Gross surgical resection (GTR) of vestibular schwannomas (VS) is curative, but how surgical intent translates to facial nerve outcomes in practice, however, is incompletely understood. The purpose of this study was to identify factors predicting tumor recurrence in our contemporary VS cohort and explore existing literature regarding extent of resection and facial nerve outcomes.

Gamma delta (γδ) T cells are a unique subset of T lymphocytes capable of bridging innate and adaptive immunity. Unlike αβ T lymphocytes, γδ T cells bypass the need for Major Histocompatibility Complex (MHC)-restricted antigen presentation, allowing them to rapidly respond to stress signals in contexts such as infections and cancer. In breast cancer (BC), γδ T cells play a dual role, exhibiting both anti-tumoral and pro-tumoral activities. Their capacity for direct cytotoxicity, cytokine production, and antigen presentation highlights their versatility within the tumor microenvironment (TME). The prognostic impact of γδ T cells in BC is complex and varies depending on their density, subset, and functional state. While Vδ1 + γδ T cells have been associated with improved survival, particularly in triple-negative BC, other subsets, such as IL-17-producing γδ T cells, contribute to tumor progression, promoting angiogenesis and immune suppression. The emerging therapeutic potential of γδ T cells resides in their MHC-independent activity and stress antigen recognition, highlighting their potential value in cancer immunotherapy, including adoptive cell therapies (e.g., chimeric antigen receptor-T approaches). Additionally, the combination of γδ T cells with immune checkpoint inhibitors or tumor-targeting antibodies has shown promise in overcoming the immunosuppressive challenges of the TME.

IntroductionThis meta-analysis aims to evaluate the impact of increasing the use of metformin in neoadjuvant treatment for breast cancer (BC) on the rate of pathological complete response (pCR) in patients.MethodsA systematic search was conducted in four electronic databases: PubMed, Web of Science, Embase, and Cochrane Library. The search scope covered all the literature from the establishment of the databases to April 2025. The risk ratio (RR) and 95% confidence interval (CI) were calculated. The outcome indicator was the pCR rate.ResultThis meta-analysis included a total of 8 randomized controlled trials (RCTs), involving 474 patients. The results showed that there was no statistically significant difference in the pCR rate between the experimental group containing metformin and the control group (RR = 1.21, 95% CI: [0.85, 1.71], P = 0.28). Subgroup analysis revealed that there were no significant differences in the pCR rate between the two groups in patients with metabolic syndrome (RR = 2.09, 95% CI [0.55, 7.85], P = 0.28), patients without metabolic syndrome (RR = 1.12, 95% CI [0.81, 1.55], P = 0.49), patients from Eastern countries (RR = 1.15, 95% CI [0.63, 2.11], P = 0.65), and patients from Western countries (RR = 1.32, 95% CI [0.75, 2.32], P = 0.34).ConclusionThis study did not observe any effect of increasing the use of metformin on the pCR rate of patients in neoadjuvant treatment for BC.

The management of advanced classical Hodgkin lymphoma (cHL) poses a major challenge in Asia, given disparities in health care resources and the variability in health care systems across the region. This article reviews the practice landscape for advanced cHL in East and Southeast Asia (hereafter referred to as Asia), offers detailed perspectives on the challenges faced by treating physicians, and proposes solutions to improve patient outcomes.

The WHO Global Breast Cancer Initiative (GBCI) aims to improve breast cancer (BC) survival through early stage at diagnosis, prompt diagnostic evaluation, and appropriate multimodality treatment. Care pathway analysis helps to evaluate delay and dropouts through this process. Little is known about the BC care pathway of women first presenting at lower level of health systems in Africa.

Exophytic squamous proliferations of the upper aerodigestive tract can exhibit distinctive papillary and verrucous architectural patterns that often complicate diagnostic interpretation. Histologic evaluation is particularly challenging in limited biopsy specimens where the base of the lesion may not be well represented; and diagnostic terminology is confounded by the lack of historical and current consensus nomenclature. The terms "papillary" and "verrucous" are merely descriptive terms that encompass a broad spectrum of benign, premalignant, and malignant entities. Entities discussed in this review include squamous papilloma, papillary hyperplasia, papillary squamous cell carcinoma, oral epithelial dysplasia, verruciform xanthoma, proliferative verrucous leukoplakia (PVL)-related lesions, verrucous carcinoma, and verrucous hyperplasia. Given these challenges, a diagnostic approach to such lesion should include comprehensive clinical correlation and careful morphological assessment. Ultimately, clear consensus guidelines and an adoption of consistent terminology are essential to improve diagnostic reproducibility and patient management.

