Ask about this productRelated genes to: NRG1 antibody
- Gene:
- NRG1 NIH gene
- Name:
- neuregulin 1
- Previous symbol:
- HGL, NRG1-IT2
- Synonyms:
- HRG, NDF, GGF
- Chromosome:
- 8p12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-19
- Date modifiied:
- 2015-01-28
Related products to: NRG1 antibody
Related articles to: NRG1 antibody
- NRG1 gene fusions have been identified in patients with various solid tumors. Such patients have aggressive tumors and respond poorly to currently available treatments. There are many gene partners described for NRG1 fusions, and the structures and roles of the chimeric proteins are not always correctly understood. Here, we gather information on 665 reported patients with a total of 115 different known gene partners, and discuss structural elements supposed to play important roles in the biology of NRG1 fusions in cancer. This gives a better understanding of the biology of NRG1 fusions, and will help in the development of new therapeutic approaches. Our methodology described in this review can also be used for the study of other genes with disease-related fusions. - Source: PubMed
Publication date: 2026/04/16
Thiollier-Schmitt ClarisseBarre ManonIssenmann MarieCros-Perrial EmelineDuruisseaux MichaëlJordheim Lars Petter - KRAS G12C-mutated non-small cell lung carcinoma (NSCLC), caused by a glycine-to-cysteine substitution at codon 12, is associated with poor prognosis and is now targetable with specific inhibitors. We retrospectively analyzed 279 KRAS G12C-mutated NSCLC cases (2017-2023) from our registry with available histologic, immunohistochemical, and molecular data. The cohort included 279 patients (125 females, 151 males; mean age 67 years, range 29-91). Most tumors were primary lung carcinomas (n = 229, 82%), while 45 (16%) were metastatic at presentation. Morphologic evaluation was available in 240 tumors: 37% showed solid squamous cell carcinoma (SCC)-like features, 61% rhabdoid/plasmacytoid morphology, and 17% sarcomatoid features. Adenocarcinoma-associated patterns were present in 67 cases, often mixed, and focal solid growth occurred in 77%. TTF1, Napsin A, and CK7 were positive in 86%, 87%, and 98%, respectively, whereas squamous markers were infrequent (p40/p63 7%, CK5/6 8%). PD-L1 expression was detected in 65%. Co-mutations most commonly involved TP53 (n = 27) and STK11 (n = 12); IDH1/2, PIK3CA, and CTNNB1 mutations occurred in four cases each, MET in two cases, and BRAF, FGFR2, FGFR3, and GNAS in one case each. Two gene fusions were identified (LRP12::NRG1, FGFR3::TACC3). Mean survival was 1.89 years, with one- and five-year survival rates of 54% and 25%. KRAS G12C-mutated NSCLC is clinically aggressive and frequently shows solid growth with rhabdoid, plasmacytoid, or SCC-like morphology, which may lead to misclassification and missed genetic testing. Immunohistochemistry and molecular profiling are essential for accurate classification and enabling targeted therapy. - Source: PubMed
Publication date: 2026/04/15
Bradová MartinaSlavík PetrVaněček TomášMartínek PetrGrossmann PetrKormunda StanislavBehenská KristýnaSvatoň MartinPešek MilošJirásek Tomᚊpůrková ZuzanaHroudová PetraMrázková HanaHořavová BarboraRoubec JaromírBaník MartinMukenšnábl PetrMichal MichalŠvajdler Marián - Alzheimer disease (AD) is a progressive neurodegenerative disorder marked by transcriptomic alterations affecting multiple genes. Many researchers have tried to predict major hallmarks of AD pathogenesis for diagnosis but the association between receptor tyrosine kinase (RTK) pathways and AD diagnosis is still unclear. This study aims to identify RTK-associated gene signatures crucial to AD pathogenesis and assess their potential as diagnostic biomarkers for AD. The study investigated changes in RTK pathway gene expression related to AD by analyzing brain transcriptome data from two independent public data sets (GSE84422 and GSE109887). Differentially expressed genes (DEGs) were analyzed from the GSE84422 and GSE109887 data sets and overlapping genes (oDEGs) were identified. RTK-related genes (ooDEGs) were subsequently selected through functional enrichment analysis. These were further refined into AD-related genes (disease-associated genes (DAGs)) through protein-protein interaction network analysis. Logistic regression and receiver operating characteristic analyses were conducted on the selected DAGs to evaluate their diagnostic potential, with additional gene expression validation performed in brain organoids and primary neurons. A total of 145 genes were identified as oDEGs in the above two data sets, and 18 genes were selected as ooDEGs. Six DAGs (ITGB1, AXL, GFAP, NRG1, CAV1, and RHOA) were selected. The diagnostic powers of the six DAGs for AD were 0.825 (GSE84422) and 0.884 (GSE109887). Human brain organoids and primary neuronal models were used to validate the biological relevance of these findings. AXL and ITGB1 were finally selected as key genes for RTK pathway in AD and were significantly increased in AD. - Source: PubMed
Publication date: 2026/04/15
