Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor with a poor prognosis. Magnetic resonance imaging (MRI) is widely used for the clinical diagnosis and prognostic evaluation of GBM. This study aimed to investigate the relationship between MRI semantic features and overall survival, and to explore the underlying biological mechanisms by transcriptomic analysis. In this study, we reviewed the MRI images of 171 patients with GBM from The Cancer Genome Atlas (TCGA) and Clinical Proteomic Tumor Analysis Consortium (CPTAC) databases and evaluated twelve MRI semantic features. Cox regression model and Kaplan-Meier survival curve were used to assess the prognostic value of the imaging features. Additionally, we investigated the relationship between imaging features and gene expression using differential gene expression and enrichment analysis in the cohort of 68 tumor samples with RNA-seq data. 171patients with GBM were included in the imaging-prognostic cohort (median age was 60.0 years and 59.6% were male). In the multivariate analyses, age (HR: 1.04, 95% CI: 1.03-1.06, P < 0.001), ependymal extension (HR:1.88, 95% CI:1.32-2.69, P < 0.001), contrast-enhancing tumor (CET) crossing midline (HR:2.38, 95% CI:1.16-4.91, P = 0.018) were significantly associated with shorter overall survival (OS). Gene set enrichment analysis (GSEA) showed that these features were significantly associated with pathways involved in inflammatory responses and tumor invasiveness, such as TNF-α signaling via NF-κB and epithelial-to-mesenchymal transition. Our study demonstrated that MRI semantic features, including ependymal extension and CET crossing the midline, can serve as prognostic indicators for patients with GBM. Additionally, several selected MRI features were found to be associated with specific biological pathways, potentially informing treatment decisions based on these distinctive semantic characteristics of GBM.

Claudin-low breast cancers (BCs), representing approximately 1.5-14% of all BCs, are characterized by high aggressiveness, enriched cancer stem cell (CSC) population, and poor prognosis. Despite the established role of Notch signaling in mammary gland development and BC progression, its status in claudin-low BCs remains inadequately explored. In this study, Notch pathway activation was evaluated in BC cell lines and 107 patient samples. Claudin-low subtype exhibited elevated Notch activity. Notch1 was observed to be the predominant receptor in the above subtype, whereas Notch3 was predominant in the claudin-high cancers. Notch1 and HES1 expression showed a significant inverse correlation with claudins 3, 4, and 7, and were positively associated with aggressive tumor features including high Ki67 index, higher grade, and increased metastasis. Immunohistochemical analysis further confirmed a correlation between nuclear Notch1 (N1ICD) expression and claudin-low status, supporting its potential as a biomarker for identification of aggressive BC. Combined treatment with celecoxib (10 µM) and doxorubicin (1 µM) in claudin-low cells not only significantly inhibited Notch signaling and claudin expression, but also suppressed viability, proliferation, migration, and BCSC populations. Since Notch signalling may be an essential factor in these latter events, our findings suggest that Notch1/N1ICD can serve as therapeutic targets for the better management of claudin-low BCs. However, validation of the same requires detailed functional studies involving modulation of each type of Notch receptor or other players involved in Notch signaling using more robust approaches.

Hodgkin lymphoma survivors (HLSs) are at risk of developing late effects (LEs), and their knowledge is crucial for prevention and treatment. We explored HLSs' knowledge and experience with LEs, their needs for information about LEs, lifestyle and rehabilitation, their needs for long-term follow-up, and factors associated with these needs.

Skin cancer has become a global public health issue. Dermoscopy is a routine diagnostic method; however, to improve accuracy, it is often combined with skin punch biopsy and stained histological slides for microscopic observation. The manual segmentation of the lesion area by doctors involves issues such as high subjectivity and time consumption. Deep learning techniques have become a mainstream solution. Compared to foreground-background segmentation in dermoscopic images, the semantic segmentation task for whole-slide skin cancer images is more complex, requiring precise differentiation of 10 distinct tissue classes (such as tumor, epidermis, dermis, hair follicle, sweat gland, fat, etc.). Among these, various epithelial and dermal tissue types exhibit similar morphological features and are interwoven, which increases segmentation difficulty. To address this, we propose a multi-frequency domain attention-based dual encoder network (MSF-VMDNet), which combines U-Net and Vision Mamba dual encoders for parallel feature extraction. The U-Net encoder incorporates an improved AFNO spectral decomposition module, which uses a frequency domain mechanism to extract high-resolution multi-class semantic information. It further strengthens spatial information through multi-scale feature aggregation, improving segmentation accuracy at class boundaries and making the contours clearer. The Vision Mamba encoder, based on a Linear State Space Model (SSM), optimizes long-range dependency modeling and enhances both global and local feature perception. By utilizing a multi-frequency domain mechanism, this encoder maps subtle class-discriminative features from the skin histological slide into the frequency domain, reinforcing contextual features and reducing misclassification rates. In the decoding phase, the SCConv module fuses features from different frequency domains and spatial levels. Experimental results show that MSF-VMDNet significantly outperforms existing methods in terms of class segmentation performance on skin cancer histological slide datasets, achieving an MIoU of 95.37% and a Dice coefficient of 95.11%. Additionally, the model demonstrates its generalization ability in extended experiments on the ISIC 2018 dermoscopic image, PanNuke pathological cell nucleus image, and Synapse image datasets.

