ReviewCancer research2017
The RAS-Effector Interaction as a Drug Target.
Review in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 79 citations in OpenAlex.
- KRAS signaling networks, mutational heterogeneity, and emerging therapeutic strategies for cancer treatment.Biomarker research · 2026Review
- Induced opening of conformational switch I in GTP-bound Ran GTPase.Protein science : a publication of the Protein Society · 2026Article
- RAS signaling and remodeling of the immune microenvironment in pancreatic ductal adenocarcinoma: implications of emerging RAS-targeted therapy.Frontiers in cell and developmental biology · 2026Review
- Integrating Ultra-Coarse-Grained Protein Models into Accessible Workflows for Multiscale Molecular Dynamics.ACS omega · 2025Article
- KRAS mutation-driven enhanced macropinocytosis: using albumin as a trojan horse for delivering nanomedicine.Nanomedicine (London, England) · 2025Review
- Evolution of computational techniques against various KRAS mutants in search for therapeutic drugs: a review article.Cancer chemotherapy and pharmacology · 2025Review
- Tumor biomarkers for diagnosis, prognosis and targeted therapy.Signal transduction and targeted therapy · 2024Review
- Monoallelic KRAS (G13C) mutation triggers dysregulated expansion in induced pluripotent stem cell-derived hematopoietic progenitor cells.Stem cell research & therapy · 2024Article
- Regulation of Ras p21 and RalA GTPases activity by quinine in mammary epithelial cells.Molecular and cellular biochemistry · 2024Article
- Structural modifications and kinetic effects ofFrontiers in molecular biosciences · 2024Article
- Role of EGFR and FASN in breast cancer progression.Journal of cell communication and signaling · 2023Review
- Physiological roles of chloride ions in bodily and cellular functions.The journal of physiological sciences : JPS · 2023Review
- A MicroRNA-Based Method for High-Viremia Detection-A New Approach on a Romanian Lot of Chronically Infected Patients with Hepatitis B Virus.Diagnostics (Basel, Switzerland) · 2023Article
- Peptidomimetics designed to bind to RAS effector domain are promising cancer therapeutic compounds.Scientific reports · 2022Article
- Stem Cell Models for Cancer Therapy.International journal of molecular sciences · 2022Review
- Small-Molecule RAS Inhibitors as Anticancer Agents: Discovery, Development, and Mechanistic Studies.International journal of molecular sciences · 2022Review
- Reconstruction and analysis of a large-scale binary Ras-effector signaling network.Cell communication and signaling : CCS · 2022Article
- Targeting KRAS mutant lung cancer: light at the end of the tunnel.Molecular oncology · 2022Review
- Review
- Machine learning-driven multiscale modeling reveals lipid-dependent dynamics of RAS signaling proteins.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
About a third of all human cancers harbor mutations in one of the K-, N-, or HRAS genes that encode an abnormal RAS protein locked in a constitutively activated state to drive malignant transformation and tumor growth. Despite more than three decades of intensive research aimed at the discovery of RAS-directed therapeutics, there are no FDA-approved drugs that are broadly effective against RAS-driven cancers. Although RAS proteins are often said to be "undruggable," there is mounting evidence suggesting it may be feasible to develop direct inhibitors of RAS proteins. Here, we review this evidence with a focus on compounds capable of inhibiting the interaction of RAS proteins with their effectors that transduce the signals of RAS and that drive and sustain malignant transformation and tumor growth. These reports of direct-acting RAS inhibitors provide valuable insight for further discovery and development of clinical candidates for RAS-driven cancers involving mutations in RAS genes or otherwise activated RAS proteins. Cancer Res; 77(2); 221-6. ©2017 AACR.
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Identifiers
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.