Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor of the gastrointestinal tract with a high mortality rate. Although positive regulatory domain zinc finger protein 1 (PRDM1) has long been thought to play a key role especially in the differentiation of B cells, its role in ESCC has never been studied. This study aimed to examine the association between PRDM1 and ESCC clinical and pathological characteristics and prognosis. Using immunohistochemical and reverse transcription quantitative polymerase chain reaction, we detected the expression level of PRDM1 in consecutive ESCC surgical resections from 163 patients. To interpret PRDM1 immunohistochemical positivity, we employed three methods: PRDM1 10 high-power field (HPF) positive cell count (PCC), PRDM1 1HPF PCC and PRDM1 positive hotspots (PPHs). Based on PPH assessment and histological morphology, we developed a novel histological grading scheme. To evaluate the relationship between PRDM1 differential expression and clinical–pathological parameters in ESCC, we used the chi-square test. To evaluate the relationship between PRDM1 expression and ESCC prognosis, we performed Kaplan–Meier survival analysis and Cox regression analysis. Immunohistochemical staining revealed that PRDM1 was expressed in tumor epithelium, stroma, and adjacent squamous epithelium in ESCC. And the expression level of PRDM1 in tumor epithelium significantly correlated with tumor differentiation (P < 0.05) and was closely related to the patient prognosis (P < 0.05). Moreover, survival analysis results indicated that our novel histological grading seem to be better than the traditional histological grading criteria in predicting the prognosis of ESCC patients. PRDM1 holds promise as a novel indicator for ESCC, with potential application value in the histological grading, diagnosis, and prognostic assessment of this disease.

Background/objectives To address the high false-positive rate of fibrosis-4 (FIB-4), we hypothesize that combining it with readily available nutritional-inflammatory indices can improve the diagnostic accuracy for advanced liver fibrosis/cirrhosis.Methods Diagnostic performance was sequentially evaluated: first, individual metrics and FIB-4 were compared via receiver operating characteristics (ROC) curve analysis; then, their incremental value was assessed using DeLong’s test, net reclassification improvement (NRI) and integrated discrimination improvement (IDI); finally, the clinical utility of four combined strategies was examined.Results In discriminating advanced fibrosis/cirrhosis, the platelet-to-albumin ratio (PAR) showed a significantly higher area under the curve (AUC) of 0.698 than the haemoglobin, albumin, lymphocyte and platelet (HALP, AUC= 0.494; p < .001). Similarly, the prognostic nutritional index (PNI) also outperformed HALP in diagnostic performance (AUC = 0.658; p < .0001). Adding PAR or PNI to FIB-4 significantly improved diagnostic performance, as evidenced by Delong’s test, NRI and IDI. Specifically, the combination of FIB-4 and PAR improved specificity (88.5% vs 38.5%) and overall accuracy (63.7% vs 54.8%) compared to FIB-4 alone, while the FIB-4 and PNI combination achieved a specificity of 80.3%. The parallel strategy (FIB-4 + ‘PAR or PNI’) maintained a sensitivity of 61.9% and achieved the highest negative predictive value (65.2%). The serial strategy (FIB-4 + ‘PAR and PNI’) provided the highest specificity (95.1%) and positive predictive value (81.8%).Conclusions In scenarios prioritizing high sensitivity, FIB-4 alone is suitable. For high specificity, a sequential strategy (FIB-4 + ‘PAR and PNI’) is recommended. For balanced performance, a parallel strategy (FIB-4 + ‘PAR or PNI’) provides optimal feasibility.

