ReviewAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Mechanistic Foundations of KRAS-Driven Tumor Ecosystems: Integrating Crosstalk among Immune, Metabolic, Microbial, and Stromal Microenvironment.
Review in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed.
- Mapping Mutations and Signaling Network Interactions to Guide Precision Therapy in Gallbladder Cancer.Cancer reports (Hoboken, N.J.) · 2026Review
- Microbiota in pancreatic cancer: Roles in tumor initiation and progression (Review).Oncology letters · 2026Review
- KRASScience advances · 2026Article
- Current advances in immunotherapy for KRAS-Mutant pancreatic cancer.Clinical and experimental medicine · 2026Review
- DARS2 serves as an independent prognostic factor and participates in multiple biological processes in bladder urothelial carcinoma.Translational andrology and urology · 2026Article
- Pancreatic Cancer in the Holobiont and Therapeutic Targets: A Review.Journal of clinical medicine · 2026Review
- Systematic and precise interventions for KRAS-mutant cancers.Experimental hematology & oncology · 2026Review
- Key Considerations for TargetingDrug design, development and therapy · 2026Review
- Bracing for the storm: emerging resistance mechanisms to KRAS inhibitors in pancreatic cancer and strategies to overcome them.Cancer drug resistance (Alhambra, Calif.) · 2026Review
- From Barrier to Gateway: Nanomaterials Reshaping the Tumor Microenvironment for Therapy.International journal of nanomedicine · 2026Review
- Novel Evolutionarily Conserved Oncogene COA4 is Driven by KRAS Mutant and Promotes Cancer Metastasis Through Dual Mitochondrial Metabolism-Dependent and -Independent Mechanisms.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanistic Foundations of KRAS-Driven Tumor Ecosystems: Integrating Crosstalk among Immune, Metabolic, Microbial, and Stromal Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- RETRACTED: The Impact ofInternational journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Kirsten rat sarcoma viral oncogene homolog (KRAS) is the most frequently mutated member of the RAS family of small GTPases (RAS). It affects about one-fifth of cancer cases. The tumor microenvironment (TME) is a multifaceted network of immune cells, metabolites, microbiota, stromal components, and extracellular matrix. It creates a dynamic ecosystem that supports malignant initiation, progression, and therapy resistance through bidirectional crosstalk with tumor cells. Emerging evidence reveals distinct TME landscapes shaped by wild-type versus oncogenic KRAS variants. Additionally, TME rewiring occurs during KRAS-targeted therapies. Deciphering these KRAS-dependent TME architectures and their therapeutic vulnerabilities represents a critical frontier for precision oncology. This review synthesizes key milestones and persistent challenges in KRAS inhibitor development. And it systematically evaluates how KRAS mutations orchestrated immunosuppressive niches, metabolic symbiosis, stromal remodeling, and microbiome dysbiosis, supported by mechanistic insights from preclinical and clinical studies. It further explores therapeutic opportunities arising from targeting TME interactions, including rational combinations of KRAS inhibitors with immune checkpoint blockade, metabolic agents, or microbiota-modulating strategies.
Indexed as
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What OpenQuestion holds
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.