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PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 200 | Additionally, we incorporated comorbidity-related modules derived from hdWGCNA analysis of core cell types. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 201 | Based on these inputs, we constructed an integrated evidence discovery table where each independent line of evidence was assigned an equal weight. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 202 | By calculating cumulative scores for cross-method integration and ranking, genes with a total score greater than 6 were prioritized as Tier 1 candidate comorbidity genes (Fig. 5A, Supplementary Table 15).Fig. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 203 | 5Identification and multi-dimensional validation of core candidate comorbidity genes. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 204 | A Integrated evidence scores across multiple analytical frameworks and cumulative prioritization scores for Tier 1 genes. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 205 | B Single-cell transcriptomic profiles showcasing differential expression of candidate genes in UC and CRC across diverse cell populations. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 206 | C–G Exon-level expression heatmaps and alternative splicing architectures for ARPC5 (C), PTGER4 (D), S100A10 (E), CIB1 (F), and PREX1 (G), illustrating tissue-specific regulatory patterns Identification and multi-dimensional validation of core candidate comorbidity genes. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 207 | A Integrated evidence scores across multiple analytical frameworks and cumulative prioritization scores for Tier 1 genes. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 208 | B Single-cell transcriptomic profiles showcasing differential expression of candidate genes in UC and CRC across diverse cell populations. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 209 | C–G Exon-level expression heatmaps and alternative splicing architectures for ARPC5 (C), PTGER4 (D), S100A10 (E), CIB1 (F), and PREX1 (G), illustrating tissue-specific regulatory patterns Among Tier 1 genes, ARPC5 regulates isoform-specific actin remodeling to determine cell motility . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 210 | In malignancy, ARPC5 is regulated by YAP to maintain focal adhesions and drive invasion , or binds TAGLN2 to activate the MEK/ERK pathway for metastasis . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 211 | Immunologically, ARPC5 maintains intestinal barrier integrity via macrophage-mediated bacterial clearance , whereas its deficiency disrupts IL-6 signaling and influences CRC progression . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 212 | Regarding intestinal homeostasis, PTGER4 mediates PGE2-induced CXCL1 secretion by mature macrophages via the MAPK pathway to promote epithelial regeneration , or activates epithelial HDAC4/5/7 and SPINK4 to support goblet cell maturation and barrier reconstruction . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 213 | CIB1 acts as a “myristoylation switch” that translocates SPHK1 to the plasma membrane, promoting S1P production and activating oncogenic signaling to drive CRC transformation . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 214 | Clinically, high CIB1 expression in CRC correlates with poor survival and tumor aggressiveness , while its inhibition may trigger NLRP3-mediated pyroptosis via sphingosine accumulation . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 215 | PREX1, a Rac-specific exchange factor, mediates cytoskeletal reorganization via Rac1 activation. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 216 | Its upregulation promotes invasion in squamous cell carcinoma and forms a feedback loop with TGFβ1 to drive metastasis in gastric cancer . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 217 | Additionally, PREX1 maintains T-cell homeostasis through STAT5 nuclear translocation and regulates early endodermal migration . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 218 | S100A10 regulates inflammation and tumor progression by inhibiting macrophage overactivation via TLR signaling and facilitating plasminogen-dependent ECM degradation . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 219 | While protecting the mucosal barrier in UC by inhibiting neutrophil-derived IL-6 , S100A10 promotes CRC invasion through plasminogen-dependent matrix degradation . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 220 | Finally, single-cell differential expression heatmaps show significant alterations of these five genes in UC or CRC (Fig. 5B). | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 221 | Exon-level analysis reveals distinct exon skipping and alternative splicing patterns in intestinal tissues compared to others, suggesting that alternative splicing contributes to tissue-specific functional regulation (Fig. 5C–G). | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 222 | Research indicates that genetic risk for ulcerative colitis (UC) and colorectal cancer (CRC) exhibits anatomical site-specificity . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 223 | Risk signals are significantly enriched in the terminal ileum and transverse colon but less so in the sigmoid colon, seemingly contradicting the typical "recto-sigmoid" clinical predominance. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 224 | Through gsMap analysis, UC/CRC genetic signals were localized to the E16.5 mouse embryonic gut. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 225 | This suggests that spatiotemporal programming during development—where coordinated axial patterning establishes regional identities—may play a role in adult disease susceptibility [65, 66]. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 226 | Previous studies found that colonic injury reactivates embryonic-specific gene profiles and cell populations . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 227 | Furthermore, specific cell types in IBD, such as S4 fibroblasts, exhibit fetal-like gene expressions enriched with disease-related genes like CCL19 and CXCL13 . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 228 | Consequently, we propose the “Genetic Programming-Microenvironment Triggering” spatiotemporal model . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 229 | This hypothesis posits that UC/CRC variants shape regional epigenetic landscapes and cellular programs during embryogenesis, creating site-specific vulnerabilities. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 230 | In adulthood, “second hits” such as dysbiosis, viral infection, or high-fat diets are more likely to trigger pathological inflammatory responses in these predisposed regions. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 231 | Notably, since this model is based on E16.5 mouse data, caution is required when extrapolating these findings to human pathology, and further validation through longitudinal studies is necessary. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 232 | Our integrated single-cell analysis reveals that genetic susceptibility to UC and CRC exhibits distinct evolutionary characteristics at the cellular level. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 233 | Consistent results from ECLIPSER, CELLECT, and scDRS shift the research focus from the traditional “epithelium-centric” view to an “immune-progenitor” interaction model. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 234 | Specifically, CD4 + T cells serve as the core genetic susceptibility subset in UC, establishing the immunological foundation for chronic inflammation . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 235 | In contrast, progenitor cells carry the primary weight of genetic risk during CRC progression, acting as the cellular origin for malignant transformation . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 236 | Analysis of hdWGCNA modules shows that CD4 + T cells undergo significant immunometabolic polarization in the UC environment. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 237 | The M4 module drives persistent mucosal damage through the Th17/IL-17 axis, serving as a primary driver of UC pathogenesis . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 238 | Meanwhile, the co-occurrence of enhanced glycolysis and PD-1 signaling in the M1 module suggests that T cells undergo tumor-like metabolic reprogramming (the Warburg effect) and exhaustion driven by chronic activation within the hypoxic inflammatory microenvironment . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 239 | Additionally, the M5 module reveals that endoplasmic reticulum stress (UPR) and p53 surveillance mechanisms are activated, reflecting intrinsic efforts by CD4 + T cells to maintain homeostasis under long-term inflammatory stress . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 240 | As the pathology progresses toward CRC, the center of genetic drivers shifts to progenitor cells. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 241 | The M10 module in CRC progenitors highlights genomic instability associated with p53 failure and MAPK signaling , likely in response to the inflammatory stress accumulated during the UC stage. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 242 | Subsequently, these cells acquire invasive phenotypes through epithelial-mesenchymal transition (EMT) and extracellular matrix reorganization mediated by the M1 module . | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 243 | Together with TGF-β and pro-angiogenic signaling in the M3 module , this completes the pathological transition from tissue destruction to the reconstruction of the tumor microenvironment. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 244 | Through the implementation of a multi-scale evidence weighting system—incorporating eCAVIAR, fastenloc, hdWGCNA, open4gene, and scDRS—this study has identified ARPC5, PTGER4, CIB1, PREX1, and S100A10 as the primary “first-tier” core comorbid genes that potentially mediate the pathological evolution from ulcerative coli... | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 245 | Viewed through the broad continuum of disease progression, intestinal barrier instability and regenerative stress appear to constitute the initial triggers of this comorbidity. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 246 | Within the specific microenvironment of UC, PTGER4-mediated PGE2 signaling drives crypt epithelial regeneration and coordinately regulates goblet cell maturation to reconstruct the mucosal barrier via the MAPK-CXCL1 axis; meanwhile, ARPC5, a central component of actin remodeling, maintains mucosal homeostasis by ensuri... | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 247 | However, the persistent interplay between chronic inflammatory damage and underlying genetic risk appears to induce a “functional switch” in key signaling nodes. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 248 | Specifically, CIB1 functions as a “myristoylation switch” regulating sphingosine metabolism: its functional inhibition during the UC stage tends to exacerbate inflammatory injury by inducing NLRP3-mediated pyroptosis, whereas its risk-driven overexpression during malignant transformation promotes the translocation of S... | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 249 | This polarization of survival signals further catalyzes the acquisition of cellular motility and the malignant reorganization of tissue architecture; PREX1 triggers cytoskeletal remodeling by activating Rac1 GTPase and establishes a metastatic feedback loop with TGFβ1, while S100A10 transitions from its role in protect... | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 250 | When integrated with differential expression analysis from single-cell transcriptomic atlases, this dynamic evolutionary landscape, constructed through the coordinated synergy of multiple genes, appears to partially delineate the shared genetic risk landscape between UC and CRC. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 251 | Despite partial progress achieved by this study, several limitations remain. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 252 | First, tissue source limitations: the eQTL/sQTL data used in this study primarily derive from post-mortem human tissues and do not reflect dynamic regulatory changes under disease states. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 253 | Future studies urgently need to obtain QTL data from different disease stages of UC (active phase, remission phase, dysplasia phase) and CRC tumor tissues. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 254 | Second, racial differences have not been fully explored: existing GWAS data are predominantly from European ancestry populations. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 255 | Future studies should deeply explore whether genetic risk operates through different cell types or pathway weights across different ethnic groups. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 256 | In addition, the relatively small sample size of the UC GWAS might limit its statistical power to some extent. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 257 | Furthermore, as the gsMap analysis relied on E16.5 mouse embryonic data, caution is required when extrapolating these developmental associations to broader human disease phenotypes. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 258 | Finally, the shared genetic loci identified in this study represent overlap in genetic susceptibility between UC and CRC rather than direct causal pathways of inflammation-to-cancer transformation. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 259 | These shared loci may reflect common biological vulnerabilities such as chronic inflammation, immune dysregulation, DNA damage repair defects, and metabolic reprogramming, which may independently lead to UC or CRC, or may increase cancer risk in UC patients. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 260 | Future studies should further validate the causal roles of these candidate genes in UC-associated CRC cohorts and conduct functional experiments to clarify the specific mechanisms of these genes in inflammation-to-cancer transformation. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 261 | In summary, this study systematically dissects the shared genetic architecture and pathogenic evolution of UC and CRC by integrating multi-scale evidence. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 262 | We propose the “genetic programming-microenvironment triggering” hypothesis, suggesting that spatiotemporal programs during embryonic development preset intestinal segmental susceptibility. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 263 | These predisposed segments may become more vulnerable to “second hits” in adulthood, though caution is warranted when extrapolating mouse data to human pathology. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 264 | Our analysis highlights a shift in genetic risk from CD4 + T cell-mediated immunometabolic dysregulation in UC to progenitor-driven malignant transformation in CRC. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 265 | Key molecular transitions involve moving from Th17/IL-17-mediated inflammation and metabolic stress toward p53-related genomic instability, EMT, and vascular remodeling. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 266 | We prioritized Tier 1 candidate genes—ARPC5, PTGER4, CIB1, PREX1, and S100A10—which likely coordinate the pathological transition from mucosal repair failure and immune imbalance to a pro-tumorigenic microenvironment. | FullText |
PMC13160972 | Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis | 267 | These findings provide a molecular framework for identifying high-risk UC patients and offer potential therapeutic targets to intercept the inflammation-to-cancer transition. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 0 | Lung adenocarcinoma (LUAD) remains a leading cause of cancer-related mortality, with therapeutic resistance largely driven by unresolved malignant epithelial heterogeneity within the tumor microenvironment. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 1 | However, the epithelial cell states that underlie poor prognosis and immunotherapy resistance remain incompletely defined. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 2 | We performed an integrative multi-omics analysis combining large-scale single-cell RNA sequencing, spatial transcriptomics, and bulk transcriptomic data with clinical outcomes. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 3 | The Scissor algorithm was applied to identify prognosis-associated epithelial cell states, followed by construction of a risk score model. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 4 | External validation was conducted across multiple independent cohorts, including immunotherapy-treated datasets. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 5 | We identified a prognostically relevant Scissor⁺ malignant epithelial cell state associated with adverse survival. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 6 | This state was characterized by activation of MYC, epithelial–mesenchymal transition, hypoxia, and NF-κB signaling, and was linked to an immunosuppressive tumor microenvironment. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 7 | Based on this state, we developed a Scissor⁺ epithelial cell–derived risk score (SERS), which demonstrated robust and reproducible prognostic performance across multiple cohorts and was associated with reduced responsiveness to immunotherapy. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 8 | Further analyses identified SLC2A1 as a key gene associated with this malignant epithelial state. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 9 | Functional experiments confirmed that SLC2A1 promotes tumor cell proliferation, migration, and invasion. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 10 | In addition, cell–cell communication analysis suggested a potential SLC2A1–CAF–collagen signaling axis linking epithelial cell states with stromal interactions. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 11 | This study defines a clinically relevant malignant epithelial cell state in LUAD and establishes a framework linking cell states, molecular features, and microenvironmental interactions. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 12 | These findings provide potential biomarkers for prognostic stratification and immunotherapy response prediction in LUAD.Lung cancer remains the leading cause of cancer-related death worldwide (Siegel et al. 2025). | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 13 | Lung adenocarcinoma (LUAD), the most common histological subtype, is characterized by pronounced heterogeneity and complex molecular features (Shen et al. 2025; Zhang et al. 2025a, b). | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 14 | Although systemic treatment for LUAD has expanded from conventional chemotherapy to include targeted therapy and immunotherapy, overall survival outcomes have improved only modestly(Herbst et al. 2018; Wang et al. 2025a, b). | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 15 | A major reason for the limited clinical benefit lies in tumor heterogeneity: chemotherapy-related toxicity, the low prevalence of actionable driver mutations, and the unpredictable response to immunotherapy all restrict the effectiveness of current treatment strategies (Bortolot et al. 2025; Reck et al. 2025; Zhao et a... | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 16 | Therefore, identifying molecular markers that reflect key tumor cell states and predict therapeutic response is critical for advancing precision treatment in LUAD. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 17 | The tumor immune microenvironment (TIME) plays a central role in LUAD progression, immune evasion, and treatment response (Xu et al. 2022). | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 18 | Dynamic interactions between tumor cells, immune cells, fibroblasts, and vascular-associated cells collectively shape the tumor ecosystem and its immunoregulatory landscape(Sun et al. 2025). | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 19 | Increasing evidence indicates that the TIME is not static but undergoes continuous remodeling during tumor evolution (Keenan et al. 2025). | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 20 | For example, the accumulation of immunosuppressive macrophages, regulatory T cells, and cancer-associated fibroblasts (CAFs) is frequently associated with immune escape and poor clinical outcomes(Huang et al. 2025). | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 21 | However, which specific cellular populations drive malignant progression in LUAD and influence patient prognosis through microenvironmental interactions remains incompletely understood. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 22 | The development of single-cell RNA sequencing (scRNA-seq) has enabled us to re-understand the heterogeneity of LUAD tumor tissue at the cellular level (Boxer et al. 2025). | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 23 | In particular, within tumor epithelial cells, different malignant states often correspond to distinct potentials for progression and interactions with the microenvironment(Andreatta et al. 2025). | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 24 | By leveraging scRNA-seq, not only can we identify key cell subpopulations associated with tumor progression, but we can also further dissect their immune regulatory features and cell communication networks, providing new biological foundations for prognostic assessment and treatment stratification (Tirosh and Suva 2024... | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 25 | Using the Scissor algorithm to integrate single-cell transcriptomics with clinical survival data, we have been able to pinpoint epithelial cell states directly linked to poor prognosis in LUAD. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 26 | However, despite increasing recognition of epithelial heterogeneity, a key gap remains: the malignant epithelial cell states that directly drive poor prognosis, their molecular regulators, and their relationship with immunotherapy response have not been systematically defined. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 27 | In particular, how these cell states can be translated into clinically applicable biomarkers remains unclear. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 28 | Based on this rationale, we integrated large-scale single-cell transcriptomic data with clinical and spatial datasets to systematically characterize malignant epithelial heterogeneity in LUAD. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 29 | We identified a prognostically relevant epithelial cell state and developed a corresponding risk score model (SERS), which was validated across independent cohorts and immunotherapy-treated samples. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 30 | Furthermore, we identified SLC2A1 as a key regulator of this malignant state and explored its functional and microenvironmental roles. | FullText |
PMC13219086 | A clinically relevant SLC2A1-associated malignant epithelial cell state predicts prognosis and immunotherapy response in lung adenocarcinoma | 31 | Together, this study defines a clinically relevant malignant epithelial cell state in LUAD and establishes a framework linking cell states, molecular drivers, and microenvironmental interactions, providing new insights into tumor progression and precision therapy. | FullText |
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