Purpose: We explored the association between metastatic cancer, chemotherapy, and the risk for suicide attempts (suicide injuries) in adult trauma patients.Methods: We conducted a retrospective analysis of the Trauma Quality Program Participant Use File (2017-2019), comprising 27,474 patients from 700 U.S. Trauma Centers. Self-harm/suicide injury (compared to controls) was the dependent variable; presence of metastatic cancer and current chemotherapy were the key independent variables. We adjusted for age, sex, race/ethnicity, method of payment, facility levels, and discharge year (Model 1), and Model 1 plus trauma type, injury location, stay length, comorbidities, Injury Severity Score, and Glasgow Coma Scale (Model 2). We employed chi-square analysis, Fisher's exact test, and unadjusted and adjusted logistic regression using Stata v18, setting statistical significance at P≤0.05.Results: Of 27,474 patients, 249 (0.91%) reported suicide injuries. Significantly higher attempts were noted among patients with metastatic cancer (201 out of 249; 80.72%) and those not receiving chemotherapy (184 out of 249; 73.90%), P<0.001. Metastatic cancer was associated with higher odds of suicide injuries (unadjusted OR:2.252, 95%CI: 1.642-3.089; adjusted OR in Model 1:1.925, 95%CI:1.302-2.848). Chemotherapy was associated with lower odds of suicide injuries (unadjusted OR:0.408, 95%CI:0.307-0.541; adjusted OR in Model 1:0.444, 95%CI:0.311-0.636). However, neither metastatic cancer nor chemotherapy was significantly associated with suicide injuries in adjusted Model 2, suggesting the crucial role of other factors in influencing this risk.Conclusion: Patients with metastatic cancer exhibited notable prevalence of suicide injuries. Findings suggested metastatic cancer was associated with higher odds, and chemotherapy with lower odds, of suicide injuries. Multifaceted factors were associated with suicide risk beyond the presence of metastatic cancer or chemotherapy status, underscoring the importance of mental health assessments and interventions in oncology care, particularly for those with advanced cancer.

Primary cutaneous T-cell and B-cell lymphomas may occur at any age and are defined by specific clinical, histopathologic, and immunophenotypic features. Clinical correlation is critical to differentiate indolent and aggressive entities, such as the lymphomatoid papulosis subtypes, which may have histopathologic and immunophenotypic features that are indistinguishable from aggressive cutaneous T cell lymphomas. Awareness of mycosis fungoides variants that overlap with benign conditions may help prevent misdiagnosis. Lymphoproliferative disorders do not require aggressive treatment or extensive staging. Watchful waiting is often appropriate.

Onychopathology (nail unit pathology) is a niche area in dermatopathology. There is a lack of familiarity with nail unit pathology and basic anatomy in general among pathologists and dermatopathologists, because of the relative rarity of such specimens in practice, and the lack of exposure and teaching regarding these lesions in training. It is however a vibrant area of dermatopathology, with knowledge evolving rapidly. In this article, we explore new information in the analysis of melanocytic and epithelial lesions of the nail unit, as well as nail inflammatory disease.

This article highlights selected cutaneous mesenchymal tumors, emphasizing histopathology, immunophenotype, and molecular alterations. It outlines diagnostic pitfalls, distinguishing features, and clinical behavior of indolent and malignant lesions. Awareness ensures accurate and appropriate treatment, and prevents overtreating benign mimics.

