ArticleBMC genomics2020
Comparison of the molecular and cellular phenotypes of common mouse syngeneic models with human tumors.
Article in BMC genomics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.
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Who cites it
115 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.
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- Pulsed photobiomodulation reprograms the tumor immune microenvironment to restore local T cell-mediated antitumor immunity.iScience · 2026Article
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- Docetaxel-Induced Immune Activation Shows Antitumor Synergy With the Tumor-Targeted CD40 Agonist KK2269.Cancer science · 2026Article
- Organ-Specific Migration License (OSML) theory: a novel paradigm for spatiotemporal regulation and intervention of cross-organ immune cell migration in tumor immune responses.Cell communication and signaling : CCS · 2026Review
- Vaccinia virus armed with IL-21 can cure murine colorectal cancer liver metastases via intravenous administration.Journal for immunotherapy of cancer · 2026Article
- Recombinant CALR polarizes and activates macrophages in tumors.Molecular therapy. Oncology · 2026Article
- The deubiquitinase USP17 regulates the expression and activity of the oncogenic driver β-catenin in colorectal cancer.Oncogene · 2026Article
- Priming versus propagating: distinct immune effects of alpha- versus beta-particle emitting radiopharmaceuticals when combined with immune checkpoint inhibition in mice.Nature communications · 2026Article
- Cyclin-dependent kinase 4 and 6 inhibitors and the breast cancer immune ecosystem: immune remodeling, resistance, and therapeutic reprogramming.Frontiers in immunology · 2026Review
- Modeling pediatric brain tumors with human stem cells.Frontiers in cellular neuroscience · 2026Review
- Targeting LRBA triggers CTLA4 degradation and antitumor immunity for cancer immunotherapy.Nature communications · 2025Article
- Cancer cells accelerate exhaustion of persistently activated mouse CD4Oncoimmunology · 2025Article
- Enhancement of melanoma aggressiveness via p38-MAPK, HIF-1α pathways, and metabolic reprogramming induced by Candida albicans.Scientific reports · 2025Article
55 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe clinical success of immune checkpoint inhibitors demonstrates that reactivation of the human immune system delivers durable responses for some patients and represents an exciting approach for cancer treatment. An important class of preclinical in vivo models for immuno-oncology is immunocompetent mice bearing mouse syngeneic tumors. To facilitate translation of preclinical studies into human, we characterized the genomic, transcriptomic, and protein expression of a panel of ten commonly used mouse tumor cell lines grown in vitro culture as well as in vivo tumors.
resultsOur studies identified a number of genetic and cellular phenotypic differences that distinguish commonly used mouse syngeneic models in our study from human cancers. Only a fraction of the somatic single nucleotide variants (SNVs) in these common mouse cell lines directly match SNVs in human actionable cancer genes. Some models derived from epithelial tumors have a more mesenchymal phenotype with relatively low T-lymphocyte infiltration compared to the corresponding human cancers. CT26, a colon tumor model, had the highest immunogenicity and was the model most responsive to CTLA4 inhibitor treatment, by contrast to the relatively low immunogenicity and response rate to checkpoint inhibitor therapies in human colon cancers.
conclusionsThe relative immunogenicity of these ten syngeneic tumors does not resemble typical human tumors derived from the same tissue of origin. By characterizing the mouse syngeneic models and comparing with their human tumor counterparts, this study contributes to a framework that may help investigators select the model most relevant to study a particular immune-oncology mechanism, and may rationalize some of the challenges associated with translating preclinical findings to clinical studies.
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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.