BACKGROUND:Systemic therapies have been widely applied in the first-line treatment of patients with unresectable hepatocellular carcinoma (uHCC). Regimens based on programmed cell death 1/ligand 1 (PD-1/PD-L1) inhibitors combined with either bevacizumab or lenvatinib have become first-line treatments, yet the optimal strategy remains controversial. This systematic review and meta-analysis aimed to compare the efficacy and safety of lenvatinib versus bevacizumab, both in combination with PD-1/PD-L1 inhibitors, as first-line therapy for uHCC. METHODS:A thorough literature search was performed in PubMed, Web of Science, Embase, CNKI and Wanfang from their inception to August 1, 2025. The primary endpoints were overall survival (OS) and progression-free survival (PFS), whereas secondary endpoints included objective response rate (ORR), disease control rate (DCR) and adverse events (AEs). A meta-analysis using a random effects model was performed to obtain hazard ratio (HRs) and 95% confidence intervals. Statistical analyses were conducted using Stata software. RESULTS:A total of 10 retrospective cohort studies involving 1659 patients were included. The analysis demonstrated that, compared with the bevacizumab-based regimen, the lenvatinib-based regimen was associated with significantly prolonged OS (I2 = 55.9%, HR: 0.69, 95% CI: 0.5-0.95, p = 0.023) and PFS (I2 = 45.7%, HR: 0.73, 95% CI: 0.59-0.9, p = 0.004). No significant differences were observed between the two groups in terms of ORR (I2 = 65%, RR: 1.09, 95% CI: 0.91-1.31, p = 0.304) or DCR (I2 = 77%, RR: 0.99, 95% CI: 0.92-1.06, p = 0.532). Regarding safety, the overall incidence of AEs was comparable between the two groups. However, the lenvatinib-based regimen was associated with a higher incidence of hand-foot skin reaction and neutropenia, whereas the bevacizumab-based regimen carried a higher risk of gastrointestinal haemorrhage. CONCLUSION:In this meta-analysis of retrospective studies, lenvatinib plus PD-1/PD-L1 inhibitor regimens were associated with superior OS and PFS compared with bevacizumab plus PD-1/PD-L1 inhibitor regimens as first-line regimen for uHCC in East Asian populations. These findings require confirmation in large-scale, prospective, multinational randomized controlled trials in other populations.

Background: Invariant natural killer T (iNKT) cells show promise as immunotherapeutic agents for solid tumors, and our prior study demonstrated that combining iNKT-cell therapy with transarterial chemoembolization (TACE) achieved a 58.3% objective response rate (ORR) in hepatocellular carcinoma (HCC). This study further examines iNKT-mediated immune modulation of post-TACE survival dynamics and associated prognostic biomarkers. Methods: Clinical data and peripheral blood samples were obtained from 77 HCC patients in Beijing you'an Hospital between 2018-2023, including 38 receiving TACE alone and 39 receiving combined iNKT-cell/TACE therapy. Serial measurements included: Hematological parameters; Liver function tests [alanine aminotransferase (ALT), aspartate aminotransferase (AST), bilirubin]; Inflammatory markers [C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR)]; Cytokine profiling [Interferon-gamma (IFN-γ), Interleukin-6 (IL-6), Interleukin-10 (IL-10)]. Potential Prognostic factors for progression-free survival (PFS) were identified through univariate/multivariate Cox regression. A risk-score model was derived using significant covariates from the multivariate analysis. Model performance was evaluated by time-dependent receiver operating characteristic (ROC) analysis [Area Under the Curve (AUC) calculation] and Kaplan-Meier survival stratification with log-rank testing. Results: The TACE group exhibited decreased lymphocytes but increased neutrophils/monocytes post-treatment, whereas iNKT + TACE maintained stable counts. Systemic inflammation indices [NLR/systemic immune-inflammation Index (SII)/systemic inflammation response index (SIRI)] rose significantly in TACE alone (all p < 0.05) but remained stable in iNKT + TACE. Cytokine profiling revealed reduced IL-6/IL-10 (p < 0.001/p = 0.012) and elevated IFN-γ/tumor necrosis factor-alpha (TNF-α) (p < 0.01/p < 0.001) in iNKT + TACE vs. TACE. Multivariate analysis identified lymphocyte count (HR = 0.18, 95%CI 0.04-0.76, p = 0.02), IL-6 (HR = 2.57, 95%CI 1.03-6.86, p = 0.04), and IFN-γ (HR = 0.14, 95%CI 0.02-0.98, p = 0.04) as independent PFS predictors. The risk model demonstrated strong discrimination (AUC = 0.891, 95%CI 0.73-1.00), with median PFS of 9.5 vs. 3.0 months for low- vs. high-risk groups (log-rank p < 0.01) in iNKT + TACE group. Conclusions: iNKT cell therapy stabilizes peripheral lymphocyte counts and attenuates TACE-induced inflammation in HCC. The combined evaluation of lymphocyte levels, IL-6, and IFN-γ represents a promising prognostic biomarker panel for PFS in iNKT + TACE-treated patients.

