ArticleOncogene2023
ASCL2 induces an immune excluded microenvironment by activating cancer-associated fibroblasts in microsatellite stable colorectal cancer.
Article in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 23 citations in OpenAlex.
- Gene regulation at the early human maternal-fetal interface.Nature reviews. Genetics · 2026Review
- Lactate as a Master Regulator of Immune Suppression: From Metabolic Waste to Epigenetic Checkpoint in Colorectal Cancer.International journal of molecular sciences · 2026Review
- Universal off-the-shelf TGF-Acta pharmaceutica Sinica. B · 2026Article
- Nanomaterials targeting cancer-associated fibroblasts to overcome stromal barriers in cancer immunotherapy.Journal of nanobiotechnology · 2026Review
- ASCL2 drives colorectal cancer metastasis through transcriptional activation of TDGF1.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- The Rayleigh Quotient and Contrastive Principal Component Analysis II.bioRxiv : the preprint server for biology · 2026Article
- Exploring phenotype-related single-cells through attention-enhanced representation learning.Genome medicine · 2026Article
- Traditional Chinese medicine as a potential barrier-oriented sensitization strategy for immune checkpoint blockade in microsatellite-stable colorectal cancer: from resistance mechanisms to translational validation.Frontiers in immunology · 2026Review
- Mechanisms of immune resistance in microsatellite-stable colorectal cancer.Frontiers in oncology · 2026Review
- FAP as a Clinical Biomarker: FAP+ CAFs Orchestrate an Immunosuppressive Stem Cell Niche via the COL1A1/2-CD44 Axis in Colon Cancer.Stem cells international · 2026Article
- Novel anti-tumor strategies: targeting the crosstalk between cancer stem cells and cancer-associated fibroblasts to resist drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2026Review
- ASCL2 contributes to clinical assessments of breast cancer and mediates tumor progression via the interaction with CLDN3.Scientific reports · 2025Article
- KLB as a potential prognostic biomarker and therapeutic target in colorectal cancer: insights from multi omics and single cell analyses.Discover oncology · 2025Article
- Gut Microbiota Reshapes the Tumor Microenvironment and Affects the Efficacy of Colorectal Cancer Immunotherapy.Cancer medicine · 2025Review
- Molecular and functional profiling unravels targetable vulnerabilities in colorectal cancer.Molecular oncology · 2025Article
- Signature Gene Mutations in Colorectal Cancer: Potential Neoantigens for Cancer Vaccines.International journal of molecular sciences · 2025Review
- Circulating IL6 is involved in the infiltration of M2 macrophages and CD8+ T cells.Scientific reports · 2025Article
- The emerging role of intestinal stem cells in ulcerative colitis.Frontiers in medicine · 2025Review
- Immune activation following PD-L1 inhibitor plus chemoradiotherapy in locally advanced rectal cancer: a retrospective, single-arm study.Frontiers in immunology · 2025Article
- GJA4 expressed on cancer associated fibroblasts (CAFs)-A 'promoter' of the mesenchymal phenotype.Translational oncology · 2024Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proficient mismatch repair or microsatellite stable (pMMR/MSS) colorectal cancers (CRCs) are vastly outnumbered by deficient mismatch repair or microsatellite instability-high (dMMR/MSI-H) tumors and lack a response to immune checkpoint inhibitors (ICIs). In this study, we reported two distinct expression patterns of ASCL2 in pMMR/MSS and dMMR/MSI-H CRCs. ASCL2 is overexpressed in pMMR/MSS CRCs and maintains a stemness phenotype, accompanied by a lower density of tumor-infiltrating lymphocytes (TILs) than those in dMMR/MSI CRCs. In addition, coadministration of anti-PD-L1 antibodies facilitated T cell infiltration and provoked strong antitumor immunity and tumor regression in the MC38/shASCL2 mouse CRC model. Furthermore, overexpression of ASCL2 was associated with increased TGFB levels, which stimulate local Cancer-associated fibroblasts (CAFs) activation, inducing an immune-excluded microenvironment. Consistently, mice with deletion of Ascl2 specifically in the intestine (Villin-Cre
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.