BACKGROUND:Colorectal cancer (CRC) is one of the most common and life-threatening intestinal tumors throughout the world. Its incidence and mortality have been going up in recent decades, and more accurate and personalized treatment for CRC are also being developed continuously. Early screening, molecular typing, and risk grouping have become critical for improving patient survival by using sensitive and special biological markers. METHODS:We analyzed the expression of four mismatch repair (MMR) genes, namely MutL homolog 1 (MLH1), MutS homolog 2 (MSH2), MutS homolog 6 (MSH6), and PMS1 homolog 2 (PMS2), in CRC and normal tissues using the Tumor, Normal and Metastatic (TNM plot) database. We used the Kaplan-Meier analysis for prognosis, and related pathways were annotated by the Kyoto Encyclopedia of Genes and Genomes. We conducted a retrospective study with 115 CRC patients, who were divided into microsatellite stable (MSS) and microsatellite instability (MSI) groups by immunohistochemistry (IHC). The diagnostic value of MMR markers was assessed through receiver operating characteristic (ROC) curve analysis. RESULTS:Online data showed that MMR genes were more highly expressed in CRC than in the normal group (P<0.05). Low expression of these genes was linked to shorter recurrence free survival (RFS, P<0.05), and the related signaling pathways also exert an impact on cell cycle regulation. In clinical samples, loss of MLH1 expression was found in female patients, those aged ≥60 years and lymph node-negative cases (P<0.05). MSI-positive tumors were mostly located in the right-sided colon (P<0.05). The combined model of MSH6 and PMS2 had the highest area under the curve (AUC) of 0.981 (95% confidence interval (CI): 0.936-0.997, P<0.001). CONCLUSION:Combined detection of MSH6 and PMS2 serves as a reliable biomarker for determining the microsatellite status in CRC. This study provides a basis for the precise diagnosis and targeted therapy of CRC.
SMARCA4-deficient non-small cell lung cancer (SMARCA4-dNSCLC) is a rare, aggressive subtype with a high propensity for early metastasis and poor prognosis. Common metastatic sites include the bone, brain, adrenal glands, liver, and spleen; metastasis to the base of the tongue, however, is exceptionally rare. We present a unique case of SMARCA4-dNSCLC with concurrent metastases to both the adrenal gland and the base of the tongue. A 44-year-old male presented with cough and shortness of breath. Imaging revealed a right hilar mass, a left adrenal gland mass, and a nodule at the right tongue base. Histopathological examination of biopsies from the tongue base and mediastinal lymph nodes confirmed the diagnosis of SMARCA4-deficient undifferentiated NSCLC with metastases (T3N2M1c, stage IVB). Following a multidisciplinary discussion, the patient received combination therapy with paclitaxel, cisplatin, and tislelizumab. After three cycles, a partial response (PR) was achieved. The treatment was well-tolerated without significant adverse events, and the patient's condition remained stable with no signs of recurrence. This case highlights the unusual co-occurrence of a common (adrenal) and a rare (tongue base) metastatic site in SMARCA4-dNSCLC, which posed considerable diagnostic challenges. It expands the known clinical spectrum of this malignancy and underscores the importance of recognizing its rare metastatic patterns to guide accurate diagnosis and treatment.
