Adopting a healthy lifestyle is crucial for preventing chronic diseases, yet sustained behavioral change remains challenging, especially in rural residents. Assessing their health behavior cognition is key to designing effective interventions. We conducted face-to-face, semi-structured interviews with 61 rural residents across three counties in Shanxi Province. Qualitative data were analyzed using thematic analysis. Three core themes emerged regarding rural residents’ cognitive frameworks of healthy lifestyles: (1) Fundamental cognition (including knowledge level and health values), (2) Risk-benefit assessment (including perceived risks and perceived benefits), and (3) Control beliefs (including self-efficacy and health locus of control). The study revealed that a considerable proportion of rural residents exhibited cognitive gaps towards healthy lifestyles. These cognitions are not merely individual-level deficits but are profoundly shaped and reinforced by structural determinants. Consequently, effective health promotion requires multi-level interventions that address both cognitive patterns and their structural drivers. Key strategies include delivering accessible health information through trusted local channels, providing low-cost check-ups to create objective health feedback, and facilitating successful behavioral experiences through social support and regular follow-up from village clinics.

Background:Ovarian mucinous tumor has been a common epithelial tumor originated from female reproductive system, and a few of the tumors might be accompanied by mural nodules including sarcomatoid nodules, sarcoma, and anaplastic carcinoma. In much rarer cases, the epithelial tumors of female genital tract coexist with germ cell tumors, for instance yolk sac tumor (YST). Up to date, only seven cases of ovarian mucinous tumors associated with YST component have been reported. In the study, we present a rare case of ovarian mucinous tumor with both anaplastic region and YST component, and reviewed all the eight cases to highlight current understanding of the pathological diagnosis and clinical features of the disease. Case Description:A 62-year-old women admitted to the hospital due to intermittent lower abdominal pain accompanied by gradually increasing abdominal distension for over two years, imaging analysis revealed a pelvic mass with the maximum diameter nearly as 20 cm. Further, postoperative pathological examination of the mass revealed three distinct regions, including cystic areas, solid areas, and certain microcystic reticular areas. Immunohistochemical (IHC) experiment showed different results among these areas which supported the final pathological diagnosis as anaplastic ovarian mucinous carcinoma with YST differentiation. The patient went through 6 periods of chemotherapy, however, the tumor recurred 62 days post-operation, currently, the recurred mass has again filled the abdominal cavity (3 months post operation). The patient is currently still alive, but her condition is extremely poor. Conclusions:We presented a rare case of ovarian mucinous carcinoma with anaplastic region and YST differentiation. The case and seven other cases retrieved from literature revealed that its current diagnosis primarily rely on pathological morphological characteristics together with IHC experiment. Gene mutations were identified in some of the cases, for instance CDKN2A and CDKN2B genes deletion, as well as KRAS and TP53 genes mutation. This tumor is highly aggressive, 75.0% (6/8) of the cases recurred or dead within one year of diagnosis.

IntroductionRho GTPases have been a well-known family of small G proteins that regulate cellular cytoskeleton dynamics and are involved in multiple critical steps of cancer progression. However, ARHGAP44 gene, a member of GAP proteins that regulate the Rho GTPases cycling between their active GTP-bound and inactive GDP-bound states, remains poorly understood in terms of its role in cancer development. This study aims to analyze the functions of ARHGAP44 gene in a broad spectrum of human cancers, thus aiding in the better understanding of the collaborative network of cytoskeleton-related genes in cancers.MethodsThe study started with the analysis of the genetic characteristics of ARHGAP44 gene, followed by its expression patterns, frequent alterations as well as survival prediction value in a broad spectrum of human cancers. Furthermore, the probable reasons for the aberrant changed expression of ARHGAP44 in cancers compared to corresponding normal control samples were investigated. Moreover, the correlation of ARHGAP44 with multiple critical clinical cancer parameters was performed in succession.ResultsThe basic genetic physicochemical properties of ARHGAP44 including its amino-acid composition, estimated molecular weight, and protein half-life were investigated. Then, genetic alteration analysis revealed that ARHGAP44 expression varies in human cancers, which was partly due to the modulation by DNA methylation and phosphorylation. Furthermore, ARHGAP44 gene was associated with multiple critical cancer traits including cancer stemness, cytoskeleton dynamics as well as immune infiltration in different human cancer types. Moreover, ARHGAP44 gene was also associated with the sensitivity of several chemotherapy-related drugs.ConclusionsBased on multiple analyses, some valuable strategies to guide the therapeutic orientation concerning the role of ARHGAP44 gene in human cancers were revealed, although more detailed experiments and clinical trials are obligatory to support further clinical medical applications of the gene, especially in each independent cancer type.