3028 Background: Pts with advanced HCC face limited treatment options beyond immunotherapy and anti-angiogenic agents. GPC3, a surface antigen overexpressed in HCC and associated with poor prognosis, represents a promising therapeutic target due to its tumor-specific expression. MRG006A, a potential first-in-class GPC3-targeted ADC, demonstrated potent pre-clinical anti-tumor activity. Here we report the preliminary safety and efficacy of MRG006A in advanced HCC with intermediate/high GPC3 expression from a phase I/II trial. Methods: MRG006A-001 (NCT07093970) is an ongoing first-in-human, open-label, multi-center phase I/II study. The phase I study comprises dose escalation (Ia) and dose optimization/expansion (Ib) stages. The dose-escalation employed an accelerated titration plus 3+3 design. Eligible pts who had failed standard treatment received MRG006A intravenously at 1.6-6.4 mg/kg every three weeks (Q3W). GPC3 expression was only required for dose expansion cohorts. The primary endpoints were safety and tolerability. Secondary endpoints included objective response rate (ORR), disease control rate (DCR), duration of response (DOR), progression-free survival (PFS), clinical benefit rate (CBR), etc. Results: As of Dec 19, 2025, the maximum administered dose was established as 6.4 mg/kg Q3W, with ≥ G3 treatment-related adverse event (TRAE) of platelet count decreased reported in all six pts at this dose level and dose-limiting toxicity (G4 platelet count decreased) observed in one patient. During dose escalation, tumor response was observed at 3.2 mg/kg and 4.8 mg/kg. Accordingly, dose optimization in phase Ib proceeded with three levels (3.2, 4.0, and 4.8 mg/kg Q3W). Twenty-six HCC pts with intermediate or high GPC3 expression were enrolled across three cohorts; 61.5% had BCLC stage C disease; median 2 (range 1-4) prior lines of therapy, and 25 (96.2%) had received immune checkpoint inhibitors and anti-angiogenic agents. Among 25 efficacy evaluable pts, ORR, DCR and CBR were 23.1%, 68.0% and 32.0%, respectively. In pts with high GPC3 expression (n=12), ORR, DCR and CBR increased to 33.3%, 75.0% and 50.0%, respectively; median PFS and DOR were 7.0 and 4.2 months (median follow-up 5.7 months). Most pts (24 [92.3%]) experienced TRAE of any Grade. TRAEs of ≥ G3 were reported in 11 (42.3%) pts . The most common TRAEs were platelet count decreased (88.5%), blood bilirubin increased (50.0%), AST increased (46.2%), white blood cell count decreased (38.5%), and nausea (30.8%). No treatment-related permanent discontinuations or deaths occurred. Conclusions: MRG006A demonstrated manageable safety and promising anti-tumor activity in heavily pretreated pts with GPC3-expressing advanced HCC. Our findings support the therapeutic potential of GPC3-directed ADC and merits further clinical investigations. Clinical trial information: NCT07093970 .

To evaluate the prognostic utility of the FIGO 2023 staging system with/without molecular classification vs. FIGO 2009 in endometrial cancer. A total of 172 patients between 2015 and 2020 diagnosed with endometrial cancer in our center were included in this study. Molecular classification subtypes were classified using DNA sequencing and immunohistochemistry. The clinical characteristics and patients’ prognosis were analyzed. Of the 172 patients, 10 patients were classified to the POLEmut, 30 patients to the MMRd group, 106 patients to the NSMP group, and 26 patients to the p53abn group. Stage migration from FIGO 2009 to FIGO 2023 occurred in 27.3