Ureteral calculi are a common cause of emergency department visits worldwide. Although small stones often pass spontaneously, medical expulsive therapy is frequently used to facilitate stone clearance and reduce the need for surgical intervention. Tamsulosin, an α1-adrenergic receptor antagonist, is commonly prescribed for this purpose, but its efficacy compared with placebo remains uncertain. We conducted a systematic review and meta-analysis of randomized controlled trials comparing tamsulosin with placebo in patients with ureteral calculi. A comprehensive search of PubMed, Embase, and the Cochrane Central Register of Controlled Trials was performed from database inception through April 2025. The primary outcome was the stone expulsion rate, and secondary outcomes included time to expulsion and the incidence of adverse events. Pooled estimates were calculated as risk ratios or mean differences with 95 percent confidence intervals, using a random-effects model. A total of 42 randomized controlled trials involving 7,117 patients met the inclusion criteria. Compared with placebo, tamsulosin significantly increased the stone expulsion rate (risk ratio 1.42, 95 percent confidence interval 1.29 to 1.56, P < 0.001) and shortened the time to expulsion by an average of 3.04 days (95 percent confidence interval 2.28 to 3.81 days, P < 0.00001). The overall incidence of adverse events did not differ significantly between groups, although subgroup analysis indicated a lower risk of moderate to severe complications with tamsulosin (risk ratio 0.35, 95 percent confidence interval 0.22 to 0.98, P < 0.0001). Substantial heterogeneity was observed across outcomes. In conclusion, tamsulosin improves stone expulsion and reduces clearance time without increasing overall adverse events. However, given the considerable heterogeneity among studies, these findings should be interpreted with caution. Further high-quality, large-scale trials are needed to confirm the benefits of tamsulosin and to identify patient subgroups most likely to benefit from therapy.
Papillary cystadenoma (PC) is a benign epithelial tumor believed to be of mesonephric origin and is recognized as one of von Hippel-Lindau syndrome (VHL)-related neoplasms. PC tends to develop frequently in male VHL patients but rarely in females and arises from the mesosalpinx or broad ligament in females. Having experienced a case of multiple PCs in a female patient, we here report it with literature review. The patient was a 34-year-old woman. In her past medical history, VHL including multiple hemangioblastomas of the central nervous system, pancreatic neuroendocrine tumor, and multiple clear cell renal cell carcinoma (CCRCC) of the bilateral kidneys was diagnosed. In addition, a PC of the left ovary was resected seven years earlier. In the present report, she was admitted to our hospital because of lower abdominal pain, and then computed tomography revealed swelling of the right ovary and ascites. She was diagnosed with right ovarian torsion and thus salpingo-oophorectomy was performed. Histopathologically, while the tumor cells with pale or eosinophilic cytoplasm showed a papillary growth with partial cystic changes, none of apparent nuclear atypia, mitotic figure, and necrosis were observed. We finally diagnosed it as PC of the right ovary. Its pathological findings were similar to those of the previously resected left ovarian lesion. Although PC is rare in females, the presence of VHL should be kept in mind when PC is encountered. Moreover, metastatic CCRCC should also be considered to be one of differential diagnoses in VHL patients.
Objectives: The significance of long non-coding RNAs (lncRNAs) in glioblastoma multiforme (GBM) has been acknowledged, but their specific role in the pathogenesis of GBM has not been thoroughly investigatedr. This study aimed to investigate the involvement of lncRNAs in the pathogenesis of GBM. Methods: We collected GBM tissues from four patients and corresponding para-carcinoma controls samples, and used HiSeq sequencing to generate lncRNA expression profiles in GBM. To identify lncRNAs associated with GBM, we employed Mendelian randomization (MR), leveraging the comprehensive extensive expression data obtained from HiSeq sequencing to infer causal relationships. Expression quantitative trait loci (eQTLs) for brain tissues were accessed from the Genotype-Tissue Expression (GTEx) Portal. Subsequently, we conducted an integrative analysis combining brain cancer genome-wide association study (GWAS) summary data (finn-b-C3_GBM) with eQTL data using MR. Differentially expressed lncRNAs were intersected with MR results to identify lncRNA candidates. Subsequently, the ENCORI database was used to identify genes regulated by the candidate lncRNAs, and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed. Result: A protein-protein interaction (PPI) network was constructed to identify hub genes associated with GBM, and these findings were validated using the Gene Expression Profiling Interactive Analysis 2 (GEPIA2) tool. A total of 106 lncRNAs exhibited significant alterations in expression levels (|log2(fold change)| > 1 and P < 0.05) in GBM tissues. Through Mendelian randomization (MR) analysis, TMEM161B-AS1 emerged as a promising candidate lncRNA. Genes regulated by TMEM161B-AS1 were significantly enriched in biological processes such as DNA replication and repair, cellular response to DNA damage stimuli, and pathways including the peroxisome proliferator-activated receptor signaling pathway, nucleotide excision repair, and the Fanconi anemia pathway. The differential expression of hub genes CUL4A, RPA1, and BRIP1 was validated using the GEPIA2 database. Conclusions: These findings suggest pathways for the development of more precise and sensitive biomarkers for the diagnosis and management of GBM, which may ultimately enhance patient outcomes.