Cold atmospheric plasma (CAP), a partially ionized near-room temperature gas (argon or helium), generates a variety of oxygen and nitrogen reactive species which can have a multitude of downstream biological effects including cell death, inflammation, and immune modulation. CAP is therefore a powerful tool with many potential medical applications, particularly in cancer treatment. As primary treatment, CAP can be administered directly through a plasma jet, or indirectly via plasma activated substances (i.e. media, biogels, etc.). CAP has been shown to directly kill cancer cells by inducing RONS-mediated cell death mechanisms, enhance anti-tumor immunity or increase the tumor's responsiveness to systemic therapies. While the chemical factors (i.e. RONS-mediated apoptosis) is the most studied mechanism of CAP efficacy, CAP can also induce necrosis of cells through ultraviolet irradiation, thermal and electromagnetic effects, which tend to lead to necrosis. CAP has been shown to cause selective cell death in various cancers, including skin, breast, colorectal, head and neck, and more recently in gliomas, with minimal side effects to surrounding normal tissues.

Uveal melanoma (UM) is an aggressive intraocular malignancy in adults arising from the melanocytes of the uveal tract. While primary UM lesions can be successfully treated, ~ 50% of UM patients develop metastases primarily in the liver. Patients with liver metastatic UM (LMUM) have poor prognosis and few therapeutic options. LMUM lesions are unresponsive to standard chemotherapies, targeted therapies, and immune checkpoint inhibitors - an effect at least in part associated with the detoxification function of the liver and the diverse hepatic immunological landscape. Here, we recount the etiology and molecular mechanisms in the development of LMUM, examine the influences of the hepatic tumor microenvironment (TME) on UM liver tropism, and review how the innate and peripheral immune response contributes to LMUM progression and therapeutic efficacy. The unique immunological properties of the liver coupled with the distinct growth patterns of LMUM lesions present significant challenges for developing effective treatments that can overcome this specialized microenvironment. Improved understanding of the interplay between the liver and LMUM is essential for the development of more effective diagnostic techniques and improved therapeutic outcomes.

Cancer stem cells (CSCs) are a subpopulation of tumor cells with self-renewal capacity and the ability to drive tumor growth, metastasis, and relapse. They are widely recognized as major contributors to therapeutic resistance. Despite extensive efforts to characterize and target CSCs, their elusive nature continues to drive therapeutic resistance and relapse in epithelial malignancies. Single-cell RNA sequencing (scRNA-seq) has transformed our understanding of tumor biology. It enables high-resolution profiling of rare subpopulations (<5%) and reveals the functional heterogeneity that contributes to treatment failure. In this review, we discuss evolving evidence for a paradigm shift, enabled by rapidly advancing single-cell technologies, from a static, marker-based definition of CSCs to a dynamic and functional perspective. We explore how trajectory inference and spatial transcriptomics redefine stemness by context-dependent dynamic-state modelling. We also highlight emerging platforms, including artificial intelligence-driven predictive modelling, multi-omics integration, and functional CRISPR screens. These approaches have the potential to uncover new vulnerabilities in CSC populations. Together, these advances should lead to new precision medicine strategies for disrupting CSC plasticity, niche adaptation, and immune evasion.

Macrophage migration inhibitory factor (MIF) is a pleiotropic cytokine with a pivotal role in immune regulation, inflammation, and tumorigenesis. Originally identified as a T cell-derived factor inhibiting macrophage migration, MIF has since been recognized as a key player in the progression of a wide range of solid tumors. This comprehensive review traces the historical discovery and evolving understanding of MIF, highlighting its structural features, receptor interactions, and intracellular signaling mechanisms. The review also explores the molecular mechanisms of MIF involvement in tumor pathogenesis through promoting proliferation, angiogenesis, immune evasion, and metastasis. Special focus is given to MIF interplay with several oncogenic pathways, modulation of the tumor microenvironment, and its dual role in both autocrine and paracrine signaling within tumors. The review also discusses emerging insights into MIF's involvement in therapeutic resistance and its potential as a diagnostic biomarker and therapeutic target. By consolidating current knowledge, the authors aim to provide a detailed perspective on MIF's multifaceted role in solid tumors and to outline future directions for research and clinical intervention.