Shin SaewoonZhu XiaohuiAmartumur SarnaiLee TaehoonYu Won JongPark SoominEtemadi NiloofarJamsranjav AriunzayaKang RianBak GyusooLee DongjoonKim JieunHan Jong WonHeo ChaejeongCho HansangChang SunghoeMook-Jung InheeLee Sang-EunPark Jong-Chan - Growth differentiation factor 15 (GDF15) is a stress-responsive cytokine strongly associated with aging, multimorbidity, and cardiovascular disease. Although prior studies have established its prognostic value in high-risk populations, its role in the general population remains less defined. The aim of this study was to determine if there is an association between plasma GDF15 levels, heart disease and mortality in a representative population-based cohort. We analyzed 1532 participants (mean age 55 years; 54.6% women) with available baseline plasma GDF15 concentrations. Participants were stratified according to an optimal cutoff of 1081 pg/mL, derived from ROC curve analysis for mortality. Associations with prevalent heart disease were assessed using multivariable logistic regression models adjusted for cardiovascular risk factors and NT-proBNP. Mortality was analyzed using Cox proportional hazards models, with model performance evaluated by C-index and time-dependent ROC curves. Individuals with GDF15 > 1081 pg/mL were older and exhibited a more adverse cardiometabolic profile with higher prevalence of comorbidities. Elevated GDF15 was independently associated with ischemic cardiomyopathy (OR 3.34, 95% CI: 1.38-8.11), particularly in men (OR 4.26, 95% CI: 1.40-12.96), but not in women. No independent associations were observed with arrhythmias, valvulopathy, or heart failure after adjustment for NT-proBNP. During a median follow-up of 6.2 years, 51 deaths occurred. Elevated GDF15 independently predicted all-cause mortality (HR 2.47, 95% CI: 1.19-5.13), though the effect was attenuated after adjustment for NT-proBNP. GDF15 improved model discrimination (ΔC-index = +0.01; LRT = 0.011) and showed robust time-dependent predictive ability, with AUCs of 0.76, 0.82, and 0.85 at 2, 4, and 6 years, respectively. In this population-based cohort, elevated GDF15 identified individuals with an adverse health profile, was independently associated with ischemic cardiomyopathy in men, and predicted mortality. Although its incremental predictive value over NT-proBNP was modest, GDF15 could provide complementary biological information and may enhance multimarker strategies for cardiovascular risk stratification in the general population. - Source: PubMed
Publication date: 2026/03/27
Martín-Carro BeatrizNieto-García LeticiaSánchez-Pablo ClaraRomero AlfonsoPérez Del Villar CandelasMoyano-Maza José CarlosDios José María deCembrero-Fuciños DavidIglesias-Colino EstefaníaMuriel PazCascón SaraMartín-Gallego AmaliaBlázquez BaltasaraSantolino InmaculadaGonzález-González LydiaLedesma María ConcepciónMaillo-Seco JavierRodríguez-Nieto JesúsRincón Luis MIsidoro-García MaríaSánchez Pedro L - : Lung cancer remains the leading cause of cancer-related mortality globally. Approximately 45% of these tumors harbor oncogenic mutations that drive carcinogenesis and are amenable to targeted therapies. Other predictive biomarkers-e.g., PD-L1, TMB, and MSI-play a crucial role in patients' management. This study aims to investigate the existence of mutation clusters (co-mutations) and evaluate the correlation of these clusters with various clinical and laboratory parameters. : A retrospective study was conducted utilizing pathological samples from lung cancer patients harboring mutations in , , , , , , , , and . Data were collected from the Institute of Pathology at Carmel Medical Center between the years 2022 and 2024. Patients were stratified using a Two-Step Cluster Analysis algorithm based on actionable mutations and co-mutations. Heatmaps and dendrograms were generated to assess the correlation between these genomic clusters, clinical metrics, and predictive biomarkers. : The study cohort included 129 patients with actionable mutations. Five distinct clusters were identified: Clusters 1, 2, and 3 exhibited a high expression of and co-mutations alongside drivers ( = 38, = 12, and = 23, respectively). Clusters 4 and 5 demonstrated high expression of alterations and tumor suppressor gene mutations ( = 31 and = 25, respectively). Cluster comparisons demonstrated statistically significant differences between clusters regarding age, gender, PD-L1 expression, and tumor mutational burden. No significant associations were found regarding ethnicity or microsatellite instability status. : By constructing clusters based on the aggregate of genomic alterations in patients with actionable mutations, it is possible to predict associations with distinct demographic and clinical characteristics. Future research should apply this analytical approach to larger cohorts to further characterize these subgroups and investigate potential correlations with therapeutic efficacy. - Source: PubMed
Publication date: 2026/04/07
Agbarya AbedShalata WalidSabo EdmondSaiegh LeonardShaham YuvalNasrallah HaitamMhameed KamelMazareb SalamSheikh-Ahmad MohammadFaber Dan Levy