This study aimed to identify and validate robust prognostic biomarkers for oropharyngeal squamous cell carcinoma (OPSCC), with a specific focus on the high-risk HPV-negative subtype. Methods: Integrated bioinformatics analysis was performed on transcriptomic data from four GEO datasets (n = 418 samples). Differentially expressed genes (DEGs) were identified, and a protein-protein interaction (PPI) network was constructed for the most dysregulated genes. Key modules were analyzed via survival analysis and multivariate Cox regression. The top candidate genes were validated at the protein level using immunohistochemistry (IHC) in an independent cohort of 304 OPSCC patients. Results: A 33-gene module related to extracellular matrix organization showed significant prognostic association. It stratified patients into high- and low-risk groups with markedly different overall survival (HR = 2.71, p < 0.001). From this module, SPP1 and PLAU were identified as independent prognostic factors through multi-step screening. Both genes were significantly overexpressed in tumors (approximately 20-fold and 10-fold, respectively, p < 0.001), with high expression strongly correlated with advanced tumor stage (p < 0.01) and, notably, the HPV-negative subtype (p < 0.001). In survival analysis, high expression of either SPP1 or PLAU was associated with poorer overall survival (SPP1: p < 0.001; PLAU: p < 0.001) and progression-free survival (p < 0.001). IHC validation confirmed high protein expression in 69.7

Introduction:C5orf46 is a recently discovered tumor-progression-related gene whose function in most cancers is still unknown, especially its potential role in regulating the tumor microenvironment (TME). The aim of the study is to explore the function of the C5orf46 gene in human pan-cancer, including kidney renal clear cell carcinoma (KIRC), for potential clinical application. Methods:The study started with the physicochemical properties of C5orf46, then the gene expression as well as alteration patterns in diverse cancers, followed by its post-transcription modulation, and then survival analysis. Moreover, the correlations between C5orf46 and multiple cancer TME-related parameters, including angiogenesis, extracellular matrix (ECM) degradation, and immune infiltration, were explored sequentially. Furthermore, C5orf46's association with other critical cancer features, for instance, cancer stemness, tumor epithelial-mesenchymal transition (EMT), and DNA repair, was also investigated. Results:Firstly, the physicochemical properties, including amino acid composition, estimated molecular weight, and protein half-life, of the C5orf46 gene were computed sequentially. Then, based on gene expression as well as survival analysis results, C5orf46 was shown to be upregulated in various human cancers, wherein KIRC showed the greatest difference in C5orf46 expression between cancer and corresponding normal tissues. The change in expression was partly due to DNA methylation modulation. Meanwhile, of greater clinical significance, the upregulated C5orf46 expression was correlated with both worse patients' overall survival and shorter recurrence-free survival. Moreover, the association between C5orf46 and multiple critical cancer traits, including microenvironment angiogenesis, immune infiltration, ECM degradation, and cancer EMT, was validated. Furthermore, the C5orf46 gene was indicated to correlate with the sensitivity of several chemotherapy-related drugs. Conclusions:Based on TCGA pan-cancer data and validation of local hospital samples, C5orf46 was indicated to potentially work as an oncogene in diverse cancers, and the gene was associated with multiple critical cancer traits.

