Given the worldwide prevalence of head and neck cancer and the importance of scientifically based treatment, current studies are discussing innovative strategies for the treatment of radiodermatitis. This review adhered to the Joanna Briggs Institute's nine-step methodological framework for scoping reviews and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews checklist. We searched eight databases: Web of Science, Science Direct, Scientific Electronic Library Online, CAPES Catalog of Theses and Dissertations, Elsevier's Scopus, Wiley Online Library, PubMed Central, and Cochrane Library. Data collection occurred in March 2024. A final sample of 21 articles was selected. The research question was formulated using the "Population, Concept and Context" framework. This led to the specific question: "What are the strategies identified in the literature used in the management of radiodermatitis in patients with head and neck cancer undergoing radiotherapy?" The included studies were published between 2011 and 2024, with China being the leading producer of articles. Clinical trials were the predominant study design. Scales were frequently used to assess various aspects of radiodermatitis. The Radiation Therapy Oncology Group criteria were commonly used. Several topical agents for preventing radiodermatitis were evaluated, including pharmacological therapies, phototherapy/photobiomodulation, and dressings. Numerous topical agents have been clinically tested for the treatment and prevention of radiodermatitis in patients with head and neck cancer. However, the current body of research is insufficient in both quantity and quality to conclusively support or refute the widespread approval of any specific product.

Pancreatic neuroendocrine neoplasms (PNENs) are rare tumors with heterogeneous outcomes. Tumor grading (G), based on mitotic count and Ki-67 index, is the main prognostic factor guiding treatment. EUS-guided fine-needle aspiration/biopsy is the current standard but shows a misgrading rate up to 25%. We evaluated an artificial intelligence-based video analysis model to predict PNEN grading from contrast-enhanced EUS (CE-EUS) recordings.

This retrospective study was conducted at Istituti di Ricovero e Cura a Carattere Scientifico San Raffaele Hospital, Milan, a European Neuroendocrine Tumor Society Center of Excellence. Patients were eligible if CE-EUS videos ≥1 minute (arterial and venous phases) and cyto-histological confirmation of PNEN were available. Exclusion criteria included mixed neuroendocrine-non-neuroendocrine neoplasms, missing Ki-67 grading, or poor video quality. CE-EUS videos were processed with a deep-learning video transformer model (GradAINet). The dataset was split into training (70%), validation (10%), and testing (20%) cohorts. Diagnostic performance was evaluated using sensitivity, specificity, positive predictive value, negative predictive value, accuracy, and F1-score.

Between 2022 and 2024, 115 patients were included (49 female, 42.6%): 70 had G1, and 45 had G2-G3 tumors. Overall, 253,751 video frames were analyzed. GradAINet achieved a sensitivity of 0.817 (95% confidence interval [CI]: 0.556-1.000), specificity 0.806 (95% CI: 0.588-1.000), positive predictive value 0.759 (95% CI: 0.500-1.000), negative predictive value 0.856 (95% CI: 0.667-1.000), and accuracy 0.811 (95% CI: 0.654-0.962).

This artificial intelligence-driven CE-EUS video model shows high accuracy for PNEN grading and potentially complements EUS-guided fine-needle aspiration/biopsy. As the first video-based rather than static-image model, it represents a methodological advance. Multicenter validation on larger cohorts is needed before clinical implementation.

The E26 transformation-specific family of transcription factors regulates the cell cycle and apoptosis that are crucial for carcinogenesis. More specifically, the PEA3 subfamily-comprising ETS variant (ETV) transcription factors ETV1, ETV4, and ETV5-has been implicated in multiple oncogenic signaling pathways and chemotherapy resistance. While cisplatin is still a widely used chemotherapeutic treatment for ovarian cancer, its therapeutic efficacy is sometimes limited by the induction of resistance mechanisms. The present study investigates the potential role of PEA3 subfamily genes in cisplatin resistance in ovarian cancer through comprehensive in silico analyses.

