Nodular fasciitis (NF) is a benign myofibroblastic neoplasm rarely found in the oral cavity. It typically presents with regional pain, numbness or paresthesia. Due to its high mitotic rate, rapid growth and local invasiveness, NF is often misdiagnosed as a malignancy. We report a case of NF in the oral cavity of a 55-year-old male. Two weeks prior to admission, a rapidly growing swelling appeared in his right buccal area, accompanied by low-grade afternoon fever. Clinical examination revealed a 4×5 cm mulberry-like mass with a pedicle and mucosal ulceration. The mass enlarged rapidly post biopsy. Histopathological examination confirmed a diagnosis of NF. The patient underwent local resection, resulting in resolution of the fever. No recurrence was observed during a 3-month follow-up. This is the first reported case of NF associated with a periodic fever, which may improve understanding of NF's inflammatory nature and aid in differential diagnosis.

Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype with limited treatment options and response to immune checkpoint inhibitors. Tumor-infiltrating lymphocytes have been extensively studied; however, the integration of peripheral immune dynamics with mechanistic regulation underlying therapeutic response remain poorly defined. Here, we integrate immune-state modeling with pathway-level mechanistic inference to analyze single-cell RNA sequencing of PBMCs from patients with advanced TNBC treated with paclitaxel alone or in combination with the anti-PD-L1 Ab atezolizumab. This framework leverages treatment arm, longitudinal sampling, and clinical response to resolve coordinated immune programs across lymphoid and myeloid compartments. We identified distinct treatment- and response-specific states before and after treatment. Chemotherapy responders displayed pretreatment adaptive immune priming, whereas combination-therapy responders exhibited preexisting effector T-cell activity coupled with tumor PD-L1 expression. In contrast, chemotherapy nonresponders developed persistent post-treatment immune dysregulation in regulatory and terminal effector programs, whereas combination-therapy nonresponders demonstrated maladaptive remodeling of adaptive and innate compartments, including dysfunctional NK and metabolically reprogrammed myeloid populations. Across regimens, pathways involving protein translation, metabolic adaptation, and stress signaling emerged as shared modulators of response. These findings suggest that coordinated adaptive-innate immune dynamics underlie therapeutic efficacy, whereas systemic immune exhaustion and myeloid immunoregulation lead to resistance. Projection of these peripheral immune programs onto independent I-SPY2 showed concordant associations with tumor immune phenotypes and pathological complete response, supporting generalizability of the findings. Our study demonstrates the utility of an integrative approach for linking peripheral immune state organization with mechanistic insights, informing response in TNBC.

Dyspnoea is one of the most distressing symptoms in patients with advanced lung cancer, substantially impairing quality of life and complicating palliative care. Traditional assessment and management approaches often rely on episodic self-report and may not fully capture the dynamic and multidimensional nature of breathlessness. Artificial intelligence (AI) technologies may support symptom assessment, remote monitoring, risk prediction and decision support. However, the types of AI technologies used for dyspnoea-related care in advanced lung cancer, the data inputs and outcomes reported and the clinical or home-care contexts in which these tools are applied remain unclear. This scoping review will map the available evidence on AI applications in dyspnoea management for patients with advanced lung cancer.

This review will follow the Joanna Briggs Institute (JBI) methodology for scoping reviews. The protocol will be prepared in line with Preferred Reporting Items for Systematic Reviews and Meta-Analysis Protocols (PRISMA-P) where applicable, and the completed review will be reported in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR). We will search PubMed/MEDLINE, Embase (Ovid), CINAHL (EBSCO), Web of Science Core Collection, Scopus, Cochrane Library, IEEE Xplore, ACM Digital Library, PsycINFO, CNKI, WanFang Data, VIP Database and SinoMed from database inception with no date restrictions. Supplementary searches will include Google Scholar, ClinicalTrials.gov, the WHO International Clinical Trials Registry Platform, medRxiv, arXiv, ProQuest Dissertations & Theses and reference lists of included studies and relevant reviews. Eligible evidence will include original quantitative, qualitative and mixed-methods studies as well as full grey-literature reports with sufficient empirical data. Systematic, scoping and narrative reviews will not be included as evidence units but will be used to identify additional primary studies. Two reviewers will independently screen titles, abstracts and full texts, with disagreements resolved by discussion or a third reviewer. Data will be charted using a piloted extraction form and will include study characteristics, AI technology type, data sources, dyspnoea-related outcomes, implementation context and reported feasibility or performance metrics where available. Findings will be synthesised descriptively and thematically.