OBJECTIVE:Vaginal cancer is a rare malignancy, and the research on it is not comprehensive yet. To explore the characteristics of human papillomavirus (HPV) infection in patients with vaginal intraepithelial neoplasia (VaIN) and vaginal cancer. MATERIALS AND METHODS:This study included patients who underwent colposcopy and biopsy of suspected sites at the Second Hospital of Shanxi Medical University from January 2014 to December 2023 due to abnormal cytology results and/or positive HPV test. Those diagnosed with benign inflammatory reaction of the vagina (ie, vaginitis), VaIN and vaginal cancer according to histologic results were selected as the study objects. Clinical data such as age, menopause, clinical manifestations and previous screening history were collected. We aimed to analyze the distribution and characteristics of HPV in VaIN and vaginal cancer patients. RESULTS:A total of 5,180 patients were included in this study. Of the total, 2,739 patients had VaIN1, 641 had VaIN2/3, and 251 had vaginal cancer. There were 235 patients with vaginal squamous cell carcinoma (VaSCC) and 16 patients with vaginal adenocarcinoma. A total of 4,548 patients were infected with HPV. The HPV positive rate was 95.5% in VaIN2/3, 86.0% in VaSCC and 43.8% in adenocarcinoma of the vagina. The most common 5 HPV types were HPV16, 52, 58, 53, and 18. The positive rate of HPV18 in the adenocarcinoma of the vagina was the highest. CONCLUSION:HPV16, 52, 58, 53, and 18 are the predominant genotypes in VaIN and vaginal cancer in Shanxi, China. HPV testing provides additional benefits for the detection of vaginal lesions during cervical cancer screening. Active HPV vaccination may help reduce the burden of these lesions.

BACKGROUND:Advanced esophageal squamous cell carcinoma (ESCC) is characterized by molecular heterogeneity and distinct patterns of immune cell infiltration. Regulatory T cells (Tregs), in particular, play a critical role in shaping an immunosuppressive tumor microenvironment (TME), which is associated with poor clinical outcomes. METHODS:We developed a prognostic model by integrating GEO-derived bulk RNA sequencing data and single-cell transcriptome. Model predictions were confirmed through RT-qPCR, Western blot, and immunohistochemistry on clinical specimens, while in vitro assays (CCK8, transwell invasion, scratch, colony formation, and immunofluorescence) validated the function of SAP18 in cell proliferation, invasion, and ECM remodeling. RESULTS:Expression patterns of the 5 Tregs-associated genes in clinical specimens aligned with model predictions, underscoring the model's robustness. The high-risk subgroup was associated with upregulated extracellular matrix (ECM) remodeling, an abundance of immune-suppressive cells, higher TP53 mutation rate, and limited benefit from immunotherapy. In contrast, the low-risk subgroup exhibited anti-tumor immunity. Cell-cell communication analysis also implicated the collagen pathway in Tregs-mediated immune evasion in ESCC. Functional assays indicated that SAP18 in the prognostic model significantly promotes proliferation, invasion, and ECM reconstruction, further highlighting its potential as a therapeutic target. CONCLUSION:Our findings elucidate the role of Tregs in the TME, underscoring significant potential of SAP18, which is essential for assessing patient prognosis and may facilitate the development of personalized therapies for ESCC.

