Clinician experience variability affects lung cancer detection using computed tomography. AI-based computer-aided diagnosis (CAD) systems can improve diagnostic accuracy, but their influence on thoracic surgeons with varying experience is unclear. This study aimed to evaluate the impact of CAD system on thoracic surgeons' assessment of pulmonary nodule malignancy.

A multireader, crossover study included 20 thoracic surgeons (8 junior, 12 senior). Each reader interpreted 100 anonymized pulmonary nodules twice-once with CAD and once without-following a washout period. Nodules were assessed using a 10-point likelihood of malignancy (LOM) scale and a binary (benign/malignant) assessment.

The CAD system demonstrated high malignancy prediction (AUROC = 0.929). CAD assistance significantly improved diagnostic accuracy across all readers (AUROC: 0.770-0.804, p = 0.0014 [BINARY]; 0.833-0.879, p < 0.001 [LOM]). Junior readers showed greater improvement (BINARY: 0.780-0.848, p < 0.001; LOM: 0.838-0.904, p < 0.001) compared with senior readers (BINARY: 0.763-0.775, p = 0.344; LOM: 0.831-0.862, p = 0.026). Specificity significantly increased with CAD (p = 0.008 overall, p < 0.001 junior readers), while sensitivity remained unchanged. Reading time slightly increased with CAD for benign cases (p < 0.05), but remained stable for malignant cases.

The CAD system improved thoracic surgeons' diagnostic performance, especially junior readers, by enhancing specificity and overall accuracy. AI-based CAD systems are beneficial for reducing diagnostic variability and supporting lung nodule malignancy assessment by inexperienced thoracic surgeons.

To describe the clinical profile of girls with central precocious puberty (CPP) and determine the factors associated with abnormal cranial magnetic resonance imaging (MRI) findings.

This retrospective study included girls aged 8 years or younger with a diagnosis of CPP who received care at King Abdullah Specialized Children's Hospital in Riyadh, Kingdom of Saudi Arabia, between 2015 and 2023. Data on clinical presentation, biochemical results, imaging findings, and treatment were obtained from medical records. Logistic regression analysis was performed to determine variables associated with MRI utilization and the occurrence of abnormal MRI findings.

The cohort comprised 70 girls with CPP. The median age at breast development was 7.12 years, and pubertal onset occurred at ≥6 years in 84.3% of patients. Cranial MRI was obtained in 43 patients (61.4%), and abnormal findings were identified in 17 patients (24.3%). Pituitary gland enlargement (n = 6) and hypothalamic hamartoma (n = 4) were the most frequent abnormalities. Girls with a bone age-to-chronological age ratio <1 year had lower odds of undergoing MRI (OR = 0.18, p-value = 0.009). Higher BMI z-scores were independently associated with abnormal MRI findings (OR = 1.95, p-value = 0.043). Other clinical and biochemical variables were not significantly associated with abnormal MRI results. GnRH analogue therapy was initiated in 81.4% of patients.

Abnormal cranial MRI findings were identified in nearly one-quarter of girls with CPP. Higher BMI z-scores were associated with abnormal MRI findings, whereas age at puberty onset and other clinical variables did not reliably predict intracranial abnormalities.

Visceral obesity may affect surgical difficulty in colorectal procedures. While body mass index (BMI) is commonly used to assess obesity, it does not accurately reflect intra-abdominal fat distribution. This study evaluated the impact of visceral fat area (VFA) on perioperative outcomes in robotic-assisted right colectomy.

We retrospectively analyzed consecutive patients undergoing robotic-assisted right colectomy with lymphadenectomy between January 2023 and May 2025. VFA was measured on preoperative computed tomography at the L4 level. Patients were categorized into low-VFA (<100 cm²) and high-VFA (≥100 cm²) groups. Surgical outcomes and lymph node yield were compared.

Sixty-one patients were included, and 29 (47.5%) were classified as high VFA. Lymph node yield was significantly lower in the high-VFA group (P < .001). Operative time, blood loss, and postoperative complications did not differ significantly between groups. Major complications occurred in 6.5% of patients.

Visceral adiposity is associated with reduced lymph node retrieval in robotic-assisted right colectomy, without increasing perioperative morbidity. VFA may serve as a practical indicator of operative complexity.

Immune checkpoint inhibitors have improved outcomes in small-cell lung cancer (SCLC), yet durable benefit remains limited, and the immune consequences of SCLC transformation from EGFR-mutant lung adenocarcinoma (LUAD) remain incompletely understood. Conventional explanations for resistance emphasize PD-L1 expression, tumor mutational burden, T-cell dysfunction, myeloid suppression, and stromal exclusion, but these factors do not fully explain how lineage-state changes alter tumor recognition. Here, we examine lineage plasticity as a potential tumor-cell-intrinsic contributor to immune resistance. We use the term "immune invisibility" narrowly to denote failure of tumor-cell recognition caused primarily by impaired MHC-I antigen processing and presentation. This state is distinguished from immune exclusion and T-cell dysfunction, although the three barriers may coexist. Evidence linking neuroendocrine state to reduced antigen presentation is strongest in primary SCLC and experimental SCLC models. In EGFR-mutant lung adenocarcinoma undergoing SCLC transformation, analogous changes remain biologically plausible but have not been established in paired longitudinal specimens. Therapeutically, checkpoint blockade alone may be insufficient when tumor recognition or T-cell entry is impaired. Clinically established approaches include chemoimmunotherapy in defined SCLC settings and DLL3-directed T-cell engagement in previously treated disease, whereas epigenetic combinations, STING/IFN activation, most antibody-drug conjugates, and cellular therapies remain investigational. Integrating lineage state, antigen-presentation capacity, immune localization, and retained surface targets may provide a framework for distinguishing immune-restoration from immune-redirection strategies.