Metastasis-associated protein 2 (MTA2), a master transcriptional regulator, through multiple target genes and interacting proteins, has been demonstrated to play a vital role in the regulation of proliferation, replication, apoptosis, autophagy, DNA damage repair, preimplantation, embryonic development and immune cell differentiation. Despite extensive research, the physiological role and pathogenic mechanisms of MTA2 remain poorly understood. Here, we mainly review in the current research the status of MTA2 and its implications in normal development and various tumor biology. Accumulating evidence suggests that MTA2 is frequently amplify in several types of cancers, closely associates with tumor cells migration and invasion, relates to the malignant characteristics and poor prognosis, which therefore has been considered as playing tumor oncogenic roles. Substantial evidence indicates that MTA2 functions by modulating downstream targets including cell growth, invasion as well as angiogenesis related genes. Confusingly, the proliferation effect of MTA2 remains elusive and even conflicting in the development of several solid tumors. Furthermore, we discuss the upstream regulation of MTA2 by transcription factors, microRNAs and lncRNAs in specific physiology and pathology conditions, which results in the abnormal MTA2 expression in various aspects of cancer. In this context, we summarize linked function of MTA2 directly to oncogenesis and might provide a significant avenue for the treatment of diseases. We hope that this review will help tumor molecular biologists further understand the molecular mechanism of MTA2 in normal development and cancer.

Advances in targeted therapy and immunotherapy have significantly improved clinical outcomes for patients with advanced non-small cell lung cancer (NSCLC), reshaping treatment paradigms. However, most patients ultimately face drug resistance, with limited options for subsequent therapies and suboptimal treatment efficacy, presenting a prominent challenge in current clinical practice. Antibody-drug conjugates (ADCs), characterized by high efficacy and favorable safety profiles, have emerged as a promising therapeutic frontier in recent years. This systematic review provides a comprehensive overview of the latest advancements in ADCs-based therapies for lung cancer, alongside discussions of the prevailing challenges in this rapidly evolving domain.
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Human epidermal growth factor receptor 2 (HER2) mutations play a role as a driver gene in non-small cell lung cancer (NSCLC). Patients with advanced NSCLC harboring HER2 mutations exhibit poor responses to conventional chemotherapy and immunotherapy, hence targeted therapies against HER2 are under extensive investigation. This review analyzes the biological characteristics of HER2, an overview of clinical trials for targeted therapy drugs, including monoclonal antibodies, tyrosine kinase inhibitors (TKIs), and antibody-drug conjugate, and research directions for drug resistance in NSCLC. Currently, Pyrotinib and Trastuzumab deruxtecan have been approved for the treatment of advanced NSCLC with HER2 mutations, suitable for patients who have failed standard therapy, which is far from meeting the clinical demands. Novel selective HER2 TKIs are gradually emerging. Future exploration trends are gradually shifting from single drugs to combination strategies, and are exploring more precise selection strategies as well as research on resistance mechanisms. These studies will provide a theoretical basis for clinical treatment strategies for advanced NSCLC with HER2 mutations, promoting the development of personalized therapy.
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Reactive oxygen species (ROS) are a diverse group of molecules that serve as both essential signalling mediators and potential drivers of oxidative stress. In tumours, ROS influence critical processes such as proliferation, angiogenesis, metabolic adaptation and therapy resistance. These processes are further modulated by reduced oxygen availability (hypoxia), a defining feature of many solid tumours that can alter redox balance and cellular signalling. The interplay between ROS and hypoxia is highly dynamic, with both factors shaping tumour behaviour in complex and often unpredictable ways. Accurately measuring ROS and tumour oxygenation remains a significant challenge due to their transient nature and variability in levels across different tumour types. In this guide, we provide a comprehensive update on the dynamic interaction between ROS and hypoxia in tumours, evaluate current strategies for ROS detection and discuss emerging therapeutic approaches that target redox vulnerabilities in cancer. Understanding the intricate relationship between ROS and hypoxia is crucial for refining therapeutic strategies and improving patient outcomes.