Background:Giant cell tumor of bone (GCTB) has been a common primary bone tumor with potential malignancy and local aggressiveness. H3F3A gene mutation has been gradually understood to be related with GCTB occurrence. However, the relationship between different mutation sites and tumor pathological morphology as well as clinical prognosis is still uncertain. This study aimed to investigate the clinical pathological characteristics of GCTB and analyze the potential correlation between H3F3A and GCTB tumor recurrence and prognosis risk. Methods:A total of 96 cases of GCTB samples diagnosed by two registered pathologists in the Second Hospital of Shanxi Medical University from January 2019 to December 2023 were collected. The clinical and pathological features of the samples were evaluated by pathological hematoxylin and eosin (HE) staining combined with immunohistochemistry (IHC) experiments. H3F3A mutation status was analyzed based on Sanger sequencing. Further, the associations between H3F3A mutation sites and GCTB clinical features, especially recurrence risk, were explored. Results:Among the 96 GCTB cases, H3F3A was detected to be mutated in 85 cases (88.54%) with the main mutation site defined as H3F3A G34W (76 cases, 89.41%), and other relatively rare mutation sites including G34V, G34L, and Y41H. Of these sites, Y41H mutation was firstly reported in the study. Meanwhile, 15 of the 96 patients encountered recurrence, with clinicopathological features including the Campanacci grading system (which is based on imaging evaluation), tumor soft tissue invasion, P53 expression, and different mutation sites of H3F3A gene associated with tumor recurrence. In particular, compared with the common H3F3A G34W mutation, other relatively rare mutation sites were revealed to be correlated with increased intravascular tumor thrombin and higher tumor cell mitosis, and these patients tended to have a greater risk of recurrence. Conclusions:Multiple clinicopathological features of GCTB including Campanacci grading system, soft tissue invasion, and H3F3A mutation in rare gene sites were associated with tumor recurrence, and the cases with rare H3F3A mutation sites encountered recurrence more frequently than those with G34W mutation. It is of clinical significance to elucidate in detail the mutation sites of H3F3A by Sanger or high-throughput sequencing analysis.

This study aimed to investigate the effects of apigenin on the proliferation, migration, and apoptosis of human diffuse large B-cell lymphoma (DLBCL) OCI-LY3 cells. OCI-LY3 cells were cultured in vitro and treated with varying concentrations of apigenin (20, 40, 80 µmol/L). The CCK-8 assay, Transwell assay, and flow cytometry were employed to detect the proliferation, migration, invasion, and apoptotic abilities of each cell group, respectively. Western blot was employed to measure the expression levels of apoptosis-related proteins (Bax, Bcl-2, Caspase-3). BALB/c mice were used to establish xenograft tumor models via subcutaneous injection of OCI-LY3 cells. Mice were randomly divided into a vehicle group, an apigenin group (10 mg/kg), and a cyclophosphamide group (20 mg/kg) to evaluate the effects of apigenin on tumor growth in vivo. Additionally, Ki-67 expression (a marker for tumor proliferation) was assessed by immunohistochemistry in tumor tissues. Compared to the DMSO group, apigenin at 20, 40, and 80 µmol/L greatly reduced cell proliferation, migration, invasion, and Bcl-2 expression while increasing apoptosis rates and the abundance levels of Bax and cleaved Caspase-3. Apigenin also suppressed the growth of xenograft tumors and reduced Ki-67 expression in tumor tissues. Apigenin exerts anti-DLBCL effects both in vitro and in vivo, offering a novel therapeutic strategy for lymphoma treatment.