Extramedullary multiple myeloma is characterized by clonal plasma cell proliferation outside the bone marrow and is associated with an adverse prognosis, particularly when accompanied by high-risk cytogenetic abnormalities. Sinonasal involvement is rare and may present with recurrent epistaxis or unilateral nasal obstruction, creating diagnostic overlap with inflammatory, vascular, lymphoid, and epithelial sinonasal lesions. We report a 54-year-old man with an eight-month history of progressive right-sided nasal obstruction and intermittent epistaxis that became increasingly frequent and refractory to nasal packing. Magnetic resonance imaging showed a right sinonasal mass involving the nasal cavity and maxillary sinus, with septal deviation and no radiological evidence of orbital floor or nasal septal erosion. Endoscopically guided biopsy demonstrated a dense plasma cell infiltrate with mature and atypical forms. Systemic evaluation revealed anemia, multiple lytic skull and humeral lesions, 32% bone marrow plasma cell infiltration, an IgG monoclonal protein with lambda light-chain restriction, and high-risk cytogenetic abnormalities including CKS1B 1q gain, deletion 17p, and deletion 13q. These findings established a diagnosis of high-risk symptomatic multiple myeloma with extramedullary sinonasal involvement rather than a solitary extramedullary plasmacytoma. This case emphasizes that recurrent epistaxis associated with a unilateral sinonasal mass warrants early biopsy and systemic evaluation, particularly when clinical or laboratory features suggest an underlying plasma cell neoplasm.

Lung cancer remains one of the most prevalent and lethal malignancies worldwide and is characterized by a complex tumor microenvironment (TME), including severe hypoxia, acidosis, elevated glutathione levels, and pronounced immunosuppression. These pathological conditions compromise the efficacy of conventional therapies and contribute to drug resistance, tumor recurrence, and metastasis. Nanodynamic therapy (NDT) is an emerging therapeutic paradigm that employs nanomaterials to amplify reactive oxygen species (ROS) generation in response to endogenous or exogenous stimuli, thereby enabling localized tumor ablation and immune reprogramming. This review systematically summarizes the biological basis of NDT in lung cancer. Particular emphasis is placed on the sequential biological processes of TME responsiveness, programmed cell death (PCD) pathway reprogramming, and immune remodeling. We comprehensively review the therapeutic applications and translational potential of four major NDT modalities-sonodynamic therapy (SDT), chemodynamic therapy (CDT), photodynamic therapy (PDT), and radiodynamic therapy (RDT)-in lung cancer. We further highlight recent advances in the integration of these modalities with lung cancer-specific therapeutic strategies. These advances include immunogenic cell death (ICD)-mediated conversion of immunologically "cold" tumors into "hot" tumors, as well as synergistic strategies incorporating EGFR tyrosine kinase inhibitor (EGFR-TKI) therapy, anti-angiogenic treatment, and inhalable pulmonary delivery systems. Finally, we critically examine major barriers to the clinical translation of NDT, including the limited availability of clinically relevant in situ models, inadequate material consistency, insufficient long-term pulmonary toxicity data, and the lack of standardized physical activation parameters. We further propose priorities for future research and clinical translation. Collectively, this review provides a systematic and integrative framework for lung cancer NDT, spanning mechanistic design, therapeutic optimization, and potential clinical translation.

Anticancer therapy can eliminate immune-visible tumour cells while simultaneously imposing selective pressures that favour residual immune-evasive populations. This mini-review conceptualizes therapy-induced immunoediting as a dynamic continuum comprising pre-existing escape, therapeutic immune activation, a selective bottleneck, residual equilibrium and secondary escape. We discuss how genetic alterations, therapy-resistant stem-like tumour-cell states and spatial remodelling of vascular, stromal and myeloid niches cooperate to reduce tumour visibility, effector susceptibility and immune-cell access. Representative approved and investigational therapies illustrate both successful pharmacological interception and the limitations of non-selective immune intensification. We further highlight residual equilibrium as a clinically actionable window that may be identified through longitudinal tissue sampling, circulating tumour DNA and spatial or single-cell profiling. Clinically, longitudinal biomarkers may identify residual equilibrium and guide mechanism-matched treatment adaptation before immune-evasive populations expand into radiographically evident relapse.