Tunicamycins trigger endoplasmic reticulum (ER) stress by inhibiting DPAGT1 (dolichyl-phosphate N-acetylglucosamine-phosphotransferase 1): the rate-limiting enzyme that initiates N-glycan biosynthesis. Aberrant N-glycan branching is a hallmark of many solid tumors, and distinct cancer-associated N-glycan structures have been identified. Evidence shows that tunicamycins suppress key oncogenic processes, including proliferation, apoptosis resistance, metastasis, and angiogenesis. Yet their high systemic toxicity and lack of selectivity have precluded therapeutic application, and the structural complexity of tunicamycins has hindered chemical modification to mitigate these liabilities. No clinically translatable antitumor efficacy has been demonstrated in animal models. This review underscores the emergence of DPAGT1 as a novel and tractable anticancer target, outlining milestones in the discovery of selective inhibitors and their potential to transform cancer therapy. We discuss how advances in DPAGT1 inhibitor design may overcome limitations of tunicamycins and pave the way toward glycosylation-targeted oncology therapeutics.

Protein homeostasis is a dynamic process essential for cellular function and survival, tightly controlled by the ubiquitin-proteasome system. Within this system, ubiquitin-specific protease 7 (USP7) plays a key role as a deubiquitinating enzyme, thus modulating the stability, localization, and activity of a wide variety of substrates. USP7 is involved in critical cellular processes such as DNA repair, apoptosis, immune response, and epigenetic regulation. The dysregulation of USP7 expressions or activity has been linked to several pathological conditions, including cancer, neurodegenerative and inflammatory diseases, and viral infections. This enzyme exerts its biological functions through the stabilization of both oncogenic and tumor suppressor proteins, highlighting its sensitive role in tumorigenesis. Despite the identification of selective USP7 inhibitors with promising preclinical activity, the development of clinically effective compounds remains a major challenge. This review summarizes the current understanding of USP7 structure, function, and biological relevance, with a particular emphasis on its potential as a therapeutic target in oncology.

Phyllodes tumors, also known as cystosarcoma phyllodes, represent a rare and complex category of fibroepithelial neoplasms that primarily affect the breast. These tumors are characterized by their unique histological architecture, which resembles leaf-like structures, as suggested by the etymology of the term "phyllodes," derived from the Greek word "phyllodes," meaning "leaf-like". The World Health Organization (WHO) has classified these tumors into three distinct categories-benign, borderline, and malignant-based on various histopathological criteria, including cellular atypia, mitotic activity, and stromal overgrowth. With a peak incidence occurring between the ages of 40 and 52, these tumors primarily affect women and constitute 0.3% to 1% of all breast tumors. Imaging modalities currently employed (mammography, ultrasound, and MRI) play a crucial role in the initial assessment of breast masses. Histopathological characteristics, such as stromal cellularity and mitotic activity, and immunohistochemical markers, like Ki-67 and p53, are important in the diagnosis, categorization, treatment plans, and prognosis of breast phyllodes tumors. Surgical intervention, with the goal of achieving complete excision of the tumor along with adequate margins, is the primary treatment option. Adjuvant therapies, such as radiotherapy, may be considered but are still debatable. Understanding the nuances of these tumors is crucial for healthcare professionals, as they present unique challenges in both diagnosis and treatment.