A subset of differentiated thyroid cancer still lacks effective treatment options, such as locally advanced or metastatic patients. Some of these patients also need to try radiation therapy. The objective of this study is to investigate the potential of the antennapedia-modified SMAC fragment (ANTP-SmacN7) as a radiation sensitizer to enhance the therapeutic efficacy of radiotherapy in papillary carcinoma of thyroid (PTC), ascertain the contribution of X-linked inhibitor of apoptosis protein (XIAP), and explore its associated mechanisms to the apoptotic response in PTC. Methods To determine whether ANTP-SmacN7 enhances radiotherapy sensitivity by promoting apoptosis through XIAP in thyroid cancer, we first performed bioinformatics analysis of XIAP in thyroid cancer (THCA) using TCGA/GTEx THCA datasets. This analysis evaluated XIAP expression levels, its correlation with clinical pathological features and prognosis, functional enrichment, and interactions with apoptosis-related genes of CASP. Subsequently, we treated TPC-1 cells with gamma ray and ANTP-SmacN7 in different groups and assessed cell proliferation, migration, and apoptosis-related protein expression (XIAP, caspase-3, caspase-8, and caspase-9) using CCK-8, colony formation, transwell assays, annexin V/PI double staining, and western blotting. To further elucidate the role of XIAP and the effects of ANTP-SmacN7, we constructed XIAP-overexpressing TPC-1 cells, treated them with gamma ray and ANTP-SmacN7 in different groups, and compared changes of cell function and apoptosis-related protein. XIAP is highly expressed in THCA and demonstrates significant correlations with aggressive clinicopathological features including advanced T stage (p = 0.018) and extrathyroidal extension (p = 0.017) in THCA, while its prognostic stratification potential is evidenced by an AUC of 0.63. It interacts closely with CASP family members involved in apoptosis, which might critically inform therapeutic strategies for radioresistant THCA. The experimental results demonstrate that TPC-1 cells are sensitive to low-dose gamma ray but exhibit radioresistant as the radiation dose increases. While ANTP-SmacN7 significantly enhances gamma ray-induced radiosensitization. When combined with gamma ray, ANTP-SmacN7 markedly reduces cell proliferation, viability, and migration, while simultaneously promoting apoptosis. This effect is mediated by XIAP inhibition, which activates the intrinsic apoptosis pathway through caspase-3 and caspase-9. Additionally, XIAP influences the extrinsic apoptosis pathway by directly or indirectly upregulating caspase-8. ANTP-SmacN7 could be a probable candidate for a pharmaceutical radiosensitizer when combined with gamma ray for the treatment of PTC. These findings may provide a theoretical basis for the development of radiosensitization strategies for locally advanced or metastatic patients.

OBJECTIVE:To evaluate detection rates of multisite lesions (cervical, vaginal, vulvar) among women attending colposcopy clinics. METHODS:Our cross-sectional study included 20,486 patients between 2014 and 2023 in Shanxi China. Detection rates for cervical, vaginal, and vulvar lesions were retrospectively analyzed across strata by HPV status, cytological diagnosis, and clinical manifestations (vaginal bleeding/discharge). Multinomial logistic regression was applied to calculate odds ratios for high-grade lesions and squamous cell carcinoma (SCC). RESULTS:High-risk HPV (hr-HPV) infection was detected in 16,636 of 20,486 women (81.2%), and 9,137 (44.6%) had ASC-US+ cytology. Following cervical lesion detection on histopathology among hr-HPV-positive women (CIN2/3: 19.9%; SCC: 5.3%; AIS/ADC: 0.4%), additional lesions were identified at other anatomical sites: vaginal lesions (VaIN2/3: 3.6%; SCC: 1.1%; AIS/ADC: 0.04%) and vulvar lesions (VIN2/3: 0.4%; SCC: 0.1%) were further identified. Overall, 21.6% of hr-HPV-positive women exhibited high-grade lesions (CIN/VaIN/VIN2/3), with 5.6% demonstrating multi-focal SCC and 0.4% showing AIS/ADC. Stratified analysis revealed that patients even with negative HPV or cytology result still had relative high detection rate of high-grade lesions. Among these HPV-negative women, those reporting vaginal bleeding/discharge carried an elevated risk, with 3.2% having high-grade lesions and 10.5% having SCC. The integrative examination combining hr-HPV, cytology, and vaginal bleeding/discharge identified 3,753 high-grade lesions and 1,154 cancers. CONCLUSION:Integrating the assessment of hr-HPV testing, cytology, and clinical symptoms (e.g., vaginal bleeding or discharge) could help finding more cases of multisite lesions (cervical, vaginal, vulvar). This is especially important for some high-risk women, including those who visit the colposcopy clinics, and more attention should be paid to the multisite examination.