Refinements in histologic criteria, staging systems (American Joint Committee on Cancer 8th edition, Brigham and Women's Hospital), clinical guidelines (National Comprehensive Cancer Network [NCCN]), and molecular tools like gene expression profiling have enhanced the precision of cutaneous squamous cell carcinoma diagnosis and treatment. In Merkel cell carcinoma, recent updates in viral pathogenesis, immunohistochemistry, and emerging biomarkers have aided in better diagnostics. As immunotherapies and precision oncology evolve, dermatopathologists remain essential in guiding patient-specific management strategies for both cutaneous squamous cell carcinoma and Merkel cell carcinoma.

Cutaneous adnexal tumors recapitulate hair follicles, sweat glands, and/or sebaceous glands. These tumors range from benign to malignant and might herald an underlying inherited tumor syndrome. Accurate classification of adnexal tumors is thus critical but can be challenging due to many knowledge gaps in this area. Recent advances have dramatically improved our understanding and diagnosis of adnexal tumors. Here, we review several recently described adnexal carcinomas and summarize new molecular drivers reported in previously established tumor entities. We highlight morphologic, immunohistochemical, and molecular clues helpful for diagnosis of these adnexal tumors.

Vulvar squamous cell carcinoma and its precursors are heterogeneous and classified into 3 biologically distinct subgroups: human papillomavirus (HPV)-associated, HPV-independent TP53-mutated, and HPV-independent TP53-wild type. Although nomenclature is established for HPV-associated high-grade squamous intraepithelial lesion and TP53-mutated differentiated vulvar intraepithelial neoplasia lesions, terminology for precursors in the TP53-wild-type subgroup is evolving. Accurate classification is essential, as prognosis, progression risk, and recurrence rates differ among subgroups. Diagnosis relies on integrated assessment of clinical presentation, histopathology, and immunophenotype, particularly p16 and p53 expression.

This article highlights current advances in melanocytic lesions and their impact on histopathologic diagnosis and patient management. Special emphasis is given to the concept of melanocytoma and the study of dysplastic nevi. Finally, the article describes the current status and possible future applications of immunohistochemistry, digital analysis, and artificial/augmented intelligence.

In the past 2 decades, several molecular methods have been developed as an adjunct for the assessment of melanocytic neoplasms. Some tests can assist in the diagnostic workup of neoplasms with ambiguous histopathologic findings. Others can optimize the selection of patients for targeted therapy. Some tests also aim to provide prognostic information. Scenarios when ordering these tests may be appropriate and helpful are discussed in this article as well as pitfalls in the interpretation of test results. Due to the inherent limitations in sensitivity and specificity of various tests, correlation with the histopathologic findings is paramount.

This study aimed to systematically review the literature regarding topical therapies for reducing the risk of cervical intra-epithelial neoplasia (CIN) grade 2 or higher (CIN II+) lesions among women with high-risk human papillomavirus (HPV) infection and histologically confirmed CIN I or either no cervical lesions.

Carcinoembryonic antigen (CEA) is commonly raised in patients with colorectal carcinoma (CRC) and has an established role in postoperative monitoring to detect early recurrence. CEA is not recommended as a screening tool for CRC; however, a de novo raised level mandates further investigation with a colonoscopy. This report describes a patient referred from primary care with a raised CEA and functional bowel symptomatology who went on to have a normal colonoscopy. The persistently rising CEA prompted a repeat colonoscopy, upper gastrointestinal and small bowel investigation and a CT of the abdomen and pelvis, without any cause being found. Finally, a CT-positron emission tomography scan revealed localised uptake in the thyroid gland, with a fine-needle aspiration confirming a diagnosis of medullary cell thyroid carcinoma with regional lymph node involvement.

Breast cancer is the most common invasive malignancy among women and represents the second leading cause of cancer-related mortality in this population, following lung cancer. While metastases typically involve the bones, liver and lungs, less common metastatic sites have also been documented. Metastatic involvement of the pancreas or duodenum from an extrapancreatic primary tumour is rare, accounting for less than 3% of all pancreatic and periampullary malignancies. We report a case of isolated ampullary metastasis originating from invasive lobular breast carcinoma in a female patient in her late 50s, more than a decade after the initial diagnosis, accompanied by a review of the relevant literature.Given the limited number of published cases, this report underscores the importance of considering metastatic breast cancer in the differential diagnosis of women presenting with obstructive jaundice, particularly in the presence of a relevant clinical history.

