ReviewTrends in cancer2017
KRAS Alleles: The Devil Is in the Detail.
Review in Trends in cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 233 papers, 2 of them syntheses 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
233 citing papers in PubMed, 2 syntheses or guidelines pooled it, 359 citations in OpenAlex.
- KRAS/BRAF mutations in brain arteriovenous malformations: A systematic review and meta-analysis.Interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences · 2021Pooled it
- Genetic Profile of Adenomatoid Odontogenic Tumor and Ameloblastoma. A Systematic Review.Frontiers in oral health · 2021Pooled it
- Hyper-mutational processes provide a head-start for weak cancer drivers: Explaining atypical KRAS variants.PLoS computational biology · 2026Article
- ARNTL2 promotes metastatic phenotypes through SERPINE1 transcription in KRAS G12D pancreatic cancer.iScience · 2026Article
- The Role of KRAS in Non-Small Cell Lung Cancer: From Molecular Background to Precision Medicine.International journal of molecular sciences · 2026Review
- Changes in the transcriptome and synthetic lethal dependencies followingProceedings of the National Academy of Sciences of the United States of America · 2026Article
- KRAS Inhibitor-Induced Cancer Cell Death Enhances Sensitivity to Immune-Mediated Bystander Killing of Drug-Resistant Subclones.Cancer research · 2026Article
- Molecular dynamics driving phenotypic divergence among KRAS mutants in pancreatic tumorigenesis.Developmental cell · 2026Article
- Targeting Oncogenic KRAS Using Peptide Nucleic Acid Oligomers Attached to Cell-Penetrating Peptides.International journal of molecular sciences · 2026Article
- A ternary association of KRas, EphA2, and integrins controls PDAC cell behavior.The Journal of biological chemistry · 2026Article
- RAS-PI3Kα signaling regulates KrasG12D-induced lymphangiogenesis in complex lymphatic anomalies.Disease models & mechanisms · 2026Article
- Carbohydrates metabolic reprogramming and tumor microenvironment in pancreatic cancer: targeting pathways.Molecular biology reports · 2026Review
- Concurrent Stereotactic Body Radiation Therapy and KRAS Inhibition Synergistically Improve Pre-clinical Pancreatic Cancer Treatment.bioRxiv : the preprint server for biology · 2026Article
- U2af1Leukemia · 2026Article
- Review
- Crosstalk between KRAS and miRNAs in pancreatic cancer: Opportunities for its diagnosis, prognosis and therapeutic intervention (Review).International journal of oncology · 2026Review
- The impact of K-Ras Gly12 mutants on homeostasis and tumorigenesis in the colonic epithelium.Oncogene · 2026Article
- Profiling KRAS mutations in whole blood by error-corrected maximum depth sequencing.NPJ precision oncology · 2026Article
- Association between 8-OHdG Levels and Eosinophil Counts in Chronic Rhinosinusitis with Nasal Polyps.International archives of otorhinolaryngology · 2026Article
- Review
173 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 is the most frequently mutated oncogene in cancer and KRAS mutation is commonly associated with poor prognosis and resistance to therapy. Since the KRAS oncoprotein is, as yet, not directly druggable, efforts to target KRAS mutant cancers focus on identifying vulnerabilities in downstream signaling pathways or in stress response pathways that are permissive for strong oncogenic signaling. One aspect of KRAS biology that is not well appreciated is the potential biological differences between the many distinct KRAS activating mutations. This review draws upon insights from both clinical and experimental studies to explore similarities and differences among KRAS alleles. Historical and emerging evidence supports the notion that the specific biology related to each allele might be exploitable for allele-specific therapy.
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.