Myelodysplastic syndrome (MDS) are clonal myeloid neoplasms that cause cytopenias and can progress to acute myeloid leukemia (AML). Hypomethylating agents (HMA) are the mainstay of treatment for higher risk disease, but they achieve responses in only half of treated patients and complete remission rates are low. Several scientifically based combinatorial regimens have been tested in clinical trials but none has demonstrated a survival benefit over HMA monotherapy. Allogeneic stem cell transplant remains the only curative therapy and is dependent on effective donor lymphocytes for its efficacy. However, access is limited by its toxicity, so alternative approaches are sorely needed. Recent clinical and translational studies have shown that MDS is not only a clonal myeloid disorder, but also associated with immune dysregulation, inflammatory signaling, T-cell repertoire restriction, immune exhaustion, and immune mediated suppression of hematopoiesis. These findings suggest that there is potential for unlocking a novel approach to the treatment of MDS by restoring and/or enhancing the lymphoid immune response. In this review, we discuss the current understanding of the role of normal T lymphocytes in MDS, the causes and manifestations of dysfunctional T lymphocytes as well as the role and dysfunction of natural killer (NK) cells. The role of therapeutic immunosuppression in lower risk MDS is reviewed, as is the impact of HMAs on dysregulated T lymphocytes and NK cells in higher risk disease. We propose that there is tremendous potential for more targeted approaches to engage the lymphoid compartment in addressing the unmet therapeutic need in MDS.

Stromal tumor-infiltrating lymphocytes (TILs) are established biomarkers in triple-negative breast cancer (TNBC), but conventional density-based assessment does not capture their spatial relationship to tumor nests. We evaluated whether an H&E-derived spatial architecture index (SAI) provides predictive information beyond stromal TIL density for pathologic complete response (pCR) after neoadjuvant therapy.

This single-center retrospective cohort included 236 patients with TNBC who had evaluable pretreatment core biopsy slides and definitive surgical response assessment. The primary SAI was the equally weighted mean of standardized close interaction ratio and lymphocyte cluster index, together with reverse-coded standardized lymphocyte-tumor distance and edge enrichment. The primary multivariable analysis included 231 patients with complete clinicopathologic data. Robustness was evaluated using bootstrap optimism correction, alternative SAI constructions, treatment-regimen and propensity-score analyses, repeated nested cross-validation, and a 60-case reproducibility assessment. During internal validation, preprocessing and SAI construction were repeated within each training fold.

Of 236 patients, 122 (51.7%) achieved pCR. In the main multivariable model, the SAI remained associated with pCR (OR 2.79 per 1 SD, 95% CI 1.79-4.35; P < 0.001), whereas stromal TIL density was not independently significant (OR 0.88 per 10% increase, 95% CI 0.74-1.04; P = 0.123). Bootstrap optimism-corrected AUROCs were 0.698 for the clinical model, 0.705 after the addition of stromal TIL density, 0.764 after the addition of the SAI, and 0.765 after the addition of both. Across six internally validated algorithms using the full feature set, mean AUROCs ranged from 0.730 to 0.752, with only modest between-algorithm differences. The SAI showed excellent interobserver reproducibility (ICC 0.93, 95% CI 0.89-0.95). Its association with pCR persisted in the chemotherapy-only subgroup (OR 2.48, 95% CI 1.52-4.05; P < 0.001), whereas the interaction with pembrolizumab-containing treatment was not significant (P = 0.222).

In this exploratory single-center retrospective cohort, the H&E-derived SAI provided internally validated predictive information beyond stromal TIL density for pCR. External multicenter validation, assessment of intersite technical reproducibility, and prospective calibration are required before clinical implementation.

Seborrheic keratosis (SK) is a common benign epidermal neoplasm, particularly affecting the elderly. Although non-malignant, it often poses cosmetic and diagnostic challenges due to its resemblance to malignant skin tumors. This review aims to provide a comprehensive update on the recent advancements in the epidemiology, pathogenesis, diagnostic modalities, and therapeutic approaches for SK.

A narrative review of current literature was conducted, focusing on molecular insights, diagnostic innovations, and therapeutic options for SK. Sources were identified through searches in PubMed, ScienceDirect, and Google Scholar over the last decade using relevant keywords.

Molecular research has highlighted the role of oncogenic mutations, including AKT pathway alterations and amyloid precursor protein (APP) involvement. Non-invasive diagnostic tools such as dermatoscopy, reflectance confocal microscopy (RCM), and optical coherence tomography (OCT) have improved lesion differentiation. Artificial intelligence (AI)-based algorithms have further enhanced diagnostic precision. While conventional therapies such as cryotherapy, excision, electrodesiccation, and laser remain effective, they may cause post-inflammatory hypopigmentation. Recent non-invasive treatments, including 30%-50% aqueous nitric-zinc oxide solution with organic acids, 65 or 80% trichloroacetic acid (TCA) solution, and 0.3% Annona muricata L. seed extract cream have demonstrated efficacy with minimal side effects. Nano-Pulse Stimulation (NPS) technology emerges as a novel low-complication treatment.

Advances in molecular understanding and technology have transformed the diagnostic and therapeutic landscape for SK. There is a growing need for accessible, effective, and cosmetically favorable treatment options, especially with rising patient demand. Further research is warranted to validate long-term efficacy and broaden availability.