Background/Objective: Immune checkpoint inhibitors (ICIs) have extended survival in patients with nonsmall cell lung cancer (NSCLC) but their therapeutic benefit is limited to a proportion of patients. Predictive biomarkers based on tissue of origin of the tumor have their limitations, and thus there is a need for solid and minimally invasive predictive biomarkers. Our aim was to investigate serum proteomics via liquid biopsy for biomarker discovery. Methods: In this retrospective extension of the TD-FOREKNOW trial, deep proteomic profiling was undertaken on pre-treatment serum samples of 72 patients with NSCLC receiving neoadjuvant therapy. Further quantitation of proteins in serum was performed by data independent acquisition mass spectrometry to obtain candidates associated with treatment outcome. Statistical regression was also used to screen for proteins related to ICI efficacy and a risk score composite model was set up to predict treatment response and prognosis. Results: From the 1,802 analyzed serum proteins, 59 serum proteins were differentially expressed in patients receiving immunotherapy plus chemotherapy. Using univariate logistic regression followed by least absolute shrinkage and selection operator (LASSO) regression, three factors, SERPINE2, DAZAP1, and MGAT4B, were identified whose baseline expression was correlated with the response to ICI therapy. The risk score model using the three proteins was an effective biomarker in predicting ICI response with an area under the curve (AUC) of 0.946 (95% CI: 0.874-1.000). Its predictive value for ICI response was validated in further survival analysis, showing that patients with a low risk score had significantly longer progression-free survival (HR = 0.13, 95% CI: 0.04-0.46, P = 0.002) and overall survival (HR = 0.14, 95% CI: 0.03-0.62, P = 0.033) than those with a high risk score. Conclusion: A pre-treatment serum-based risk score that effectively predicts response to ICI therapy in patients with NSCLC was developed and validated. Our findings reveal the great prospect of human serum proteomics as a powerful liquid biopsy platform for biomarker discovery and construction of clinical prognostic models.
BACKGROUND:Bladder cancer (BLCA) is a common malignant tumor of the urinary system with a poor prognosis, especially in cases of invasive or advanced patients. Although mitochondrial dysfunction is associated with tumor progression, there are relatively few mitochondrial-related prognostic models for bladder cancer. The intention of study was to construct a five-gene mitochondrial-related prognostic marker for bladder cancer, and perform external validation, and then explore its association with the tumor immune microenvironment and potential immune treatment response. METHODS:Transcriptome and clinical data were obtained from TCGA and GEO databases - intersecting bladder cancer-related differentially expressed genes (BLCA-related DEGs) with the mitochondrial-related gene database (MitoCarta 3.0 genes) to find the mitochondria-related differentially expressed genes (Mitochondria-related DEGs). Construction of a prognosis model using univariate (uni), lasso, and multivariate Cox regression analyses, was used for verificaiotn in 2 gene expression profile public databases (GEO cohorts). Functional enrichment (func enrich), tumor microenvironment (tumor microenv), immune infiltration (immune infil), mutation (mut), and single-cell transcriptomic analyses were carried out. RESULTS:A prognosis model was created containing five genes: COX7A1, MTHFD1L, MTG1, SCO2, and ACP6. The survival rate of high-risk patients was found to be poorer compared with that of low-risk patients. The high-risk tumor stromal score was higher, the fibroblast-related characteristics were enriched, with differences in the immune pattern. Single-cell analysis found COX7A1 in endothelial cells and mast cells, MTHFD1L in T cells, and SCO2 in endothelial cells. Functional analysis associated the high-risk group with extracellular matrix remodeling, stromal activation, and changes in immune pathways. This model also has potential value in estimating the response to immunotherapy. CONCLUSIONS:A five-gene prognosis marker related to mitochondria for bladder cancer was developed and verified. This model may become a useful tool for survival stratification of bladder cancer patients and characterization of tumor microenvironment heterogeneity.
