ArticleMedComm2020
Enhancing anticancer activity of checkpoint immunotherapy by targeting RAS.
Article in MedComm, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Current status of KRAS G12C inhibitors in NSCLC and the potential for combination with anti-PD-(L)1 therapy: a systematic review.Frontiers in immunology · 2025Pooled it
- Domvanalimab plus zimberelimab in unresectable and immunotherapy refractory biliary tract cancers: a phase 2 trial.Nature communications · 2026Trial
- Plasma-Activated Medium Suppresses Lung Cancer H1299 Cell Migration through the MAPK Pathway.Cell biochemistry and biophysics · 2026Article
- Mutation in CDC42 Gene Set as a Response Biomarker for Immune Checkpoint Inhibitor Therapy.Cancer medicine · 2025Article
- An Explainable Graph Neural Framework to Identify Cancer-Associated Intratumoral Microbial Communities.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- From structural design to delivery: mRNA therapeutics for cancer immunotherapy.Exploration (Beijing, China) · 2024Review
- TG468: a text graph convolutional network for predicting clinical response to immune checkpoint inhibitor therapy.Briefings in bioinformatics · 2024Article
- PTPLAD1 Regulates PHB-Raf Interaction to Orchestrate Epithelial-Mesenchymal and Mitofusion-Fission Transitions in Colorectal Cancer.International journal of biological sciences · 2024Article
- HPIP is an essential scaffolding protein running through the EGFR-RAS-ERK pathway and drives tumorigenesis.Science advances · 2023Article
- Review
- Cancer immune evasion through KRAS and PD-L1 and potential therapeutic interventions.Cell communication and signaling : CCS · 2023Review
- TargetingGastroenterology report · 2023Review
- Targeting the undruggable oncogenic KRAS: the dawn of hope.JCI insight · 2022Review
- Role of the Epigenetic Modifier JMJD6 in Tumor Development and Regulation of Immune Response.Frontiers in immunology · 2022Review
- Novel Dihydrooxadiazinones as PDE3 Inhibitors for Treating Cancer.ACS medicinal chemistry letters · 2021Article
- Near Complete Pathologic Response to PD-1 Inhibitor and Radiotherapy in a Patient with Locally Advanced Pancreatic Ductal Adenocarcinoma.OncoTargets and therapy · 2021Article
- Identification of Key Pathways and Genes Related to Immunotherapy Resistance of LUAD Based on WGCNA Analysis.Frontiers in oncology · 2021Article
- Article
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 at 4 institutions in 1 country.
Funding
Abstract
Approximately 30% of human cancers harbor a gain-in-function mutation in the RAS gene, resulting in constitutive activation of the RAS protein to stimulate downstream signaling, including the RAS-mitogen activated protein kinase pathway that drives cancer cells to proliferate and metastasize. RAS-driven oncogenesis also promotes immune evasion by increasing the expression of programmed cell death ligand-1, reducing the expression of major histocompatibility complex molecules that present antigens to T-lymphocytes and altering the expression of cytokines that promote the differentiation and accumulation of immune suppressive cell types such as myeloid-derived suppressor cells, regulatory T-cells, and cancer-associated fibroblasts. Together, these changes lead to an immune suppressive tumor microenvironment that impedes T-cell activation and infiltration and promotes the outgrowth and metastasis of tumor cells. As a result, despite the growing success of checkpoint immunotherapy, many patients with RAS-driven tumors experience resistance to therapy and poor clinical outcomes. Therefore, RAS inhibitors in development have the potential to weaken cancer cell immune evasion and enhance the antitumor immune response to improve survival of patients with RAS-driven cancers. This review highlights the potential of RAS inhibitors to enhance or broaden the anti-cancer activity of currently available checkpoint immunotherapy.
Indexed as
Identifiers
What Socratic 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 Socratic graph.