Background:Accurate identification of pathological high-risk factors (PHRFs) in early-stage lung adenocarcinoma (LUAD) is critical for optimizing surgical decision-making. However, reliance on intraoperative frozen section (FS) assessment is limited by insufficient sensitivity. This study aimed to retrospectively develop and prospectively validate a deep learning model (a knowledge-based graph convolutional network, KB-GCN) based on preoperative CT scans to identify PHRFs in LUAD. Methods:We retrospectively developed and externally validated a KB-GCN using two cohorts (A: 268 patients/297 lesions for training and internal validation; B: 68 patients/75 lesions for external validation). We then conducted a pre-registered, single-center, prospective observational validation in 200 consecutive surgical candidates with early-stage LUAD. Before prospective enrollment, the model architecture, weights, preprocessing pipeline, and the decision threshold (0.40, determined from the retrospective phase) were locked. For each patient, a preoperative prediction was generated before intraoperative FS and final pathology (FP); the clinical team was blinded to the model output. The performance of the locked model and FS was compared with FP. Results:In retrospective validation, the KB-GCN model achieved an area under the curve (AUC) of 0.92 (95% CI: 0.86-0.97) in the internal validation cohort and 0.88 (95% CI: 0.81-0.94) in the external validation cohort. The KB-GCN model outperformed all 6 compared classical 2D/3D CNN models (best comparative AUC: 0.79). In prospective validation, intraoperative FS achieved an overall sensitivity of 59% and accuracy of 77% for detecting PHRFs, misclassifying 40.6% (39/96) of PHRF-positive cases. In contrast, the KB-GCN model demonstrated significantly higher overall sensitivity (82%) and AUC (0.83), although with lower specificity (75% vs FS: 92%). The KB-GCN model showed superior performance in part-solid nodules (PSN, AUC: 0.86) and in 2-3 cm tumors (AUC: 0.86), with moderate performance in ≤1 cm tumors (AUC: 0.82) and in 1-2 cm tumors (AUC: 0.79). Conclusion:This study retrospectively developed and, for the first time, prospectively demonstrates that a deep learning model based on preoperative chest CT predicts PHRFs, achieving significantly higher sensitivity for identifying PHRFs in early-stage invasive LUAD than conventional intraoperative FS. Despite slightly lower specificity, the KB-GCN model effectively compensates for the critical sensitivity deficit of FS, particularly for tumors (1-3 cm) containing solid components. Preoperative deep learning assessment combined with intraoperative FS provides thoracic surgeons with more comprehensive and accurate information to optimize surgical decisions (e.g., extent of resection: lobectomy or sublobar resection). Future development requires integrating this preoperative model with intraoperative FS assessment into standardized workflows.

BACKGROUND:Proficiency in cytopathologic diagnosis depends heavily on extensive hands-on practice and immediate error correction. Traditional teaching models, however, are constrained by limited practice opportunities and delayed feedback, which fails to meet the core skill-development needs of residents. METHODS:In total, 45 pathology residents were enrolled and assigned to two groups. The experimental group (n = 20) adopted a tripartite teacher-artificial intelligence-resident collaborative teaching model, whereas the control group (n = 25) received conventional instruction. Both groups underwent an identical 8-week teaching cycle. RESULTS:The questionnaire results from the experimental group indicated that 19 of 20 residents (9%) deemed the new model highly necessary, and 15 of 20 (75%) believed it significantly improved their diagnostic competence. Semistructured interviews further revealed that the model enhanced diagnostic ability, facilitated personalized learning, and alleviated learning anxiety. For objective metrics, the experimental group demonstrated a significantly higher postintervention concordance rate for gray-zone cell identification (78.65%) compared with both their preintervention baseline (64.38%) and the contemporaneous control group (66.84%; t = 8.962; p < .001). In addition, the experimental group exhibited a markedly faster diagnostic speed (mean ± standard deviation, 3.05 ± 0.52 minutes per case) compared with their preintervention performance (5.92 ± 0.85 minutes per case) and the control group (5.63 ± 0.79 minutes per case; t = 14.821; p < .001). No statistically significant changes were observed in the control group (p > .05). CONCLUSIONS:This study demonstrates that artificial intelligence technology integrated with real-time visual interaction effectively improves the cytopathologic diagnostic skills of residents and merits wider promotion in pathology education.