Background Osteosarcoma has been a common bone malignancy occurring in children and adolescents. Attributing to high tumor heterogeneity, none specific breakthrough has been received in targeted gene therapy for osteosarcoma, although it’s still of great potential for immunotherapy in clinical application. In the study, 5 GEO profiles containing transcriptome information of 109 osteosarcoma samples, single cell sequencing data composed of 6 cases of samples, as well as 43 cases of local hospital tissue samples were combine used to identify the promising immune related candidate genes in osteosarcoma. Methods Based on osteosarcoma transcriptome microarrays from GEO database as well as immune related gene profile from IMMPORT database, differently expressed meanwhile immune related gene candidates in osteosarcoma comparing to normal control samples were identified. Then, protein-protein interaction network (PPI), survival analysis followed by LASSO analysis were in succession applied to construct a gene signature based on the selected candidate genes. After understanding the basic genetic physicochemical properties and evaluating the prognosis risk association of the gene signature using local hospital cancer samples, its association with immune microenvironment features including macrophages included various immune cells infiltration, different immune checkpoints expression, immune related signaling pathways involvement were next step assessed. Results From GEO transcriptome datasets which contains a total of 109 osteosarcoma samples, a total of 108 high level differently expressed meanwhile immune related gene candidates were identified. Then, PPI network and LASSO analysis highlighted a 6 genes containing cluster from the 108 candidate genes. Further, ROC curve as well as Cox regression analysis assisted scaled the 6 hub genes down to 2 key genes, namely STC2 and FPR1, and a gene signature was constructed based on them. After understanding the basic genetic physicochemical properties of STC2 and FPR1, double staining immunochemistry (IHC) experiment based on 43 cases of local hospital samples and single cell sequencing date of 6 tissue samples revealed that STC2 was mainly expressed in osteosarcoma cancer cells, meanwhile, FPR1 was mostly enriched in macrophages focused immune cells which has also been the main immune cell type in osteosarcoma microenvironment. Moreover, the combining STC2/FPR1 dual genes signature was also associated with distribution of multiple immune checkpoints, especially TIM-3. Further, the correlation between the signature and other immune features including immune related cell death (ICD) and ESTIMATE immune score were additionally evaluated. Conclusions Based on osteosarcoma transcriptome genes analysis, a dual genes containing signature composed of STC2 and FPR1 genes was constructed. Immune correlation analysis indicated the signature was associated with the macrophages infiltration which has been a main immune cell type in osteosarcoma, ans it was also related with TIM-3 included multiple immune checkpoints expression. The results shall benefit further osteosarcoma immune researches and assist revealing promising prediction markers for clinical immunotherapy.

Background Exosomes have been important particles that mediate not only cellular communication, but also participate in multiple critical processes of cancer development. The aim of the study is to explore the role of a specific exosome C5orf46 gene in the development of human pan-cancer for potential clinical application. Methods The study started with the physicochemical property, and then gene expression as well as alteration patterns of C5orf46 in cancers, followed by post transcription modulation of the gene and then survival analysis in cancers. Moreover, the correlation between C5orf46 and multiple critical cancer parameters including angiogenesis, cancer stemness, DNA repair, and immune infiltration were in succession explored, which were partly validated using local hospital KIRC samples. Results Firstly, physicochemical properties of C5orf46 were computed including its aminoacid composition, estimated molecular weight and protein half life. Then, based on gene expression as well as survival analysis result, C5orf46 was shown to be up-regulated in KIRC included various human cancers which was partly due to DNA methylation modulation. And of more clinical significance, the changed expression correlated with worse patients survival. Moreover, the association between C5orf46 and multiple critical cancer traits including microenvironment angiogenesis, immune infiltration, extra cellular matrix (ECM) degradation and epithelial-mesenchymal transition (EMT) were validated. Further, C5orf46 gene was indicated to correlate with the sensitivity of several chemotherapy related drugs. Conclusions Based on TCGA pan-cancer data and local hospital samples experiments, we discovered that exosome containing C5orf46 potentially works as an oncogene which was associated with multiple important clinical cancers traits. Although more detailed experiments are needed to validate the gene function, the study shall reveal valuable strategy concerning the role of C5orf46 gene in the development of human cancers.

