer a promising platform for localized antibody delivery. Their inherent tumor tropism, intratumoral administration, and high genetic manipulability enable the engineering of OVs to express exogenous antibodies within the tumor microenvironment, enhancing therapeutic specificity and synergizing oncolytic and immune-mediated effects. In this review, we summarize the biological properties of OVs, strategies for engineering antibody payloads, the mechanistic interplay between OV-induced oncolysis and immune modulation, and current challenges and opportunities for clinical translation. By integrating these aspects, we provide insights into optimizing OV-based antibody therapies for enhanced tumor-targeted efficacy and reduced systemic toxicity.

Natural killer (NK) cells are core components of innate antitumor immunity, the dysfunction of NK cells in the tumor microenvironment is a major obstacle to the antitumor efficacy. Runt-related transcription factor 3 (RUNX3) acts as a critical tumor suppressor and regulates immune cell function, while its biological role in NK cells remains largely unexplored. Herein, we investigated the interaction between RUNX3 and NK cells in tumor microenvironment.

The Cancer Genome Atlas (TCGA) database was utilized to determine the genetic alteration of RUNX3 in pan-cancer. TIMER and GEPIA website were used to evaluate the correlation between RUNX3 and immune cell infiltration. Single-cell RNA sequencing (scRNA-seq) analysis was applied to characterize RUNX3 expression and pseudotime trajectory in NK cells. In vitro experiments were further performed to validate RUNX3's role in regulating NK cell functions.

RUNX3 was significantly downregulated in lung adenocarcinoma and hepatocellular carcinoma tissues. Clinical analyses have demonstrated that defective RUNX3 expression was correlated with adverse prognosis. Immune infiltration analyses revealed that RUNX3 was positively associated with immune cell infiltration, particularly NK cells and CD8⁺ T cells. scRNA-seq indicated RUNX3 enrichment in intratumoral NK cells, and differential genes of RUNX3 were enriched in the MAPK signaling pathway. Pseudotime trajectory analysis indicated RUNX3 participated in NK cell differentiation. Moreover, RUNX3 overexpression enhanced NK cell viability, chemotactic capacity, cytotoxicity against tumor cells, and secretion of pro-inflammatory cytokines and granzyme B, while upregulating NK cell activation receptors.

Our findings identify RUNX3 as a key regulator of NK cell-mediated antitumor immunity in LUAD and LIHC, providing a novel molecular target for enhancing innate immune surveillance and developing targeted immunotherapies for the aggressive malignancies.

Solitary fibrous tumors (SFTs) were initially perceived as benign, pleural-based neoplasms but have since been recognized for their potential for local recurrence and distant metastasis, occurring across various anatomical sites. This manuscript delves into the clinicopathological characteristics, treatment outcomes, and follow-up data of patients with SFTs treated at our institution.

A retrospective review was conducted on patient charts diagnosed with and treated for extra-pleural SFT at our institute between 2006 and 2017. Data encompassing clinical presentations, diagnostic imaging, therapeutic interventions, histopathological findings, and follow-up details were extracted from electronic case records.

Eight patients (four males, four females) with SFT were included. Tumor sizes ranged from 2 cm to 17 cm, with a mean of 9.6 cm. Locations varied, with tumors found in soft tissues and bones. Surgical resection was performed on all patients, with varying outcomes. Five patients remained disease-free during follow-up, while others experienced relapse and metastasis.

Historically considered benign, SFTs exhibit variable clinical courses, with local recurrence and distant metastasis reported in a subset of cases. The advent of IHC has improved diagnostic accuracy, revealing characteristic markers such as CD34 and STAT6 positivity. Predicting malignancy remains challenging, necessitating comprehensive histopathological assessment. Surgical resection remains the primary treatment for SFTs, although the roles of adjuvant therapies such as chemotherapy and radiation therapy remain uncertain. The unpredictable nature of SFTs underscores the importance of prolonged follow-up and further research into their molecular biology to develop more effective treatment strategies.

Breast cancer has surpassed lung cancer as the most diagnosed cancer globally. This retrospective audit, conducted in Eastern India, aimed to evaluate the clinicopathological profile and 5-year survival outcomes of 584 non-metastatic invasive breast cancer patients treated with curative intent between June 2016 and May 2023.

Clinical and pathological data were analyzed, and patients underwent various treatments, including neoadjuvant therapy, surgery, and adjuvant therapy. Hormone receptor and HER2/neu status were considered in the analysis.

The majority of patients were postmenopausal (60.5%), with T2 tumors (52.2%), clinical node-positive disease (61.5%) and most commonly clinical stage at presentation was Stage IIA (52.7%). Hormone receptor positivity was observed in 61.5% of cases, and HER2/neu positivity in 38.4%. Neoadjuvant therapy was administered to 39.4% of patients. The 5-year disease-free survival was 68.1%, and overall survival was 78.8%. Recurrence, particularly distant recurrence (72%), was the primary cause of treatment failure. Factors influencing survival included clinical nodal positivity and presence of lymphovascular invasion. HER2/neu-positive patients had a 5-year DFS of 65.9%, while triple-negative disease patients had the lowest DFS at 63.5%.