Background: Myolipoma is a rare benign mesenchymal tumor composed of mature adipose tissue, smooth muscle bundles and blood vessels, which predominantly occurs in the retroperitoneum, inguinal region and abdominal wall. Primary uterine involvement is extremely uncommon, and the presence of bizarre-nucleated cells within such tumors is even rarer. The morphological features of these cells may mimic malignant neoplasms, posing great challenges for clinical and pathological diagnosis. Methods: We report a 61-year-old female patient with imaging and ultrasonographic findings suggestive of a uterine space-occupying lesion. Histopathological examination and immunohistochemical staining were performed on the surgically resected specimen, with the detected markers includingsmooth muscle actin (SMA), Desmin, HMB45, Melan A, S-100 and Ki-67. Results: Pelvic magnetic resonance imaging (MRI) revealed a well-demarcated heterogeneous signal mass in the anterior wall of the uterine corpus, consistent with the manifestations of a benign tumor containing adipose components. Gross examination showed a well-circumscribed intramural mass of the uterus with a grayish-yellow and heterogeneous cut surface. Microscopically, mature adipocytes and benign smooth muscle cells were scattered with bizarre-nucleated cells characterized by markedly enlarged and irregular nuclei; no mitotic figures or necrotic foci were identified. Immunohistochemically, the smooth muscle component showed diffuse and strong positivity for SMA and Desmin, while HMB45, Melan A and S-100 were all negative. The Ki-67 proliferation index was extremely low (<1%), confirmingthe diagnosis of uterine myolipoma with bizarre-nucleated cells. Conclusion: Uterine myolipoma with bizarre-nucleated cells is an exceedingly rare benign tumor, and no recurrence or metastasis was observed during postoperative follow-up, indicating its indolent biological behavior. Accurate diagnosis requires the combination of imagingfeatures, adequate sampling, meticulous histological evaluation and targeted immunohistochemical detection to distinguish it from leiomyosarcoma, liposarcoma and perivascular epithelioid cell tumor (PEComa).
Breast cancer exhibits a well-documented but incompletely explained predilection for the upper outer quadrant (UOQ), accounting for 45-50% of all cases, followed by the lower inner quadrant (LIQ) as the second most common site. We propose a mechanical hypothesis: chronic, repetitive mechanical stress from sexual partner-initiated breast manipulation-specifically the four-finger pinch grasp-creates sustained micro-injury and subsequent reparative proliferation preferentially targeting the UOQ, thereby increasing local mutational burden. The thumb opposes on the LIQ, offering a natural explanation for its secondary incidence pattern. This hypothesis generates specific, testable predictions, including dose-response relationships between cumulative exposure and quadrant specific risk, as well as lateral asymmetry based on partner handedness. A large-scale epidemiological questionnaire study is proposed as the initial validation step. If confirmed, this hypothesis may transform breast cancer risk reduction into a modifiable behavioral domain.