BACKGROUND:Digestive system malignancies are a major global health burden, and the role of fatty acid binding protein 5 (FABP5) in these tumors remains controversial. AIMS:This meta-analysis aimed to evaluate the correlation between FABP5 expression and clinicopathological features, as well as survival outcomes in digestive system malignancies. MATERIALS AND METHODS:Data from 11 studies (1207 patients) retrieved from PubMed, Embase, Cochrane Library, CNKI, and WanFang were analyzed. RESULTS:FABP5 overexpression was associated with poorer overall survival (OS), larger tumor size, advanced UICC stage, and increased risk of vascular invasion and lymph node metastasis. Notably, FABP5 overexpression is particularly associated with poorer OS in the subgroup of digestive tract malignancies and larger tumor sizes in the subgroup of Chinese patients. DISCUSSION:Cellular experiments demonstrated that FABP5 overexpression enhances proliferation, migration, and invasion in hepatocellular carcinoma (Huh7) and gastric cancer (HGC-27) cell lines, while FABP5 knockdown reduces these effects. Mechanistically, FABP5 may drive tumor progression through PPARβ/δ signaling, epithelial-mesenchymal transition induction, angiogenesis regulation, and potential effects on fatty acid metabolism and hypoxia-related pathways. CONCLUSION:FABP5 overexpression correlates with adverse clinicopathological features and prognosis in digestive system malignancies, suggesting its potential as a biomarker for these tumors. Further research is warranted.

The objective of this study is to evaluate the clinical presentations, treatment strategies, and prognostic factors for prostate diffuse large B-cell lymphoma (DLBCL), aiming to improve patient management and outcomes. We conducted a retrospective analysis of four prostate DLBCL cases treated at Beijing Chaoyang Hospital between 2014 and 2024, integrating these findings with data from the surveillance, epidemiology, and end results (SEER) dataset (2000-2021) to provide a broader context. All four patients underwent thorough diagnostic evaluations, and immunohistochemistry (IHC) confirmed their diagnoses. Kaplan-Meier survival curves and Cox regression analysis were applied to the SEER dataset to assess overall survival and treatment efficacy. P-values below 0.05 considered statistically significant. All four patients were diagnosed with prostate DLBCL via biopsy and confirmed by IHC, with extraprostatic involvement in three cases. Two patients achieved complete response, and one had partial response. In the SEER database, Kaplan-Meir analysis found that 59 patients had a 5-year survival rate of 59 months when it dropped in half, while multi-variable Cox regression highlighted age (HR 10.45, p < 0.001), surgery (HR 0.38, p = 0.0292), and radiation (HR 0.35, p = 0.0212) as the survival predictors. Although chemotherapy was administered in clinical practice, its impact was not statistically significant in our analysis. Prostate DLBCL is aggressive with diverse clinical presentations, making early detection and personalized treatment essential. Surgery and radiotherapy significantly improve patient outcomes, but the prognostic impact of chemotherapy, despite its widespread use, requires further validation through clinical trials.

BackgroundInvariant natural killer T (iNKT) cells are an unconventional lymphocyte subset that has garnered increasing attention due to their shared features with both natural killer cells and conventional T cells, as well as their unique dual immunological functions. In this study, we conducted a comprehensive bibliometric analysis to trace the evolution of research in the iNKT cell field, identify emerging trends, and highlight current research hotspots and frontier directions.MethodsWe performed a literature search in the Web of Science Core Collection database to retrieve all publications related to iNKT cells published to December 31, 2024. We then used the visualization tools CiteSpace and VOSviewer to conduct a bibliometric analysis of the retrieved data.ResultsWe identified 2,579 relevant publications authored by 12,108 individuals from 2,218 institutions across 70 countries. These publications appeared in 540 journals and collectively cited 60,342 references from 4,322 different journals. The publication volume in the iNKT cell field has significantly increased since 2008, peaking at 151 articles in 2018. This surge highlights the sharp rise of research interest in this area. The United States led in publication output within this field. Among the journals, the Journal of Immunology was the most prolific and also ranked first in total citations. Besra was the most published author, while Bendelac’s research was highly influential. Research on iNKT cells is undergoing a paradigm shift from mechanistic exploration to clinical application.ConclusionsOur bibliometric analysis delineates the thematic evolution within the iNKT cell research landscape. Future investigations will converge on several pivotal frontiers, including improving the tumor microenvironment, reprogramming the functional activity of iNKT cells within tumors, and advancing engineered immunotherapies. Additionally, strategies to engineer iNKT cells for more targeted and effective therapeutic interventions are likely to gain momentum, as researchers aim to overcome the current limitations in the field and transition from basic mechanistic studies to more impactful clinical applications.

