cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.30552965.v1
title: Molecular features influencing clinical outcome of advanced HER2-positive gastric cancer receiving trastuzumab plus chemotherapy

description: Less than half of the human epidermal growth factor receptor 2 (HER2)-positive gastric cancer (GC) patients respond to trastuzumab plus chemotherapy, and the outcomes are unsatisfactory. Understanding the underlying mechanisms remains crucial for identifying patients who are more likely to benefit from treatment. We performed targeted DNA sequencing on paired pre-treatment and progressive tumour tissues from 22 HER2-positive advanced GC patients undergoing first-line treatment with trastuzumab and chemotherapy. Clinicopathological and genomic characteristics were assessed for the correlation with clinical outcomes. A performance status (PS) of 0–1 was associated with improved progression-free survival (PFS) and overall survival (OS) than a PS of 2. Poorly differentiated tumours exhibited shorter PFS than moderate or moderate-poor ones. Pre-treatment amplification of <i>MYC</i> or <i>TOP2A</i> gene was association with increased PFS, and suggested a potential benefit for OS. Patients with higher tumour mutation burden (TMB) experienced significantly worse PFS, while higher chromosome instability (CIN) appeared to be correlated with longer PFS. Compared to non-responders, responders had a higher CIN but similar TMB and intratumoural heterogeneity (ITH). PS and <i>MYC</i> amplification emerged as independent factors related to PFS according to multivariate survival analysis. Additionally, after treatment, TMB significantly increased in non-responders, while CIN significantly decreased in responders. Pre-treatment <i>MYC</i> amplification and PS were independently associated with clinical outcomes in HER2-positive advanced GC patients treated with first-line trastuzumab plus chemotherapy. Dynamic post-treatment changes in TMB and CIS provide valuable insights into the relationship between therapeutic response and distinct evolutionary trajectories.
DOI: 10.6084/m9.figshare.29061591
title: Circulating fibroblast growth factor 21 is associated with blood pressure in the Chinese population: a community-based study

description: Our research team previously found that fibroblast growth factor (FGF) 21, a circulating hormone, was significantly associated with atherosclerosis in human and animal models. The relationship between FGF21 and blood pressure (BP) is rarely studied in the Asian population. Therefore, we aimed to explore the relationship of FGF21 with BP in a Chinese population. We analysed data on 1051 participants from the Shenzhen–Hong Kong United Network on Cardiovascular Disease (SHUN-CVD) study. The medians of FGF21 level were 355.1 pg/mL (IQR 234.3–574.8 pg/mL) for hypertensive patients and 253.5 (IQR 136.9–403.3 pg/mL) for non-hypertensive participants. Ln-transformed FGF21 level was associated with both systolic and diastolic BP (systolic BP: <i>B</i> = 4.45 [95% CI 3.41–5.49]; <i>p</i> &lt; .001; diastolic BP: <i>B</i> = 2.72 [95% CI 2.03–3.42]; <i>p</i> &lt; .001). After adjusting for sex, age, body mass index, hypercholesterolaemia, diabetes, alcohol consumption, smoking and physical activity, the association remained significant (systolic BP: <i>B</i> = 1.99 [95% CI 1.01–2.97]; <i>p</i> &lt; .001; diastolic BP: <i>B</i> = 1.36 [95% CI 0.69–2.04]; <i>p</i> &lt; .001). Serum FGF21 level was associated with hypertension (quartile 4 vs. quartile 1, OR = 4.19 [95% CI 2.65–6.61]; <i>p</i> for trend &lt; .001). This is the first study to elucidate the relationship of FGF21 with BP in the Asian population. FGF21 is significantly associated with BP. Besides its use as a biomarker, FGF21 may be a new drug target for hypertension treatment.
DOI: 10.6084/m9.figshare.29061591.v1
title: Circulating fibroblast growth factor 21 is associated with blood pressure in the Chinese population: a community-based study