Objectives: Overcoming chemoresistance is a major therapeutic challenge to improve patient's outcome, and lncRNAs are involved in the carcinogenesis and progression of NSCLC. Accordingly, this study was aimed to explore the roles and functions of lncRNA FENDRR in the progression and drug resistance of NSCLC. Methods: The University of California Santa Cruz (UCSC) Xena browser was used to validate the putative profile of lncRNA FENDRR in pan-cancer tissues, whereas Kaplan-Meier analysis was conducted to assess the overall survival rate. The potential mechanism underlying cisplatin (DDP) resistance was then investigated usingtransfection of siRNA-FENDRR or pcDNA3.1/FENDRR in vitro and in vivo. Simultaneously, subcellular localization of FENDRR, along with targeted DiGeorge syndrome critical region 8 (DGCR8), was predicted using lncATLAS database and further ascertained by RNA immunoprecipitation, fluorescence in situ hybridization and western blotting. Results: LncRNA FENDRR was lowly expressed in 28 types of tumor tissues, especially in A549/DDP-resistant cells and the patients with DDP resistance. LncRNA FENDRR downregulation was associated with poor survival for patients with NSCLC. Conversely, FENDRR overexpression was observed to suppress cell viability and clonogenic ability, enhance sensitivity to cisplatin in DDP-resistant NSCLC cells and simultaneously induced their apoptosis. However, FENDRR knockdown led to opposite effects on A549 cells. Furthermore, FENDRR was predominantly located in nucleus, where its overexpression suppressed tumor proliferation in A549/DDP cells by directly targeting DGCR8. Conclusions: Taken together, these findings suggest evidence of FENDRR in the emergence of NSCLC and further reveal a key role of the FENDRR/DGCR8 axis in the progression and drug resistance in this cancer, thereby implicating a FENDRR-targeted therapeutic strategy for combating DDP resistance in NSCLC.
Acute promyelocytic leukemia (APL) is characterized by a translocation t(15;17), which leads to the fusion of the promyelocytic leukemia (PML) gene with the retinoic acid receptor alpha (RARA) gene. This entity represents a true medical emergency due to the high risk of coagulopathy and disseminated intravascular coagulation (DIC); thus, early diagnosis is crucial to initiate treatment and achieve a better outcome. Here, we present a challenging case of APL in a 25-year-old male that mimicked classic acute myeloid leukemia (AML) based on morphologic and immunophenotypic features. Furthermore, marked myelofibrosis was identified in our patient-an unusual finding for APL. By sharing this observation, we emphasize the importance of a comprehensive approach in achieving an accurate and timely diagnosis of APL, including the integration of morphologic assessment, immunohistochemistry, flow cytometry, and molecular techniques.
Objective: This study aims to investigate the impact of P2RX5 on the clinical pathological characteristics and prognosis of endometrial carcinoma, and to explore its potential underlying mechanisms. Methods: The clinical samples, including 150 specimens with endometrial carcinoma (Case group) and 100 endometrial samples without cancer (Control group), were collected for analyzing the amount of P2RX5 expression. Cell biology experiments were also used for exploring the effects of P2RX5 expression on biological behaviors of endometrial carcinoma. Results: The results showed that P2RX5 expression in endometrial carcinoma tissues were significantly higher than in endometrial tissues from the control group. Additionally, expression levels showed a positive correlation with tumor size, differentiation grade, and tumor stage, with risk values of 3.57, 6.07, and 9.78, respectively. This increase in risk was statistically significant (P < 0.001). Kaplan-Meier survival analysis demonstrated that increasing P2RX5 expression was associated with lower overall survival rates (P < 0.05). Functional assays showed that knocking-down P2RX5 expression in the HEC-1B cell line significantly reduced the capacity of cell proliferation, migration, invasion, and clone formation. Following gene knockout, the rate of late apoptosis in tumor cells significantly increased (P < 0.001), while the number of cells in the S phase and G2/M phase significantly decreased (P < 0.05). Conclusion: These findings suggest a critical role of P2RX5 in endometrial cancer progression and thereby establish the value of P2RX5 as a prognostic biomarker and provide a promising therapeutic target for endometrial cancer treatment.
OBJECTIVE:To elucidate the molecular mechanisms by which endocrine-disrupting chemicals (EDCs) initiate and sustain prostate carcinogenesis, thereby establishing a mechanistic foundation for the early detection and targeted intervention of castration-resistant prostate cancer (CRPC). MATERIALS AND METHODS:A total of 402 transcriptomic profiles from public GEO cohorts were integrated. Differential expression analysis, weighted gene co-expression network analysis (WGCNA), and network toxicology were jointly applied to prioritize candidate targets. Subsequently, an explainable XGBoost-SHAP machine-learning framework was employed to distill the core gene signature. The interaction affinities between selected EDCs and the corresponding proteins were computationally validated by molecular docking, with binding free energy (ΔG) serving as the quantitative metric. RESULTS:Five genes - NR3C1, CALM1, MET, STAT3 and CES1 - were identified as robust diagnostic biomarkers across multiple independent cohorts (AUC > 0.90). All five exhibited high-affinity binding to representative EDCs (ΔG < -7 kcal mol-1). CONCLUSIONS:For the first time, a seamless "transcriptome-network toxicology-structural biology" causal chain was established. By integrating explainable artificial intelligence with structural biology, this study closes a critical knowledge gap in the systems-level mechanism linking EDC exposure to prostate cancer initiation and progression, and offers novel, actionable targets for risk stratification and precision prevention.