Aims In recent years, patients with programmed cell death-Ligand 1 (PD-L1)-positive oesophageal squamous cell carcinoma (OSCC) have been able to benefit from immunotherapy. However, method for improving the treatment efficacy of PD-L1-positive patients is a problem that needs further consideration. Studies on the relationship between human epidermal growth factor receptor 2 (HER2) and PD-L1 expression have recently been reported in certain cancers, but the relationship between PD-L1 and HER2 expression in OSCC is still unclear. Methods A total of 263 patients with OSCC were included in the study. PD-L1 protein expression and HER2 protein expression were analysed by immunohistochemistry (IHC), and fluorescence in situ hybridisation (FISH) was performed to assess HER2 gene amplification. The significance of differences between HER2 status, PD-L1 status and clinicopathological parameters was assessed. The relationship between PD-L1 status and HER2 status was examined. Results Of the 263 OSCC cases, the PD-L1-positive expression rates were 39.2% and 77.2% in OSCC for Tumour Proportion Score (TPS) and Combined Positive Score (CPS), respectively, and PD-L1 expression was associated with the degree of tumour differentiation. The HER2 expression was positive in 24% (63/263) of cases based on IHC and FISH. HER2 expression was not significantly associated with clinicopathological characteristics. PD-L1 TPS expression and CPS expression were significantly positively correlated with HER2 expression in OSCC. Conclusions PD-L1 expression was significantly positively correlated with HER2 expression in OSCC. The results provide valuable insight for the future application of HER2-targeted therapy combined with immunotherapy in OSCC.

Research on the DNA methylation status of gastric cancer (GC) has primarily focused on identifying invasive GC to develop biomarkers for diagnostic. However, DNA methylation in noninvasive GC remains unclear. We conducted a comprehensive DNA methylation profiling study of differentiated-type intramucosal GCs (IMCs). Illumina 850K microarrays were utilized to assess the DNA methylation profiles of formalin-fixed paraffin-embedded tissues from eight patients who were Epstein-Barr virus-negative and DNA mismatch repair proficient, including IMCs and paired adjacent nontumor mucosa. Gene expression profiling microarray data from the GEO database were analyzed via bioinformatics to identify candidate methylation genes. The final validation was conducted using quantitative real-time PCR, the TCGA methylation database, and single-sample gene set enrichment analysis (GSEA). Genome-wide DNA methylation profiling revealed a global decrease in methylation in IMCs compared with nontumor tissues. Differential methylation analysis between IMCs and nontumor tissues identified 449 differentially methylated probes, with a majority of sites showing hypomethylation in IMCs compared with nontumor tissues (66.1% vs 33.9%). Integrating two RNA-seq microarray datasets, we found one hypomethylation-upregulated gene: eEF1A2, overlapped with our DNA methylation data. The mRNA expression of eEF1A2 was higher in twenty-four IMC tissues than in their paired adjacent nontumor tissues. GSEA indicated that the functions of eEF1A2 were associated with the development of IMCs. Furthermore, TCGA data indicated that eEF1A2 is hypomethylated in advanced GC. Our study illustrates the implications of DNA methylation alterations in IMCs and suggests that aberrant hypomethylation and high mRNA expression of eEF1A2 might play a role in IMCs development.

ABSTRACT:Hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths worldwide. Its high recurrence rate and lack of effective control drugs result in a 5-year survival rate of only about 10%. HCC is a tumor regulated by the immune system. Significant breakthroughs have occurred in treating solid tumors with immunotherapy in recent years. Various immunotherapies, such as immune checkpoint inhibitors (ICIs), including combination therapies, have demonstrated promising therapeutic effects in both clinical applications and research. Other immunotherapies, such as adoptive cell therapies and oncolytic viruses, are also emerging, offering hope for addressing long-term survival issues in HCC. This article reviews current commonly used immunotherapy strategies and the latest research findings for reference.