description: Our research team previously found that fibroblast growth factor (FGF) 21, a circulating hormone, was significantly associated with atherosclerosis in human and animal models. The relationship between FGF21 and blood pressure (BP) is rarely studied in the Asian population. Therefore, we aimed to explore the relationship of FGF21 with BP in a Chinese population. We analysed data on 1051 participants from the Shenzhen–Hong Kong United Network on Cardiovascular Disease (SHUN-CVD) study. The medians of FGF21 level were 355.1 pg/mL (IQR 234.3–574.8 pg/mL) for hypertensive patients and 253.5 (IQR 136.9–403.3 pg/mL) for non-hypertensive participants. Ln-transformed FGF21 level was associated with both systolic and diastolic BP (systolic BP: <i>B</i> = 4.45 [95% CI 3.41–5.49]; <i>p</i> &lt; .001; diastolic BP: <i>B</i> = 2.72 [95% CI 2.03–3.42]; <i>p</i> &lt; .001). After adjusting for sex, age, body mass index, hypercholesterolaemia, diabetes, alcohol consumption, smoking and physical activity, the association remained significant (systolic BP: <i>B</i> = 1.99 [95% CI 1.01–2.97]; <i>p</i> &lt; .001; diastolic BP: <i>B</i> = 1.36 [95% CI 0.69–2.04]; <i>p</i> &lt; .001). Serum FGF21 level was associated with hypertension (quartile 4 vs. quartile 1, OR = 4.19 [95% CI 2.65–6.61]; <i>p</i> for trend &lt; .001). This is the first study to elucidate the relationship of FGF21 with BP in the Asian population. FGF21 is significantly associated with BP. Besides its use as a biomarker, FGF21 may be a new drug target for hypertension treatment.
DOI: 10.6084/m9.figshare.29424720
title: Association between heavy metal exposure and chronic cough: the mediating roles of inflammation

description: Right now, epidemiological research examining the connection between blood heavy metal exposure and chronic coughing is still deficient. Therefore, the survey was aimed at the effects of multiple heavy metals on chronic cough. In this investigation, 2647 individuals from NHANES were included. This study applied multiple statistical models to systematically explore the associations between single and mixed blood metal with the prevalence of chronic cough, including logistic regression, weighted quantile sum (WQS) regression, bayesian kernel machine regression (BKMR), and the Shapley Additive Explanations (SHAP) model. Finally, this research conducted mediation analyses to investigate the mediated effects of inflammation on the association between metal and chronic cough. In the logistic regression model of single exposure, blood cadmium was positively associated with the prevalence of chronic cough (OR: 3.17; 95% CI: 2.08–4.83). Consistent findings from the WQS, BKMR, and SHAP models revealed that cumulative exposure to multiple blood metals was positively linked to chronic cough, with cadmium emerging as the predominant contributor among the five examined metals. Mediation analyses indicated that WBC and neutrophils, with a proportion of 2.74% and 5.06%, respectively, mediated the link of cadmium in blood with chronic cough. Exposure to heavy metal mixtures was linked to an increase in the prevalence of chronic cough. And blood cadmium may primarily drive this association, with activated inflammation partially mediating it. Our findings offer novel insights into the impact of blood cadmium to chronic cough.
DOI: 10.6084/m9.figshare.29424720.v1
title: Association between heavy metal exposure and chronic cough: the mediating roles of inflammation

description: Right now, epidemiological research examining the connection between blood heavy metal exposure and chronic coughing is still deficient. Therefore, the survey was aimed at the effects of multiple heavy metals on chronic cough. In this investigation, 2647 individuals from NHANES were included. This study applied multiple statistical models to systematically explore the associations between single and mixed blood metal with the prevalence of chronic cough, including logistic regression, weighted quantile sum (WQS) regression, bayesian kernel machine regression (BKMR), and the Shapley Additive Explanations (SHAP) model. Finally, this research conducted mediation analyses to investigate the mediated effects of inflammation on the association between metal and chronic cough. In the logistic regression model of single exposure, blood cadmium was positively associated with the prevalence of chronic cough (OR: 3.17; 95% CI: 2.08–4.83). Consistent findings from the WQS, BKMR, and SHAP models revealed that cumulative exposure to multiple blood metals was positively linked to chronic cough, with cadmium emerging as the predominant contributor among the five examined metals. Mediation analyses indicated that WBC and neutrophils, with a proportion of 2.74% and 5.06%, respectively, mediated the link of cadmium in blood with chronic cough. Exposure to heavy metal mixtures was linked to an increase in the prevalence of chronic cough. And blood cadmium may primarily drive this association, with activated inflammation partially mediating it. Our findings offer novel insights into the impact of blood cadmium to chronic cough.
DOI: 10.6084/m9.figshare.29956330
title: A systematic review of the association between ultrasound-detected features and laboratory inflammatory biomarkers in hand osteoarthritis

