ReviewClinical cancer research : an official journal of the American Association for Cancer Research2015
KRAS as a Therapeutic Target.
Review in Clinical cancer research : an official journal of the American Association for Cancer Research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02704156 (Stereotactic Body Radiation Therapy Plus Pembrolizumab and Trametinib vs. Stereotactic Body Radiation Therapy Plus Gemcitabine for Locally Recurrent Pancreatic Cancer After Surgical Resection), which is not on this map. Cited by 192 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.
Stereotactic Body Radiation Therapy Plus Pembrolizumab and Trametinib vs. Stereotactic Body Radiation Therapy Plus Gemcitabine for Locally Recurrent Pancreatic Cancer After Surgical Resection: an Open-label, Randomized, Controlled, Phase 2 Trial
Who cites it
192 citing papers in PubMed, 325 citations in OpenAlex.
- Dynamism and evolvability in nucleic acid enzymes.Nature communications · 2026Article
- Nintedanib inhibits the VEGFR-ERK signaling pathway in human KRAS-mutated cancer cells.Cell death & disease · 2026Article
- Article
- Phage Display Driven Identification and Computational Mapping of Macrocyclic Peptides Targeting RhoA G17V.Biochemistry · 2026Article
- Overcoming Chemotherapy Resistance in Triple-Negative Breast Cancer with Nanocarrier-Delivered siRNA Therapeutics.Journal of clinical medicine · 2026Review
- Exploring the GDP binding to KRasEuropean biophysics journal : EBJ · 2026Article
- Allele-specific knockdown by an engineered DNAzyme capable of RNase H1 evasion.Nucleic acids research · 2026Article
- Interaction between microRNA and KRAS in Glioblastoma.Current medicinal chemistry · 2026Review
- Colorectal Adenocarcinoma: A Comprehensive Narrative Review of Molecular Pathogenesis, Metabolic Vulnerabilities, and Therapeutic Potential of Sorghum Polyphenols.Analytical cellular pathology (Amsterdam) · 2026Review
- First-line treatments for KRAS-mutant non-small cell lung cancer: current state and future perspectives.Cancer biology & therapy · 2025Review
- Broad-Spectrum RAS Inhibition in Pancreatic Ductal Adenocarcinoma: Mechanistic Advances and Therapeutic Promise.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Genomic alteration and clinical significance of circulating tumor DNA in patients with advanced urothelial cancer: SCRUM-Japan monstar screen project.NPJ precision oncology · 2025Article
- Allostery in Disease: Anticancer Drugs, Pockets, and the Tumor Heterogeneity Challenge.Journal of molecular biology · 2025Review
- Article
- KRAS G12C Inhibition in Solid Tumors: Biological Breakthroughs, Clinical Evidence, and Open Challenges.Cancers · 2025Review
- Review
- Oncogenic RAS induces a distinctive form of non-canonical autophagy mediated by the P38-ULK1-PI4KB axis.Cell research · 2025Article
- Recent advances in therapeutic strategies of Erdheim-Chester disease.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- ADT-1004: a first-in-class, oral pan-RAS inhibitor with robust antitumor activity in preclinical models of pancreatic ductal adenocarcinoma.Molecular cancer · 2025Article
- Deciphering allosteric mechanisms in KRAS activation: insights from GTP-induced conformational dynamics and interaction network reorganization.RSC advances · 2025Article
132 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
KRAS proteins play a major role in human cancer, but have not yielded to therapeutic attack. New technologies in drug discovery and insights into signaling pathways that KRAS controls have promoted renewed efforts to develop therapies through direct targeting of KRAS itself, new ways of blocking KRAS processing, or by identifying targets that KRAS cancers depend on for survival. Although drugs that block the well-established downstream pathways, RAF-MAPK and PI3K, are being tested in the clinic, new efforts are under way to exploit previously unrecognized vulnerabilities, such as altered metabolic networks, or novel pathways identified through synthetic lethal screens. Furthermore, new ways of suppressing KRAS gene expression and of harnessing the immune system offer further hope that new ways of treating KRAS are finally coming into view. These issues are discussed in this edition of CCR Focus.
Indexed as
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.