Cisplatin response data for ovarian cancer were obtained from the Cancer Treatment Response Database version 2 (CTR-DB2), and the relevant dataset was analyzed. Candidate genes, including members of the PEA3 transcription factor subfamily, were analyzed with a multigene biomarker model, and a receiver operating characteristic analysis was used to measure predictive ability. GEPIA2, KMplotter, and cBioPortal were used for survival analysis, while the TNMplot, cBioPortal, and Clinical Proteomic Tumor Analysis Consortium datasets were used for multiomics characterization and differential expression.

The ETV4-CIC gene pair in the CTR-DB2 validation dataset achieved the highest predictive performance for cisplatin response in ovarian cancer with an area-under-curve of 0.939, clearly separating responders from nonresponders. No other gene combinations outperformed this model, demonstrating only moderate predictive capacity. The ETV4-CIC gene pair was also associated with disease-free survival. Differential expression analysis showed downregulation of CIC and upregulation of ETV4 in tumor tissues. Genomic and proteomic analyses confirmed alterations in both genes, while correlation analysis suggested complementary biological roles.

The ETV4-CIC gene pair effectively discriminated between cisplatin responders and nonresponders in ovarian cancer. Accordingly, the ETV4-CIC signature may serve as a useful biomarker for cisplatin response prediction and patient stratification in precision oncology.

While the presence of metastases in neuroblastoma (NB) is a well-established prognostic factor, the clinical significance of dissemination patterns and tumour burden and their impact on response and survival remains poorly understood.

To characterise metastatic dissemination patterns and tumour burden in NB, evaluate their response to induction therapy, and determine their prognostic impact.

We retrospectively analysed 53 patients with metastatic NB between 2010 and 2024 in a reference tertiary care hospital and treated as per SIOPEN protocol or standard-of-care recommendations. Responses were recorded as per INRC 2017. Survival was estimated using Kaplan-Meier analysis, and associations between metastatic patterns and outcomes were evaluated by univariate analysis.

The most frequent metastatic sites were bone (77%), regional lymph nodes (64%), and bone marrow (55%). MSI (metastatic site index) was 1 (n = 13), 2 (n = 13), 3 (n = 15), or ≥4 (n = 12). Overall response according to INRC after induction therapy achieved complete (n = 1), partial (n = 41), minor (n = 6) responses, stable (n = 4) or progressive disease (n = 1). Regarding metastatic response, regional and distant lymph nodes, renal and pulmonary decreased in size by 66%, 85%, 90 and 99%, respectively. The median SIOPEN score decreased from 16.5 to 0. Bone marrow infiltration disappeared in 82%. High tumour burden strongly correlated with poor outcomes.

Presence of renal metastases, ascites, bone marrow infiltration, high tumour burden at diagnosis and post-induction pulmonary or renal metastases are negative prognostic markers. Incorporating these factors into risk stratification may guide personalised treatment strategies. Future work should elucidate the genomic background and underlying causes of these different metastatic patterns.

Central nervous system (CNS) tumors are the most common solid malignancies in children, comprising a highly heterogeneous group of neoplasms defined by distinct molecular alterations and clinical behaviors. Advances in molecular genetics have underscored the relevance of specific signaling pathways in driving pediatric tumorigenesis, among which the fibroblast growth factors (FGFs) and their receptors (FGFRs) have emerged as critical regulators of CNS development and tumor biology. The strict regulation of this system is frequently disrupted in cancer contexts, leading to abnormal activation that promotes tumor growth, invasion, and therapy resistance. Recent genomic profiling studies confirm that FGFR gene aberrations (i.e., activating point mutations, amplifications, and fusions) occur in a non-negligible fraction of pediatric CNS tumors. Notably, FGFR alterations are found in approximately 9% of pediatric gliomas, representing a higher incidence compared to adult gliomas. Across a broader survey of pediatric solid and brain tumors, activating FGFR aberrations were measurable in approximately 3% of cases. This prevalence establishes the FGF/FGFR axis as a measurable therapeutic vulnerability in defined patient subsets. Therefore, a deeper understanding of the role of the FGF/FGFR system across different pediatric CNS tumor subtypes is essential for elucidating disease mechanisms and identifying novel therapeutic opportunities. This review outlines the characteristics of major pediatric CNS tumors and discusses the role and potential therapeutic targeting of the FGF/FGFR system.