Supplementary Table S11. Multivariable adjusted association of molecular alterations and overall survival in HGSC and ENOC among patients with residual disease* status.

Supplementary Table S8. Antibodies and reagents.

Supplementary Figure S1. Patients and tumor samples analyzed in this study.

Background: Pneumoconiosis is a kind of lung dysfunction caused by the inhalation of mineral dust. However, the potential molecular mechanism of pneumoconiosis have not been fully elucidated. Methods: In this study, the silica -treated pneumoconiosis mice model was constructed and the transcriptome sequencing data including lncRNA, circRNA, and mRNA were obtained. Firstly, differentially expressed lncRNA, circRNA, and mRNA (DElncRNA, DEcircRNA, DEGs) between control and pneumoconiosis/silicosis samples were screened, the target miRNAs (co-pre-miRNAs) were obtained by intersecting the miRNAs predicted by DElncRNA and DEcircRNA, respectively, and the target mRNAs (co-mRNA) were obtained by intersecting the mRNAs predicted by target miRNA and DEGs. Then, the lncRNA/circRNA-miRNA-mRNA networks were constructed by Cytoscape. Next, the key mRNAs were obtained by protein-protein interaction (PPI) analysis, and the key lncRNAs/circRNAs were selected by correlation analysis. Moreover, the expression of the key lncRNAs, circRNAs and mRNAs on chromosome were studied by the "circlize" package. Furthermore, the TFs-miRNA-mRNA network was constructed and the function of DEGs were explored by Ingenuity Pathway Analysis (IPA). To demonstrate the feasibility and value of the constructed ceRNA networks, we validated key genes and mmu-miR682 pathway. Finally, We used the Drug -Gene Interaction database to predict potential drugs that could interfere with key genes,which may help to find promising treatment. Results: There were 427 DElncRNAs, 107 DEcircRNAs and 1,597 DEGs between silicosis and control groups. Totals of 77 co-pre-miRNAs and 96 co-mRNA were screened, and the lncRNA/circRNA-miRNA-mRNA networks were constructed with 27 lncRNA/25 circRNAs, 74 miRNAs and 96 mRNAs. Then, 6 key mRNAs including Igf1, Klf4, Ptgs2, Epas1, Gnao1, and Il1a were obtained by PPI, and all of these key mRNAs and 10 key lncRNAs and 8 circRNAs were significantly different between the pneumoconiosis and normal groups, in which 10 lncRNAs and 9 circRNA that have not been previously studied in pneumoconiosis/silicosis can be used as new potential therapeutic targets. Moreover, the TFs-miRNA-mRNA network were constructed with 11 TFs, 1 key miRNA (mmu-miR-682) and 3 key mRNAs (Igf1, Epas1, Ptgs2). And the validation of key genes revealing by RNA-seq through experimental approaches shows the the predictive power of this study. Finally, IPA results indicated that 41 pathways were activated and 2 pathways were suppressed in pneumoconiosis/silicosis groups, and Pathogen Induced Cytokine Storm Signaling Pathway was the most significant pathway affected by pneumoconiosis/silicosis. In addition, 93 drugs were screened out by Drug -Gene Interaction database. Among them, Hydroxychloroquine was a kind of drug which associated with Il1a and Ptgs2, may be a promising treatment. Conclusion: This study constructed the lncRNA/circRNA-miRNA-mRNA and TFs-miRNA-mRNA networks, which could deepen the potential molecular regulatory mechanism of pneumoconiosis/silicosis.