This audit provides important insights into breast cancer management at a tertiary care center in Eastern India. Most patients presented with Stage II or Stage III disease, reflecting the persistent burden of locally advanced presentation in the Indian setting. Survival outcomes were comparable to those reported in other large Indian series. These findings emphasize the need for improved early detection and the role of continuous institutional audits in refining healthcare delivery and improving outcomes.

Follicular dendritic cell sarcoma (FDCS) is a rare, aggressive malignant neoplasm usually arising in lymph nodes of the head and neck, but it can also occur at extranodal sites (ENFDCS). Due to its rarity, optimal management is not well defined, underscoring the need for further research.

We conducted a retrospective analysis of patients with histologically confirmed ENFDCS treated in the gastrointestinal oncology unit of a tertiary cancer center. Clinical features, treatments, and outcomes were reviewed.

Fourteen patients (10 males, 4 females; median age 41 years) were included. Primary sites were colon (n = 6), retroperitoneum (n = 3), rectum (n = 2), mesentery (n = 1), liver (n = 1), and pelvis (n = 1). Four tumors (28.6%) were initially misdiagnosed. Final diagnosis was based on morphology and immunohistochemistry for CD21, CD23, and CD35; Epstein-Barr virus testing was not performed. Five patients underwent primary surgery at our center; two patients with metastatic disease at presentation received systemic therapy alone. Among the five primary surgeries, three were preceded by perioperative chemotherapy (n = 1), neoadjuvant chemotherapy (n = 1), or neoadjuvant radiotherapy (n = 1). Seven patients presented with residual or recurrent disease after prior surgery elsewhere; three underwent re-resection following appropriate systemic therapy, and four received only systemic therapy. At a median follow-up of 26 months (range 7-153), median overall survival was not reached, and median disease-free survival was 24 months. Four of five patients primarily operated at our center remained disease free; one recurred at 39 months, was successfully treated with re-resection and systemic therapy, and was alive at 153 months. Of the three patients re-resected at our center, one remained disease free at 17 months, one developed systemic recurrence and eventually received best supportive care at 11 months, and one was disease free until 94 months before being lost to follow-up. Overall, 10 patients were alive, two died of disease progression, and two were lost to follow-up.

ENFDCS is frequently misdiagnosed; surgery is the cornerstone of treatment, and multimodality therapy for recurrences can yield durable survival. Outcomes appear better when patients are managed at specialized oncologic centers, highlighting the importance of early recognition and timely referral.

2-deoxy-2-[18F]fluoro-D-glucose (¹⁸F-FDG) positron emission tomography/computed tomography (PET/CT) plays a pivotal role in the evaluation of vertebral lesions and systemic disease assessment. When vertebral lesions and thyroid incidentaloma are detected simultaneously, determining their relationship can be challenging. Metabolic similarity between lesions is often considered suggestive of a common origin, such as a primary tumor with its metastasis, whereas marked metabolic disparity may suggest separate primary tumors. However, both assumptions may be misleading.

We report two cases demonstrating opposite diagnostic pitfalls related to ¹⁸F-FDG metabolic patterns. In the first case, a mildly ¹⁸F-FDG-avid thyroid incidentaloma accompanied by a markedly hypermetabolic vertebral lesion raised suspicion for an unrelated primary bone tumor, such as plasmacytoma. Histopathological examination, however, confirmed follicular thyroid carcinoma with vertebral metastasis, illustrating a misleading metabolic discordance. In contrast, the second case showed comparable ¹⁸F-FDG uptake in both thyroid incidentaloma and vertebral lesion, initially suggesting a metastasis of thyroid carcinoma to the vertebrae. Surprisingly, the vertebral lesion was pathologically proven to be Langerhans cell histiocytosis (LCH) in a patient with a follicular thyroid neoplasm, representing a deceptive metabolic concordance.

These cases highlight that both discordant and concordant ¹⁸F-FDG uptake patterns on PET/CT may lead to diagnostic pitfalls when used as the sole criterion for determining the relationship between coexisting lesions. Careful integration of metabolic findings with morphologic imaging features and histopathological confirmation is essential. When interpreted in appropriate clinical context, PET/CT remains invaluable for whole-body assessment, therapeutic planning, and individualized management.