Focal treatment has emerged as a precision-oriented alternative to whole-gland treatment approaches for localized prostate cancer. It aims to selectively destroy clinically significant tumor foci while preserving surrounding structures that are essential for urinary continence and sexual function. Irreversible electroporation (IRE) is a relatively new and increasingly investigated focal treatment modality. By delivering short high-voltage pulses, IRE creates permanent nanopores in cell membranes and induces cell death predominantly through non-thermal mechanisms.This theoretical advantage - tissue ablation with relative preservation of the collagen-rich extracellular matrix - has heightened interest in IRE, particularly for tumors located near sensitive structures such as the neurovascular bundles, the urethral sphincter complex, and the rectal wall.In this review, we outline key procedural and technical aspects and summarize the clinical evidence for IRE in localized prostate cancer. Data from both prospective and retrospective case series demonstrate encouraging early and intermediate-term oncologic outcomes, although patterns of recurrence and the need for retreatment vary between cohorts and depend on the respective follow-up protocols. Functional outcomes are consistently excellent: continence is preserved in the vast majority of patients, and potency preservation is often high, typically ranging from approximately 75 to 95% among men who were potent prior to treatment.Despite these promising findings, widespread adoption in routine clinical practice is limited by the lack of robust long-term endpoints and the absence of randomized comparisons with established standards such as radical prostatectomy, radiotherapy, or risk-adapted active surveillance. While prospective comparative studies are highly challenging as they require large sample sizes, long follow-up periods, and careful endpoint definition, they are essential to clarify the role of irreversible electroporation within treatment algorithms, optimize patient selection, standardize follow-up and salvage strategies, and ultimately confirm durable tumor control with a sustained functional benefit.

Although immune checkpoint inhibitors (ICIs) and targeted therapies (TTs) have transformed the treatment of non-small cell lung cancer (NSCLC) across disease stages, real-world access remains highly unequal worldwide. Persistent cost barriers, fragmented reimbursement frameworks, and heterogeneous regulatory pathways limit equitable availability. The rapid proliferation of me-too agents has been proposed to counter monopolies; yet, this expansion has not consistently improved affordability. Heterogeneous evidentiary requirements-along with differences in clinical end points, comparator selection, crossover policies, and treatment duration-fragment therapeutic markets and complicate assessment of incremental clinical benefit. Divergent regulatory decisions, particularly between the US Food and Drug Administration and European Medicines Agency, underscore how trial design and geographic representation influence drug availability, especially when approvals rely on single-country data sets. These challenges are amplified in perioperative treatment strategies and rare oncogene-defined subgroups, where feasibility constraints and limited clinical equipoise hinder large randomized trials. As a result, an increasingly crowded therapeutic landscape makes cross-trial comparisons difficult and allows disparities in patient access to persist despite multiple approved therapies. Dose selection has historically followed maximum tolerated dose principles, even when preclinical and pharmacologic data suggest activity plateaus at lower exposure of ICI and TT. Dose and schedule optimization-through reduced dosing, extended intervals, or other deintensified strategies-therefore represents a rational and ethically grounded approach with a meaningful clinical impact. Such strategies may preserve efficacy while improving tolerability, reducing treatment burden, and mitigating financial toxicity, particularly in resource-limited settings. Aligning regulatory frameworks with dose optimization could promote more scalable, equitable, and sustainable NSCLC innovation.

Reviewing pathology reports requires physicians to integrate complex histopathologic, immunohistochemical, and molecular findings from multiple reports and institutions, often under time constraints that increase the risk of error and fatigue. Large language models (LLMs) offer a potential solution by generating concise, coherent summaries from complex pathology data.

Immune checkpoint inhibitors (ICIs) can essentially treat cancer but only in a small subset of patients. Treatment strategies capable of effectively and robustly sensitizing refractory patients to ICIs represent a highly coveted yet unmet clinical need. In this study, we identified DJ-1 as a negative T cell regulator. DJ-1 knockout boosts antitumor immunity and significantly potentiates PD-1 and TIM-3 blockades in murine cancer models. Single-cell sequencing of tumor-infiltrating CD45+ cells revealed that DJ-1 deficiency indirectly activates T cells by reprogramming macrophages. Mechanistically, loss of DJ-1 increases reactive oxygen species (ROS) in macrophages, activating NF-κB/STAT3 signaling to promote differentiation into Cxcl9+ immune-stimulatory phenotypes while reducing immune-suppressive Spp1+ macrophages. Notably, this reprogramming may be stable across tumor microenvironments because the transplanted DJ-1-deficient macrophages maintain T cell-activating capacity. Pharmacological inhibition of DJ-1 by disulfiram markedly potentiated antitumor efficacy of PD-1 blockade. This designates DJ-1 as a promising target for overcoming immune checkpoint resistance and optimize combination therapies.