Objective. We aimed to investigate the clinicopathological features and pathogenesis of scrotal calcinosis. Methods. Hematoxylin and eosin (HE)-stained slides were performed on 14 patients with scrotal calcinosis, and the clinicopathological characteristics were analyzed together with clinical data. Meanwhile, 81 patients with extrascrotal calcinosis cutis and 7480 patients with epidermoid cysts without calcification in the skin of various parts of the body were collected and analyzed to explore the etiology and pathogenesis of scrotal calcinosis in conjunction with the literature review. Results. All our patients were adult men with a mean age of 38.2 years, with clinical manifestations of multiple scrotal nodules of varying sizes, microscopically characterized by intradermal calcium deposits, of which 3 lesions had a cystic cavity lined with squamous epithelium. Conclusions. Scrotal calcinosis is a rare benign disease that presents clinically as single or multiple hard nodules in the scrotum, usually asymptomatic, and it is histopathologically characterized by intradermal calcium deposition. There is still controversy as to whether it is idiopathic. We believe that scrotal calcinosis is not idiopathic and originates from epidermoid cysts. Prolonged local compression or injury may be one reason for the development of calcification, and perhaps there are other unknown factors contributing to the development of the disease. Surgical excision is the main treatment for this disease with satisfactory therapeutic effectiveness.

Parathyroid carcinoma(PC) is an extremely rare malignant tumor of the parathyroid glands. The lung is the most common target organ for PC distant metastases. In this study, twelve patients diagnosed with PC with lung metastases were enrolled in the study. Hematoxylin and Eosin(H&E) stained, immunohistochemical stained and next-generation sequencing (NGS) of a 425-gene panel were performed on tumor tissue samples. At the same time, we also evaluated its histopathologic characteristics. The results indicate that the microscopic examination of metastatic lesions reveals the same structure and characteristics as PC; the tumor was composed of relatively uniform cells organized in nests and separated by thin fibrous bands and abundant blood vessels. Immunohistochemical evaluation of Ki67, CyclinD1, PTH, SYN, CgA, and CD56 was useful in diagnosing PC with lung metastases. The most frequently genetic alterations were mutations of CDC73 and copy number variation (CNV) of MCL1, with a mutation rate of 25 %. In addition, the mutations of CDC73, ATM, TP53, ALK, ERBB2, MAP3K4, TSC1, CCND1 and CNV of CDK4, MCL1, SMARCB1 overlap between metastatic lesions and primary lesions. In conclusions, PC is a rare endocrine malignant tumor that is very difficult to diagnose preoperatively and prone to clinical recurrence or distant metastasis. Genetic mutations, presentation and histological characteristic were the basis for diagnosing PC with lung metastases.

ObjectiveThe objective of this study is to evaluate the clinical presentations, diagnostic approaches, and treatment modalities for primary prostate sarcoma postradical prostatectomy, aiming to enhance its diagnosis and management.MethodsWe retrospectively reviewed the clinical records of three male patients diagnosed with primary prostate sarcoma at Beijing Chaoyang Hospital, affiliated with Capital Medical University, from February 2014 to February 2024. All patients underwent transrectal prostate biopsies, which informed the decision to proceed with laparoscopic radical prostatectomies. After surgery, one patient received a combination of epirubicin and ifosfamide as immunotherapy, along with external beam radiotherapy. After comprehensive discussions regarding potential benefits and risks, the remaining two patients decided against undergoing radiotherapy and chemotherapy.ResultsBased on the pathological examination results, two patients were diagnosed with stromal sarcoma and one with spindle cell sarcoma, all classified as high-grade sarcomas. Immunohistochemical analysis showed that all three cases were positive for VIMENTIN, but other results did not show significant specificity. During the follow-up period, one patient died within 12 months, and two patients were lost to follow-up after 6 months. However, there were no evident signs of recurrence observed during the follow-up period.ConclusionsPrimary prostate sarcoma is extremely rare and typically has a poor prognosis once diagnosed. Early diagnosis should be based on pathological and immunohistochemical testing results, followed by prompt surgical treatment and adjuvant radiotherapy and chemotherapy. Despite these measures, recurrence is common, underscoring the need for a detailed and appropriate treatment plan and systematic therapy for affected patients.