Metallic nanoparticles (MNPs) have emerged as versatile platforms for addressing unmet clinical needs in diagnosis, therapy, and theranostics. This review synthesizes recent advances in the clinical application of iron-, gold-, hafnium-, gadolinium-, silver-, copper-, titanium-, and zinc-based nanoparticles across oncology, infection control, biomedical coatings, and diagnostic imaging. In oncology, superparamagnetic iron oxide nanoparticles (SPIONs) have demonstrated a median overall survival of 13.4 months in patients with recurrent glioblastoma and achieved intratumoral temperatures of 42-48.5 °C during magnetic hyperthermia. Gold-silica nano shells generated tumor-free ablation zones in up to 87.5% of prostate lesions, with oncologic success reported in 73% of treated patients. CYT-6091, a ~27 nm PEGylated gold nanoparticle conjugated with TNF-α, enabled systemic delivery of this cytokine without inducing severe hypotension, showing a substantially improved safety profile compared with free TNF-α. In antimicrobial applications, Nano Silver Fluoride reduced dentin caries progression by more than 30% compared with controls, while copper nanoparticle-reinforced universal adhesives preserved mechanical performance and retention rates over 48 months. Collectively, these findings highlight the capacity of MNPs to integrate diagnostic and therapeutic functions, including MRI/CT contrast enhancement, magnetic hyperthermia, photothermal and photodynamic therapies, and gene delivery. Despite significant progress, challenges related to heterogeneous biodistribution, long-term toxicity, and regulatory approval remain, emphasizing the need for the development of safer and more efficient metallic nanomedicines aligned with emerging clinical demands in personalized medicine.

Innate immune recognition plays a central role in determining the outcome of human papillomavirus (HPV) infection and the subsequent development of cervical cancer. This mini-review highlights how the reproductive tract's innate immune system, particularly Pattern Recognition Receptors (PRRs) such as Toll-like receptors (TLRs), NOD-like receptors (NLRs), and RIG-I-like receptors (RLRs), detects HPV-associated molecular patterns and initiates antiviral defenses. HPV has evolved sophisticated strategies to evade these responses by suppressing PRR signaling, altering cytokine networks, reprogramming cellular metabolism, and reshaping the cervical microenvironment. These viral mechanisms contribute to the formation of a persistent post-infection microenvironment (PIM), characterized by impaired antigen presentation, regulatory immune cell infiltration, chronic inflammation, and metabolic and stromal remodeling, which collectively promote immune tolerance and carcinogenesis. Emerging evidence also highlights the roles of inflammasomes, type I interferon pathways, and extracellular vesicles in modulating innate immune responses during HPV infection. Understanding how innate immunity senses HPV and how the virus circumvents these pathways provides crucial insight into cervical cancer progression and offers opportunities for developing more effective immunotherapies, vaccines, and prevention strategies. This review synthesizes current advances in HPV-driven innate immune dysregulation within the reproductive tract and their implications for reproductive immunology and infection-associated malignancy.

This study integrates single-cell RNA sequencing with Mendelian randomization to elucidate the role of nuclear factor of activated T cells (NFAT)-related genes in the progression of hepatocellular carcinoma (HCC). The GSE162616 dataset was analyzed to identify differentially expressed cells and NFAT-related genes through quality control, clustering, and z-score algorithms. Mendelian randomization analysis of expression quantitative trait loci (eQTL) data was performed to identify hub genes causally linked to HCC. Validation in The Cancer Genome Atlas-Liver Hepatocellular Carcinoma cohort included survival analysis, clinical correlation, and nomogram construction. Sixteen cell clusters were resolved and annotated into five types: natural killer (NK) cells, T cells, B cells, hepatocytes, and monocytes. Differentially expressed NFAT-related genes were predominantly enriched in immune and cytokine pathways. Three genes-CACYBP, CTLA4, and RGCC-were identified as causally associated with HCC and designated as hub genes. T cells and NK cells emerged as key cellular populations, and pseudotime analysis delineated T cell differentiation trajectories. Cell-cell communication analysis revealed robust interactions between NK and B cells and between NK and T cells, primarily via the MIF-(CD74+CXCR4) axis. All three hub genes were upregulated in HCC tissues. A nomogram integrating these genes exhibited excellent diagnostic performance (AUC = 0.9). These results establish CACYBP and RGCC as risk factors and CTLA4 as a protective factor for HCC. The nomogram offers a potential tool for early diagnosis and immunotherapy guidance. Our findings highlight the value of integrating single-cell transcriptomics with Mendelian randomization for prioritizing causal genes and provide novel insights into NFAT-mediated immune regulation in HCC.

Malignant peripheral nerve sheath tumor (MPNST) represents a life-threatening complication of neurofibromatosis type 1 (NF1). This report describes a male patient with NF1 and concomitant MPNST treated at our institution. A 55-year-old male first presented with multiple, skin-colored neoplasms distributed across his body over the course of three decades, without any identifiable predisposing factors. Two years before presentation, a firm subcutaneous nodule appeared on his left back, causing intermittent mild discomfort, leading to a diagnosis of multiple neurofibromas. Despite participation in a clinical trial, the lesion on his left back progressively enlarged, and associated pain intensified. A multidisciplinary team subsequently recommended resection of the dorsal mass via Mohs surgery under general anesthesia. Postoperative histopathological analysis confirmed NF1 with concurrent MPNST. No adjuvant targeted therapy was administered, and no recurrence was observed during the six-month follow-up. This case highlights the coexistence of NF1 and MPNST, aiming to enhance clinical awareness of the malignant transformation risks in NF1, thereby promoting earlier diagnosis and minimizing the potential for misdiagnosis and delayed intervention.