description: To systematically review observational studies for the relationship between ultrasound (US)-detected features and laboratory inflammatory biomarkers in hand osteoarthritis (OA). A systematic literature search was performed in MEDLINE, EMBASE, CINAHL, and Web of Science from their inception to June 2025 to identify relevant observational studies. Study quality was evaluated using the Newcastle–Ottawa Scale (NOS), with two independent reviewers validating the papers. Correlation coefficients and corresponding confidence intervals and P values between US-detected features and biomarkers were extracted and analysed. Out of 5,128 citations, four studies (546 participants, 91.75% female, mean age 56.1–66.3 years) scored &gt;5 on the NOS. Significant correlations (<i>r</i> = 0.3–0.57) were found between serum inflammatory markers (e.g. TNF, MIP-β, PDGF-bb, IP-10) and grey-scale synovitis (GSS) specifically in erosive hand OA. No significant correlations were observed between other US-detected features (e.g. power Doppler (PD) signals, osteophytes (OST), effusion, cartilage thickness) and inflammatory biomarkers, with coefficients generally &lt;0.2. These findings highlight a critical gap in research linking US-detected features and serum inflammatory markers in hand OA. While some evidence suggests that US-detected GSS may reflect subclinical inflammation, particularly in erosive hand OA, inconsistent results across studies underscore the need for larger, standardised research to support phenotyping and inform targeted diagnostic and therapeutic strategies.
DOI: 10.6084/m9.figshare.29956330.v1
title: A systematic review of the association between ultrasound-detected features and laboratory inflammatory biomarkers in hand osteoarthritis

description: To systematically review observational studies for the relationship between ultrasound (US)-detected features and laboratory inflammatory biomarkers in hand osteoarthritis (OA). A systematic literature search was performed in MEDLINE, EMBASE, CINAHL, and Web of Science from their inception to June 2025 to identify relevant observational studies. Study quality was evaluated using the Newcastle–Ottawa Scale (NOS), with two independent reviewers validating the papers. Correlation coefficients and corresponding confidence intervals and P values between US-detected features and biomarkers were extracted and analysed. Out of 5,128 citations, four studies (546 participants, 91.75% female, mean age 56.1–66.3 years) scored &gt;5 on the NOS. Significant correlations (<i>r</i> = 0.3–0.57) were found between serum inflammatory markers (e.g. TNF, MIP-β, PDGF-bb, IP-10) and grey-scale synovitis (GSS) specifically in erosive hand OA. No significant correlations were observed between other US-detected features (e.g. power Doppler (PD) signals, osteophytes (OST), effusion, cartilage thickness) and inflammatory biomarkers, with coefficients generally &lt;0.2. These findings highlight a critical gap in research linking US-detected features and serum inflammatory markers in hand OA. While some evidence suggests that US-detected GSS may reflect subclinical inflammation, particularly in erosive hand OA, inconsistent results across studies underscore the need for larger, standardised research to support phenotyping and inform targeted diagnostic and therapeutic strategies.
DOI: 10.6084/m9.figshare.30596078
title: TCGA molecular subtypes in endometriosis-associated ovarian cancer: a systematic review and meta-analysis

description: Endometriosis-associated ovarian cancer (EAOC) mainly includes endometrioid ovarian cancer (ENOC) and clear cell ovarian cancer (CCOC). The Cancer Genome Atlas (TCGA) revealed four molecular subtypes of endometrial cancer (EC) in 2013, which have been proven pivotal in the diagnostic, prognostic and therapeutic domains of EC. Existing evidence indicates that EC and EAOC molecular analysis have similar significance. This review aims to investigate the distribution, staging and prognostic characteristics of molecular subtypes in EAOC. PubMed, Embase and Web of Science were systematically searched from January 2013 to December 2023 using predefined keywords. Patient characteristics, including stage and prognostic characteristics, were extracted from the selected studies. Data analysis was carried out using Stata 14MP. A total of 6 studies involving 1,133 patients with ENOC and 4 studies comprising 377 patients with CCOC were included. ENOC had a higher frequency of the POLE mutation (POLEmut) subtype (odds ratio (OR) = 2.29, 95% CI: 1.03–5.11, <i>p</i> = 0.043) and the mismatch repair deficient (MMRd) subtype (OR = 3.54, 95% CI: 2.05–6.11, <i>p</i> = 0.000) than CCOC; ENOC had a lower frequency of the no specific molecular profile (NSMP) subtype (OR = 0.55, 95% CI: 0.41–0.73, <i>p</i> = 0.000) and the p53 abnormal (p53abn) subtype (OR = 0.97, 95% CI: 0.67–1.42, <i>p</i> = 0.893). The hazard ratios (HR) of the p53abn subtype in ENOC were disease-free survival (DFS) (HR = 3.25, 95% CI: 1.46–7.21, <i>p</i> = 0.004) and progression-free survival (PFS) (HR = 4.11, 95% CI: 2.86–5.92, <i>p</i> = 0.000). The DFS of the p53abn subtype in CCOC was calculated (HR = 5.52, 95% CI: 3.43–8.90, <i>p</i> = 0.000). The TCGA subtypes of EC may exhibit similarities in prognosis between ENOC and CCOC.
DOI: 10.6084/m9.figshare.30596078.v1
title: TCGA molecular subtypes in endometriosis-associated ovarian cancer: a systematic review and meta-analysis