Five years after the emergence of SARS-CoV-2 and the declaration of the COVID-19 pandemic, the long-term implications of COVID-19 for cancer biology remain incompletely understood. Beyond the major disruptions in cancer screening, diagnosis, and treatment observed worldwide, increasing attention has focused on whether SARS-CoV-2 infection and post-acute sequelae of COVID-19 (Long COVID) may induce persistent biological alterations relevant to tumor progression or recurrence.

Current evidence does not support SARS-CoV-2 as a classical oncogenic virus or demonstrate direct viral carcinogenesis. However, experimental, transcriptomic, and clinical studies suggest that SARS-CoV-2 infection can induce persistent inflammatory and immune alterations that overlap with pathways implicated in cancer biology. Among the most consistently reported findings are chronic activation of IL-6/STAT3 and NF-κB signaling, immune dysregulation, T-cell exhaustion, oxidative stress, mitochondrial dysfunction, and senescence-associated inflammatory programs. Additional proposed mechanisms include perturbation of tumor suppressor pathways, epigenetic remodeling, and microRNA alterations involving the let-7/LIN28B/STAT3 axis. Experimental models have further suggested that inflammatory remodeling induced by respiratory viral infection may influence dormant tumor cell behavior and tissue microenvironments under defined conditions. However, many of these observations derive from in vitro systems, animal models, or association studies, and their long-term relevance to human oncogenesis remains uncertain.

Collectively, current evidence supports the existence of convergent biological mechanisms between SARS-CoV-2-induced inflammatory stress responses and pathways involved in cancer progression, rather than direct oncogenic transformation. Future longitudinal studies integrating immune profiling, inflammatory biomarkers, transcriptomic and epigenetic analyses, and clinical cancer outcomes will be essential to determine whether persistent post-infectious alterations contribute to tumor progression, recurrence, or susceptibility in selected patient populations.

Melanoma is an aggressive skin cancer that, once metastatic, accounts for a disproportionate share of skin-cancer mortality. Contemporary management includes surgical excision with sentinel-node assessment, adjuvant or neoadjuvant systemic therapy, radiotherapy in selected settings, targeted inhibition for BRAF/MEK-mutant disease, and intralesional modalities; nevertheless, many patients require effective systemic options. Immunotherapy has transformed outcomes by restoring antitumor T-cell activity. Within this paradigm, activation of CD40, a pivotal costimulatory receptor on antigen-presenting cells (APCs), has emerged as a means to reprogram tumor immunity in melanoma. Available agents span several classes, including agonist monoclonal antibodies, CD40L-based fusion proteins, and engineered bispecific or conditionally activatable formats. A principal mechanism is dendritic-cell licensing that enhances cross-priming of melanoma-specific CD8⁺ T cells. This review summarizes the latest evidence on CD40 agonist therapy in melanoma, moving from biological rationale to translational data. We summarize mechanistic underpinnings, delineate therapeutic classes and leading agents, and critically appraise findings from preclinical models and early-phase clinical studies, including signals of activity and salient safety considerations. Finally, we outline future perspectives for integrating CD40 agonists with established standards of care and for prioritizing biomarker-guided development to translate preclinical promise into durable clinical benefit.