As this review will use published and publicly available literature and will not involve primary patient data, ethical approval will not be required. Findings will be disseminated through a peer-reviewed results paper, conference presentations and summary briefs for clinicians, researchers and policymakers.

This scoping review protocol has been registered in the International Prospective Register of Systematic Reviews (PROSPERO, registration number CRD420251112279).

MMPs are essential for the physiological tissue turnover within the oral cavity and maxillofacial structures but their dysregulation may lead to pathogenic, tissue-destructive oral diseases. Within oral tissues, matrix metalloproteinases (MMPs) are produced by a variety of cells, including fibroblasts, keratinocytes, epithelial cells, immune cells, osteoclasts, osteoblasts, and odontoblasts. Activation of MMPs in periodontal tissues degrades extracellular matrix components which may lead to periodontal attachment loss and alveolar bone destruction. Various MMPs serve as putative biomarkers in dental diseases, and their levels can be easily measured from oral fluids. In addition to their role in periodontal manifestations, MMPs are associated with caries, pulpal inflammation, oral potentially malignant disorders and cancers. MMP inhibitors and chairside test measuring active MMP8 have demonstrated potential clinical usability in adjunctive periodontal therapy and diagnostics. In the next chapters, we discuss the importance and function of MMPs and their use as biomarkers in oral diseases.

An organized microbial communities encapsulated in a protective matrix are called biofilms, that have a major impact on how different types of cancer form and spread. The effect of biofilms produced by Helicobacter pylori, Fusobacterium nucleatum, Porphyromonas gingivalis, Escherichia coli, and Candida spp on the development and spread of cancer is examined in this study. Because they cause cellular damage, genetic mutations, and persistent inflammation, H. pylori biofilms are strongly linked to stomach cancer, such as F. nucleatum biofilms have been connected to colorectal cancer, where they stimulate the formation of tumors by modifying the immune system and activating pathways associated to cancer. A common periodontal infection, P. gingivalis, has been linked to pancreatic and oral malignancies by increasing tumor invasiveness and facilitating immune evasion. Some of the enterotoxigenic pathovars of E. coli can cause chronic inflammation and have genotoxic effects, often are related to colorectal cancer. Moreover, Candida species, specifically Candida albicans can form biological films in the gastrointestinal and oral tracts, helping in epithelial invasion and synthesizing carcinogenic byproducts resulting in esophageal and other malignancies. Examining the mechanisms of cancer emergence and progression by biofilms can provide insights on the influence of microbes on the development of cancer. Targeting the biofilm development can provide novel approaches for the treatment regimen of cancer.

Biofilms of pathogenic bacteria are traditionally defined as microcolonies encased in an endogenously produced matrix upon host tissue. However, realistically, it is a highly heterogenous microenvironment composed of the bacterial cells and their extracellular polymeric substances (EPS), and host necrotic tissue, fibrotic tissue, fibrosis-associated cells and their extracellular matrix. This diverse milieu makes biofilms a potent immune evasion strategy. Its immune non-clearance can lead to relapse, potentially resulting in a persistent dysfunctional immune response; chronic inflammation. Characterised by repeated proinflammatory signalling, chronic inflammation may lead to localised or systemic instability by elevating mutagenesis and promoting anti-apoptotic pathways in host cells. This combined with the biofilm microenvironment's relative isolation from the host immune system significantly promotes tumourigenesis. The tumour microenvironment develops in continuum with the biofilm microenvironment as an immunosuppressive vascularised tissue. This tripartite pathophysiology of biofilm-induced chronic inflammation and tumourigenesis presents these clinical conditions, traditionally studied independently of each other, as an intricate web of interdependent disorder. Such interventions may include biofilm-disrupting agents, inflammatory pathway inhibitors targeting NF-κB/STAT3 signalling, and immune checkpoint-directed therapies aimed at dismantling the tumour-protective inflammatory niche.

Vaginal bleeding in prepubertal girls merits thorough investigation, as it is always pathological and its etiology is broad and includes inflammatory conditions, endocrine disorders, local irritation from a foreign body, neoplasms, injuries, and sexual abuse. The diagnostic approach used should be immediate, systematic, and multidisciplinary.

We present the case of a 7-year-old girl who was admitted to a tertiary pediatric hospital with a history of prolonged vaginal bleeding. During the clinical, pediatric, and forensic investigation, the presence of a foreign body within the vagina was revealed, which consisted of a single hair with presumptively blood-positive material. No findings of recent or past injury to the genitals or anus were found, while the hymen was intact. Autosomal Short Tandem Repeat (STR) analysis of the hair did not yield an interpretable genetic profile; therefore, no inference could be made regarding the presence or absence of DNA from the child or any third party.