OBJECTIVE:To investigate the mechanism of Hesperidin (Hsp) in inhibiting the proliferation and metastasis of breast cancer cell line MDA-MB-231. METHODS:The effect of Hsp on cell survival rate was analyzed using the MTT assay. The anti-migration and anti-invasion abilities of Hesperidin were evaluated using the scratch test and Transwell migration assay. The activity of matrix metalloproteinases (MMP)-2/MMP-9 was analyzed using gelatin zymography. The expression of epithelial-mesenchymal transition (EMT)-related proteins (Vimentin, Snail, ZO-1) was detected by Western blot. RESULTS:Low concentrations of Hsp (2-10 μmol/L) showed no significant cytotoxicity; 20-40 μmol/L significantly reduced survival rate (P<0.01). Scratch test results showed that Hsp inhibited wound healing in a concentration-dependent manner. Transwell migration assay showed that the number of migrating cells decreased with increasing Hsp concentration. Gelatin zymography results indicated that MMP-2/MMP-9 activity decreased with increasing Hsp concentration; Western Blotting results showed that Hsp downregulated the metastasis-related proteins Vimentin and Snail and upregulated the adhesion protein ZO-1. CONCLUSION:Our findings suggest that Hsp inhibits tumor cell invasion and metastasis by potentially reducing MMP-2/MMP-9 hydrolase activity, blocking extracellular matrix degradation, and reversing the EMT process (downregulating Vimentin/Snail and upregulating ZO-1). Hsp may represent a promising candidate for adjuvant therapy in breast cancer.
Purpose: Colon cancer (CC), a malignancy with high global incidence and mortality, remains a major public health burden. As a pivotal aspect of tumor metabolic reprogramming, fatty acid metabolism has drawn significant research interest. This study was designed to elucidate the relationship between fatty acid metabolism-related gene expression and prognosis in patients with CC. Method: We obtained the mRNA expression profiles and corresponding clinical information of colon cancers from The Cancer Genome Atlas (TCGA) database. Expression data of fatty acid metabolism-related genes and survival data were extracted for subsequent analysis. Univariate Cox regression and least absolute shrinkage and selection operator (LASSO) regression analyses were employed to identify fatty acid metabolism-related genes associated with prognosis in CC patients. Subsequently, a prognostic model based on these six genes was constructed to predict survival probability. Patients were stratified into high-risk and low-risk groups based on the model. Differences between the two groups were analyzed, including gene set enrichment analysis (GSEA), immune cell infiltration, immunotherapy efficacy, and immune checkpoint expression levels. Furthermore, a novel nomogram incorporating the risk score, age, gender, and clinical stage was developed to predict individual patient outcome. Finally, the expression levels of the identified risk genes were validated in cell lines using quantitative real-time PCR (qRT-PCR). Results: 449 CC and 41 normal samples were included in this study. A prognostic model based on six fatty acid metabolism-related genes (ENO3, ELOVL3, ACOT11, ALAD, ELOVL6, ACADL) were built to evaluate the prognosis of CC patients. Patients in the high-risk group had poorer overall survival than those in the low-risk group (P < 0.001), with AUC value of 0.701. M0 macrophage infiltration and T helper cells were higher in the high-risk group, and regulatory T cells (Tregs) and infiltration of natural killer cell (NK) cells was less. The expression levels of PD-1, LAG3, and CTLA4 were higher in high-risk patients, and the high-risk group had a higher TIDE score, indicating a worse response to immunotherapy. The Calibration plots, receiver operating characteristic (ROC) curve, and Decision Curve Analysis (DCA) all showed that the nomogram method can accurately predict the survival rate of CC patients. In addition, qRT-PCR showed downregulated expression of ACOT11, ALAD, and ACADL, and upregulated expression of ELOVL6 and ENO3 in all colon cancer cell lines tested. There was no significant difference in the expression level of ELOVL3 between colon cancer cells and colon epithelial lines. Conclusion: Targeting fatty acid metabolism-related genes represents a promising therapeutic strategy for colon cancer (CC) that could pave the way for personalized treatment and enhanced patient survival.