Background and Objectives: Breast cancer (BC) is a global health concern for women; the disease contributes to significant morbidity and mortality. A key element in the diagnosis of BC involves the histopathological diagnosis, which determines patient management and therapy. However, BC is a multifaceted disease, limiting access to early diagnosis and, therefore, treatment. Artificial intelligence (AI) is transforming diagnostics in the medical field, especially in the detection of BC. Due to the increased availability of digital slides, it has facilitated the effective integration of AI in breast cancer diagnosis. Diagnosis poses a great challenge, even for experienced pathologists, due to the heterogeneity of this malignancy. Analysing microscopic slides by pathologists requires a considerable amount of time. Implementation of AI into routine workflows holds potential to improve diagnostic sensitivity and inter-observer concordance, and to increase efficiency by reducing the review time, thereby helping to alleviate the burden of diagnosing BC. Previous studies mainly address imaging modalities or oncology broadly, while a few specifically concentrates on the histopathological aspect of breast cancer. This review aims to explore the novel synthesis of AI advancements in digital pathology, including tumour classification, grading, lymph node staging, and biomarker evaluation, and discuss their potential incorporation into clinical workflows. We will also discuss the current barriers and prospects for future advancements. Materials and Methods: A literature search was conducted in PubMed and Google Scholar using the mentioned keywords. Articles published in English until July 2025 were reviewed and synthesised narratively. Results: Recent studies demonstrate that AI models such as convolutional neural networks (CNNs), YOLO, and RetinaNet achieve high accuracy in tumour detection, histological grading, lymph node metastasis localisation, and biomarker analysis. The reported performance values range from 75% to over 95% accuracy across various tasks, with gains in diagnostic sensitivity and inter-observer concordance, and reduced review time in assisted workflows. However, certain limitations, such as data variability, external validation in clinical practice, and ethical concerns, restrict the growth and optimal performance of AI and its clinical applicability. Conclusions: The future for AI looks promising, as it is rapidly evolving. By analysing evidence across multiple domains, this review evaluates both opportunities and persisting barriers, offering practical overviews for future clinical transition. AI cannot replace pathologists; however, it has the capabilities to enhance diagnostic precision, efficiency, and ultimately patient outcomes. It is only a matter of time before AI is adopted into healthcare.

Background and Objectives: Neuroendocrine neoplasms (NENs) are rare, mainly gastro-entero-pancreatic tumors with heterogeneous biology and multiple therapeutic options. Assessing treatment response remains challenging. Standard evaluation relies on RECIST 1.1, although its limitations are well recognized. Tumor growth rate (TGR), defined as the monthly percentage change in tumor size between two imaging assessments, has been proposed as a dynamic parameter to complement conventional criteria. This review explores the role of TGR in NEN. Results: Two different evaluations of TGR, once conducted between baseline diagnostic scan and a radiological assessment 12-24 weeks after (TGR0), and another conducted between baseline scan and a diagnostic evaluation three months after (TGR3m), proved to be well correlated to progression free survival (PFS) in G1 and low-G2 NEN, with cut off of 4%/month and 0.8%/month, respectively. Conclusions: TGR offers additional insights into tumor kinetics and may help refine treatment monitoring in NEN. While retrospective evidence supports its prognostic utility, prospective studies are required to validate TGR as a standard clinical tool.

The oral microbiome plays a key role in oral cancer pathogenesis through mechanisms such as chronic inflammation, dysregulated proliferation, and increased tumor invasiveness. Dysbiosis, frequently present in premalignant and malignant lesions, may initiate or accelerate malignant transformation. Oral squamous cell carcinoma (OSCC), representing over 90% of oral cancers and affecting more than 350,000 people worldwide each year, is strongly linked to microbial shifts. Common periodontal pathogens such as Fusobacterium nucleatum and Porphyromonas gingivalis are often enriched in OSCC. These bacteria may promote tumorigenesis by activating NF-κB and STAT3 pathways, suppressing apoptosis, and modulating host immune responses. Additional potential mechanisms include the production of reactive oxygen species (ROS) and genotoxins, inhibition of tumor suppressors such as p53, disruption of cell-cycle regulation via cyclin-dependent kinase pathway, and upregulation of β-catenin and toll-like receptor signaling. These molecular alterations cause DNA damage, immune surveillance evasion, angiogenesis, promoting tumor progression. Microbiota-modulating therapies, such as Lactobacillus probiotics, may complement standard treatments by restoring balance, boosting immunity, and limiting tumor growth. Engineered bacteriotherapy, microbiome-targeted immunomodulators, and microbiota-based diagnostics expand therapeutic options in oral cancer and, combined with advances in precision medicine, may support more personalized treatments and improved outcomes.