IntroductionThe etiology and clinical presentation of vulvar carcinomas, especially vulvar lesions, are not fully understood. Because the vulva and cervix are anatomically connected, human papillomavirus (HPV) is the main cause of cervical lesions. Thus, this study explored the potential characteristics and effects of specific HPV infection types across vulvar lesions and concurrent cervical lesions.MethodsThis retrospective, cross-sectional study analyzed patients with cervical HPV or cytological results and concurrent vulvar biopsy who were seen in our hospital colposcopy clinic in Shanxi Province, China, between 2013 and 2023. Data on age, menopause status, vulvar manifestations, and cytology and HPV infection testing results were collected. Attributable fractions and multinominal logistic models were used to evaluate HPV genotyping and clinical characteristics across vulvar lesions.ResultsAmong the 1,027 participants, 83 (8.1%) had vulvar intraepithelial neoplasia (VIN) of high grade or worse (VIN2+), and 127 (12.4%) had non-neoplastic epithelial disorders of the vulva (NNEDV). A total of 175 patients had either VIN2+ or cervical intraepithelial neoplasia (CIN) lesions of grade 2 or worse (CIN2+). The most common HPV genotypes for VIN2+ or concurrent VIN2+/CIN2+ were HPV16, HPV52, and HPV58, although attributable fractions differed among lesions. Patients with normal cytological or histopathological result were more likely to have NNEDV detected, while abnormal cervical diagnosis was associated with higher detection of VIN2+. Multinominal logistic modeling showed that age and HPV16 infection were risk factors for VIN2+ or concurrent VIN2+/CIN2+; however, only vulvar presentation with depigmentation was a risk factor for NNEDV. Among patients with low-grade CIN1/VIN1, compared with those who were HPV16 negative, those who were HPV16 positive were at 6.63-fold higher risk of VIN2+/CIN2+ [95% confidence interval (CI): 3.32, 13.21]. Vulvar depigmentation was also associated with increased risk of NNEDV (odds ratio: 9.98; 95% CI: 3.02, 33.04).ConclusionsChinese women may be at specific, high risk for HPV infection types associated with VIN or CIN. The use of cervical cell HPV detection along with vulvar presentation during cervical cancer screening may also contribute to vulvar lesion detection.

Abstract Background Osteosarcoma has been the most common primary bone malignant tumor in children and adolescents. Despite the considerable improvement in the understanding of genetic events attributing to the rapid development of molecular pathology, the current information is still lacking considering the comprehensive and highly heterogeneous nature of osteosarcoma. The study is to identify more potential responsible genes during the development of osteosarcoma, thus identifying promising gene indicators and aiding more precise interpretation of the disease. Methods Firstly, from GEO database, osteosarcoma transcriptome microarrays were used to screen the abnormally expressed genes (AEGS) in cancer comparing to normal bone samples, followed by GO/KEGG interpretation, risk score assessment and survival analysis of the genes to select a credible key gene. Further, the basic physicochemical properties, predicted cellular location, gene expression in human cancers, association with clinical pathological features and the potential signaling pathways involved in the key gene’s regulation on osteosarcoma development were preliminary explored. Results A total of 24430 genes were identified to express abnormally in osteosarcoma versus normal bone samples, and the genes were classified into four groups based on the difference level, further genes interpretation indicated that the high abnormal level (>8 fold) genes were mainly located extracellular and related to matrix structural constituent regulation. Meanwhile, module function analysis of the 67 high abnormal level (>8 fold) AEGS revealed a 22-gene containing extracellular matrix regulation associated hub gene cluster. Further survival analysis of the 22 genes revealed that STC2 was an independent prognosis indicator in osteosarcoma. Moreover, after the validation of changed expression of STC2 in cancer vs normal tissues using local hospital osteosarcoma samples by IHC experiment, the gene’s physicochemical property revealed STC2 as a cellular stable and hydrophilic protein, and the gene’s association with osteosarcoma clinical pathological parameters, expression in pan-cancers and the probable biological functions and signaling pathways it involved were explored. Conclusions Using multiple bioinformatic analysis and local hospital samples validation, we revealed the aberrant gain of expression of STC2 in osteosarcoma, which associated statistical significantly with patients survival, and the gene’s clinical features and potential biological functions were also explored. Although the results shall provide inspiring insights into further understanding of the disease, further experiments and detailed rigorous clinical trials are needed to reveal its potential drug-target role in clinical medical use.