OBJECTIVE:To evaluate the effectiveness of PAX1 methylation gene testing in cervical lesions where the squamocolumnar junction (SCJ) is incompletely visible. METHODS:For patients with TCT ≥ ASCUS or HR-HPV positivity, whose colposcopy results indicate incomplete visibility of the SCJ, cervical exfoliated cells were collected for PAX1 gene methylation testing. Using histopathology results as the gold standard, the study calculated the positive rate of PAX1 methylation testing across various lesion grades, assessing the sensitivity, specificity, positive predictive value, negative predictive value, and positive concordance rate with histopathology for high-grade cervical lesions. RESULTS:The PAX1 positivity rates in the cervicitis, LSIL, HSIL, and CC groups were 30% (3/10), 30.43% (7/23), 51.28% (20/39), and 71.42% (5/7), respectively. The positivity rate in the LSIL group (cervicitis and LSIL), at 29.72% (11/37), was significantly lower than in the HSIL+ group (HSIL and CC), which was 54.76% (23/42) (P < 0.05). For HSIL+ lesions, PAX1 methylation testing showed a sensitivity of 54.76%, specificity of 70.27%, positive predictive value of 67.65%, negative predictive value of 57.78%, positive likelihood ratio of 1.84, and negative likelihood ratio of 0.22. In comparison, HPV testing for HSIL+ showed a sensitivity of 100% and specificity of 13.51%; TCT testing for HSIL+ had a sensitivity of 35.71% and specificity of 94.59%. The positive concordance rate with histopathology was 97.1% for the PAX1 group, 95.9% for the high-risk HPV group, and 100% for the TCT group. CONCLUSION:The overall efficacy of PAX1 in diagnosing high-grade cervical lesions is relatively high, enhancing diagnostic accuracy to a certain extent and making it suitable for further clinical application and promotion.
Introduction: S100A16, a member of the S100 family of calcium-binding proteins, is involved in the progression of several malignancies. However, its specific mechanism of action in gastric cancer is not completely understood. The objective of this study, therefore, was to examine the correlation between the expression of S100A16 and clinicopathological characteristics and to investigate its potential significance in gastric adenocarcinoma. Methods: S100A16 messenger RNA (mRNA) expression in stomach cancer was analyzed using bioinformatics to determine the link(s) between diagnostic utility, prognostic importance, tumor mutational burden (TMB), and immune cell infiltration of S100A16 mRNA in patients with gastric cancer. Results: S100A16 mRNA expression was elevated in gastric adenocarcinoma, particularly in samples with microsatellite instability. S100A16 mRNA demonstrated significant diagnostic efficacy for gastric cancer. There was a strong correlation between S100A16 mRNA expression and TMB, and a negative correlation between S100A16 mRNA levels and Tumor Immune Dysfunction and Exclusion (i.e., "TIDE") score. Immunohistochemistry results revealed significant differences in S100A16 expression across groups with various histological differentiation in gastric cancer. There was a positive association between S100A16 and P53 expression in those with gastric cancer. Conclusions: There was significant upregulation of S100A16 in gastric adenocarcinoma, which was associated with the level of differentiation and expression of P53. S100A16 may play a role in gene mutations, microsatellite status, and TMB in gastric adenocarcinomas. In addition, S100A16 may be associated with the ability of gastric adenocarcinoma cells to evade the immune system.