Anisodus tanguticus (Maxim.) Pascher has been documented in Tibetan ethnomedicine. Traditional records indicate that A. tanguticus has traditionally been used to relieve pain, treat parasitic infections, and heal skin wounds caused by viral infections. A. tanguticus is rich in tropane alkaloids, including anisodamine, scopolamine, and atropine, which are pharmacologically active constituents with well-known parasympatholytic effects. These alkaloids have shown promise in controlling cancer cell proliferation and metastasis, with preclinical studies indicating antitumor activity against liver, breast, and colorectal cancers. The extraction of A. tanguticus traditionally involves methods such as juice pressing or boiling; however, modern techniques like ultrasonic, reflux, and supercritical fluid extraction have enhanced alkaloid yield and quality. While the pharmacological properties of A. tanguticus suggest that some constituents of A. tanguticus may have preclinical antitumor relevance, most studies remain preclinical, and clinical data is limited. This review highlights the need for further pharmacological, toxicological, and translational studies. Current evidence suggests that A. tanguticus and several of its constituents exhibit preclinical antitumor activity; however, their clinical relevance remains uncertain, and further pharmacological, toxicological, and clinical validation is required. This narrative review summarizes the traditional use, phytochemical composition, extraction methods, antitumor-related findings, and proposed mechanisms of A. tanguticus, while highlighting the need for further pharmacological, toxicological, and translational studies.

This study employs VOSviewer, Biblioshiny, CiteSpace, and other software to conduct a visual atlas analysis of literature pertaining to the management of lung adenocarcinoma (LUAD) with Chinese medicine over the previous thirty years. The goal is to clarify research advancements, pinpoint key areas of interest, and predict future trends in this field, thereby offering a theoretical foundation and guidance for further studies on managing LUAD with traditional Chinese medicine (TCM).

Literature on herbal treatments for LUAD collected from the Web of Science over the past 30 years (1990-2024) was exported in plain text format. Key nodes such as authors, institutions, countries, and journals were selected using VOSviewer, Biblioshiny, and CiteSpace. This analysis facilitated the assessment of the growth of scientific research papers and identified the leading authors, institutions, countries, and journals. Furthermore, this study utilized network pharmacology to investigate the potential targets and mechanisms of action linked to the most frequently used herbal components in Chinese herbal treatments for LUAD.

The annual publication count in this field has risen in recent years, with China and the United States dominating the research landscape. As the most concentrated region for cooperation, Asia has established extensive networks with other countries. This trend may indicate an increasing interest in the application of TCM for LUAD treatment.

Afatinib, a tyrosine kinase inhibitor, has become a significant focus of research in LUAD treatment over the last 5 years. However, its side effects, such as diarrhea, rash, and mucositis, have raised considerable concerns. In contrast, the multi-target and multi-signal pathway strategies of TCM have increasingly attracted interest. Astragali Radix and Prunellae Spica are the most commonly used Chinese herbs in LUAD therapeutic formulas. Enrichment analysis of Gene Ontology pathways revealed that their effects on LUAD are mainly linked to the regulation of apoptosis signaling pathways, enhancement of cell migration, response to lipopolysaccharides, inhibition of cell proliferation, and promotion of phosphorylation.

Intravascular papillary endothelial hyperplasia (IPEH), or Masson's tumor, is a rare benign vascular proliferation that uncommonly involves the parotid gland.

This report details the case of a 53-year-old female who presented with an 8-year history of a right parotid mass that exhibited significant growth over 2 years, accompanied by the development of multiple bluish cutaneous lesions in the subauricular and cervical region.

Clinical and radiological evaluations were nonspecific. A cutaneous biopsy revealed a cavernous hemangioma. The patient underwent a superficial parotidectomy with complete facial nerve preservation. Histopathological examination of the parotid specimen confirmed a diagnosis of IPEH, characterized by papillary fronds lined by bland endothelial cells. Notably, one of the excised skin lesions also showed histological features of IPEH, alongside hemangioma.

This case is exceptional as it represents a mixed-form IPEH arising in association with a preexisting vascular lesion and demonstrates rare multifocal involvement of both the parotid gland and the skin. It underscores the diagnostic challenge this entity poses, often mimicking other salivary gland tumors, and highlights histopathology as the diagnostic cornerstone. Complete surgical excision remains the treatment of choice and is curative. This case contributes to the limited literature on parotid IPEH and illustrates its potential for multifocal presentation in the context of underlying vascular pathology, making this the seventh documented case in the literature.