The case highlights that the presence of a foreign body, even a rare form such as a single hair, must be considered in the differential diagnosis of prepubertal vaginal bleeding. The combined pediatric, gynecological, and forensic approach facilitated a comprehensive evaluation of the case. The available findings were not supportive of a sexual abuse etiology; however, the absence of supportive findings should not be interpreted as definitive exclusion of sexual abuse.

We sought to present a rare case of MGA::NUTM1 fusion sarcoma, with a discussion of the differential diagnoses and approach to diagnosing these ultra-rare cases, which represent an emerging subset of NUTM1-rearranged mesenchymal neoplasms characterized by varied clinical behavior. Our review of the literature (17 cases) indicated bimodal age distribution, variable anatomical distribution, and frequent metastasis in these cases. Differential diagnosis has included synovial sarcoma and BCOR-associated sarcoma. The reported survival rates vary widely, from 1 month to 15 years.

Here we report the case of a 16-year-old girl who presented with a large pelvic-abdominal mass and metastatic disease on a positron emission tomography/computed tomography scan. Based on TLE-1 positivity, the mass was initially diagnosed as synovial sarcoma at an outside center.

Histologically, the patient's tumor showed monomorphic spindle to epithelioid cells within dense hyalinized stroma. Immunohistochemistry demonstrated diffuse nuclear NUT positivity along with TLE-1 and BCOR expression. Next-generation sequencing confirmed MGA::NUTM1 fusion, with additional alterations in TP53, CCND2, and PIK3CD. Despite chemotherapy, the patient's disease progressed, highlighting poor therapeutic response in these cases.

This case highlights the overlapping and distinguishing features between MGA::NUTM1 fusion sarcomas and other common entities. Because survival in the reported MGA::NUTM1 fusion sarcomas varies widely, we hypothesized that more aggressive cases harbor second-hit alterations in the tumor suppressor genes (eg, our case had TP53 missense mutations). As the true biological nature of MGA::NUTM1 fusion sarcomas is still evolving, exploring this hypothesis by studying the second-hit alterations will be worthwhile in future cases and studies. The current lack of effective targeted therapies underscores the need for further research into novel treatment strategies for this disease.

Nested variant of urothelial carcinoma is a rare entity characterized by a particularly aggressive clinical course and a poor prognosis. Although disease progression can involve the lung parenchyma, pulmonary carcinomatous lymphangitis is an exceptionally rare manifestation. Up until the date of this publication, evidence in literature is limited, highlighting the rarity of this pattern of dissemination and the importance of its timely recognition.

A 72-year-old man with initial macroscopic hematuria, who was diagnosed with nested variant of urothelial carcinoma with infiltration of the lamina propria. Despite transurethral resection of the tumor and subsequent systemic treatment with platinum-based chemotherapy, the patient experienced rapid disease progression, which was characterized by pelvic and mediastinal lymph node infiltration, pulmonary lymphangitic dissemination, bilateral hydronephrosis, and thrombosis of the right internal jugular vein, as well as the left common iliac, external iliac, and femoral veins.

This report documents a case of muscle invader nested variant of urothelial carcinoma, whose evolution was complicated by pulmonary carcinomatous lymphangitis, an extremely rare manifestation. Early recognition of this variant is essential to guide the diagnostic and therapeutic approach in patients with high-risk histological variants.

Congenital melanocytic nevus (CMN) is present at birth or appears during the first year of life. Certain dermoscopic features allow differentiation from other pigmented lesions and assessment of its evolution. We report a case of CMN with melanocytic distribution limited to hair follicles, associating dermoscopic findings with reflectance confocal microscopy (RCM).

A 2 year and 7 month old male patient with no relevant medical history presented with a 10 × 7 mm melanocytic macule on the left posterior lumbar region, present since birth. Dermoscopy revealed a central gray-blue area with dark brown globules distributed perifollicularly and radially from the follicular ostium, forming a "sky full of stars" pattern. RCM showed melanocytic proliferation at the dermoepidermal junction, organized in dense aggregates and nests, with a mixed mesh and globular pattern.

Perifollicular aggregates observed on dermoscopy correspond to melanin deposits within follicular openings. The "sky full of stars" pattern, which has been rarely described, may be associated with melanocytes confined to the infundibulum and noncontiguous hair follicles. It is important to differentiate this pattern from the globular pattern, which indicates melanocytic activity. RCM may provide useful information for clinical follow-up.