description: Endometriosis-associated ovarian cancer (EAOC) mainly includes endometrioid ovarian cancer (ENOC) and clear cell ovarian cancer (CCOC). The Cancer Genome Atlas (TCGA) revealed four molecular subtypes of endometrial cancer (EC) in 2013, which have been proven pivotal in the diagnostic, prognostic and therapeutic domains of EC. Existing evidence indicates that EC and EAOC molecular analysis have similar significance. This review aims to investigate the distribution, staging and prognostic characteristics of molecular subtypes in EAOC. PubMed, Embase and Web of Science were systematically searched from January 2013 to December 2023 using predefined keywords. Patient characteristics, including stage and prognostic characteristics, were extracted from the selected studies. Data analysis was carried out using Stata 14MP. A total of 6 studies involving 1,133 patients with ENOC and 4 studies comprising 377 patients with CCOC were included. ENOC had a higher frequency of the POLE mutation (POLEmut) subtype (odds ratio (OR) = 2.29, 95% CI: 1.03–5.11, <i>p</i> = 0.043) and the mismatch repair deficient (MMRd) subtype (OR = 3.54, 95% CI: 2.05–6.11, <i>p</i> = 0.000) than CCOC; ENOC had a lower frequency of the no specific molecular profile (NSMP) subtype (OR = 0.55, 95% CI: 0.41–0.73, <i>p</i> = 0.000) and the p53 abnormal (p53abn) subtype (OR = 0.97, 95% CI: 0.67–1.42, <i>p</i> = 0.893). The hazard ratios (HR) of the p53abn subtype in ENOC were disease-free survival (DFS) (HR = 3.25, 95% CI: 1.46–7.21, <i>p</i> = 0.004) and progression-free survival (PFS) (HR = 4.11, 95% CI: 2.86–5.92, <i>p</i> = 0.000). The DFS of the p53abn subtype in CCOC was calculated (HR = 5.52, 95% CI: 3.43–8.90, <i>p</i> = 0.000). The TCGA subtypes of EC may exhibit similarities in prognosis between ENOC and CCOC.
DOI: 10.6084/m9.figshare.28252894
title: Cardiovascular safety of Janus kinase inhibitors in inflammatory bowel disease: a systematic review and network meta-analysis

description: Janus kinase (JAK) inhibitors (JAKinibs) are effective for inflammatory bowel disease (IBD), but their cardiovascular safety is inconclusive. We aim to assess the cardiovascular risks associated with JAKinibs in IBD patients. Systematic searches of seven databases and ClinicalTrials.gov from inception to February 2024 were conducted. Outcomes included major adverse cardiovascular events (MACE), venous thromboembolism events (VTE) and cardiovascular events (CVE), which were separately evaluated based on whether or not the dose was considered. P-score was applied to rank interventions. A total of 26 trials involving 10,537 IBD patients were included, and results showed no significantly increased risk of MACE, VTE and CVE was associated with JAKinibs. However, when the dose was considered, Tofacitinib 5 mg BID (versus placebo) showed a trend towards an increased risk of MACE [odds ratio (OR)=1.05, 95% confidence interval (CI): 0.23–4.82], as well as Upadacitinib 30 mg QD (versus placebo) showed a trend towards increased risks of VTE (OR=1.36, 95% CI: 0.23–8.03) and CVE (OR=1.08, 95% CI: 0.24–4.85), and ranked higher than placebo for the risk of VTE [P-score=0.766 (versus 0.722)]. Notably, Deucravacitinib ranked lowest for all cardiovascular risks, and significantly decreased the risks of VTE (OR=0.03, 95% CI: 0.00-0.87) and CVE (OR=0.03, 95% CI: 0.00-0.87) compared with placebo. Although a trend of increased cardiovascular risks was found considering dose, no significantly increased cardiovascular risk was associated with JAKinibs in IBD patients, and Deucravacitinib significantly decreased the risks of VTE and CVE. This is the first network meta-analysis specifically assessing the cardiovascular risks associated with JAKinibs in IBD patients, and findings demonstrated that no significantly increased cardiovascular risk was found and Deucravacitinib significantly decreased the cardiovascular risks.
DOI: 10.6084/m9.figshare.28252894.v1
title: Cardiovascular safety of Janus kinase inhibitors in inflammatory bowel disease: a systematic review and network meta-analysis