Purpose: Chronic rhinosinusitis is a prevalent condition in the field of otorhinolaryngology; however, its pathogenesis remains to be elucidated. The immunological defense of the nasal mucosa is significantly influenced by dendritic cells (DCs). We identified specific biological indicators linked to DCs and explored their significance in cases of chronic rhinosinusitis with nasal polyps (CRSwNP).Patients and Methods: We categorized cells using single-cell RNA (scRNA) sequencing, and combined transcriptome sequencing was used to identify potential candidate genes for CRSwNP. We selected three biomarkers based on two algorithms and performed enrichment and immune correlation analyses. Biomarkers were verified using training and validation sets, receiver operating characteristic curves, immunohistochemistry, and quantitative real-time reverse-transcription PCR (qRT-PCR). Variations in biomarker expression were validated using pseudotime analysis. The networks of competing transcription factor (TF)-mRNA and competing endogenous RNA (ceRNA) were established, and the protein drugs associated with these biomarkers were predicted.Results: Both scRNA-seq and transcriptome data showed that DCs immune infiltration was higher in the CRSwNP group than in the control group. Three DC-related biomarkers (NR4A1, CLEC4G, and CD163) were identified. In CRSwNP, NR4A1 expression decreased, whereas CLEC4G and CD163 expression increased. All biomarkers were shown to be involved in immunological and metabolic pathways by enrichment analysis. These biomarkers were associated with gamma delta T cells, effector memory CD4 + T cells, regulatory T cells, and immature DCs. According to pseudotime analysis, NR4A1 and CD163 expression decreased from high to low, whereas CLEC4G expression remained low.Conclusion: We screened and identified potential DC-associated biomarkers of CRSwNP progression by integrating scRNA-seq with whole transcriptome sequencing. We analyzed the biological pathways in which they were involved, explored their molecular regulatory mechanisms and related drugs, and constructed ceRNA, TF-mRNA, and biomarker-drug networks to identify new CRSwNP treatment targets, laying the groundwork for the clinical management of CRSwNP.

Abstract Background Bone marrow fibrosis (BMF) severely impacts both the quality of life and the efficacy of diagnostic procedures. However, the correlation between BMF and clinicopathological features, cytogenetic changes, and prognosis of newly diagnosed multiple myeloma (NDMM) remains unclear. This study determined the incidence, patient characteristics, and clinical outcomes of patients with NDMM with BMF. Methods The clinical data, histological features, and clinical outcomes of patients with NDMM were collected. Reticular fiber staining was performed on the enrolled cases, and the degree of reticular fiber overgrowth was graded. Patients with MF-2 and MF-3 were classified as the BMF+ group, and those with MF-0 and MF-1 were classified as the BMF- group, and BMF incidence was calculated. The differences in clinical data, histological features, and clinical outcomes between the BMF+ group and the BMF– group were compared. Results A consecutive series of 146 patients with NDMM were included. The incidence of MF-0, MF-1, MF-2, and MF-3 was 7.53% (11/146), 34.93% (51/146), 51.37% (75/146), and 6.16% (9/146), respectively. The incidence of BMF—MF-2 and MF-3—was 57.53% (84/146). A significant correlation was identified between the pattern of infiltration and BMF (P < 0.001). In the BMF- group, the distribution of cases with interstitial, nodular, and diffuse infiltration of plasma cells was 16 (25.8%), 21 (33.9%), and 25 (40.3%), respectively. Conversely, in the BMF+ group, these values for interstitial, nodular, and diffuse tumor cells were 9 (10.7%), 15 (17.9%), and 60 (71.4%). Furthermore, BMF was associated with a diffuse infiltration pattern. The overall survival (OS) of the BMF+ group (39.1 months; 95% confidence interval [CI]: 34.0–44.3) was lower than that of the BMF- group (45.4 months; 95% CI: 39.5–51.3), but there was no significant difference between the two groups (P = 0.221). Univariate and multivariate analyses showed that the BMF+ status was not associated with OS in patients with NDMM (P = 0.381 and P = 0.748, respectively). Conclusions Our findings suggest that BMF is linked to a diffuse infiltration pattern, and its occurrence is not related to the prognosis of patients with NDMM, providing a basis for further exploring the BMF value in NDMM diagnosis and treatment.