description: Janus kinase (JAK) inhibitors (JAKinibs) are effective for inflammatory bowel disease (IBD), but their cardiovascular safety is inconclusive. We aim to assess the cardiovascular risks associated with JAKinibs in IBD patients. Systematic searches of seven databases and ClinicalTrials.gov from inception to February 2024 were conducted. Outcomes included major adverse cardiovascular events (MACE), venous thromboembolism events (VTE) and cardiovascular events (CVE), which were separately evaluated based on whether or not the dose was considered. P-score was applied to rank interventions. A total of 26 trials involving 10,537 IBD patients were included, and results showed no significantly increased risk of MACE, VTE and CVE was associated with JAKinibs. However, when the dose was considered, Tofacitinib 5 mg BID (versus placebo) showed a trend towards an increased risk of MACE [odds ratio (OR)=1.05, 95% confidence interval (CI): 0.23–4.82], as well as Upadacitinib 30 mg QD (versus placebo) showed a trend towards increased risks of VTE (OR=1.36, 95% CI: 0.23–8.03) and CVE (OR=1.08, 95% CI: 0.24–4.85), and ranked higher than placebo for the risk of VTE [P-score=0.766 (versus 0.722)]. Notably, Deucravacitinib ranked lowest for all cardiovascular risks, and significantly decreased the risks of VTE (OR=0.03, 95% CI: 0.00-0.87) and CVE (OR=0.03, 95% CI: 0.00-0.87) compared with placebo. Although a trend of increased cardiovascular risks was found considering dose, no significantly increased cardiovascular risk was associated with JAKinibs in IBD patients, and Deucravacitinib significantly decreased the risks of VTE and CVE. This is the first network meta-analysis specifically assessing the cardiovascular risks associated with JAKinibs in IBD patients, and findings demonstrated that no significantly increased cardiovascular risk was found and Deucravacitinib significantly decreased the cardiovascular risks.
DOI: 10.6084/m9.figshare.30759571
title: Unveiling the prognostic and immunological role of IFI44 in glioma

description: Gliomas are aggressive central nervous system tumors with limited understanding of their molecular drivers. Identifying novel prognostic and therapeutic biomarkers remains crucial. Using TCGA, GTEx, GEO, and CGGA datasets, we performed differential expression, Cox regression, and LASSO analyses to identify prognostic genes. IFI44, one of eight significant candidates, was analyzed for its association with survival, clinical features (IDH mutation, 1p/19q codeletion) and tumor immune microenvironment. Functional assays were conducted to evaluate its effects on glioma cell proliferation, migration, and invasion. Transcriptomic analysis of 1,142 normal and 398 glioma samples identified 61 consistently dysregulated genes, predominantly enriched in immune-related rather than classical oncogenic pathways. In CGGA cohorts, eight progression-associated genes were identified, six associated with poor prognosis. IFI44 expression correlated with higher grade, older age, IDH wild type, and 1p/19q non-codeletion. High IFI44 tumors were enriched for NF1 mutations, while low IFI44 tumors carried IDH1, NOTCH1, and CIC mutations. Mechanistically, IFI44-high gliomas exhibited immune-suppressive pathway enrichment, increased checkpoint expression (PD-1/PD-L1, CTLA4, LAG3), and macrophage infiltration. Protein interaction analysis linked IFI44 to cytokine signaling and T-cell regulation. In U87 and U251 cells, IFI44 overexpression promoted proliferation, migration, and invasion, whereas knockdown suppressed these phenotypes. IFI44 may drive glioma progression through dual mechanisms of immune microenvironment remodeling and promotion of tumor cell aggressiveness, supporting its potential as a prognostic biomarker and therapeutic target. Although preliminary knockdown and overexpression assays were performed, the underlying mechanisms of IFI44-mediated immune regulation and tumor progression require further investigation.