ReviewCancers2023
The Therapeutic Landscape for
Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 33 citations in OpenAlex.
- KRAS in Colorectal Cancer: Tumorigenesis, Surgical Implications and Evolving Treatment Target.Current oncology (Toronto, Ont.) · 2026Review
- KIAA1429 Stabilizes FAM84B mRNA to Enhance Colorectal Cancer Tumorigenesis via Wnt/β-Catenin Pathway.Biochemical genetics · 2026Article
- α-ketoglutarate accumulation orchestrates immunosuppressive metabolic remodeling to drive cetuximab resistance in metastatic colorectal cancer.Cell death & disease · 2026Article
- LNA GapmeR silencing of KRAS G12V impairs growth and function in SW480 cells.Molecular and cellular biochemistry · 2026Article
- KRAS mutation subtypes refine prognostic stratification in colorectal cancer: a retrospective cohort study.Journal of gastrointestinal oncology · 2026Article
- Cancer-associated fibroblasts drive metabolic heterogeneity in colorectal cancer cells: predictions from metabolic modeling.NPJ systems biology and applications · 2026Article
- Exploring the GDP binding to KRasEuropean biophysics journal : EBJ · 2026Article
- Disrupting the KRAS-SOS1 protein-protein interaction: mechanistic rationale for pan-KRAS pathway suppression and combination therapy.Frontiers in chemistry · 2026Review
- Targeting KRAS mutations: orchestrating cancer evolution and therapeutic challenges.Signal transduction and targeted therapy · 2025Review
- Targeting KRAS in colorectal cancer (Review).Molecular and clinical oncology · 2025Review
- Poor-prognosis young-onset colorectal cancer is defined by the mesenchymal subtype and can be predicted by integrating molecular and histopathological characteristics.ESMO gastrointestinal oncology · 2025Article
- Adagrasib in the treatment of colorectal cancer.Future oncology (London, England) · 2025Review
- Colorectal Cancer: Therapeutic Approaches and Their Complications.Biomedicines · 2025Review
- EGFR controls transcriptional and metabolic rewiring in KRASEMBO molecular medicine · 2025Article
- Systemic Therapy for Metastatic Colon Cancer: New Frontiers.Clinics in colon and rectal surgery · 2025Review
- Anaplastic carcinoma of the ovary: A single-institution experience and molecular analysis.Gynecologic oncology · 2025Article
- Real-world genomic landscape of colon and rectal cancer.FEBS open bio · 2025Article
- Establishment and genomic profiling of cholangiocarcinoma cells with functional characterization.Scientific reports · 2025Article
- Mechanisms and Strategies to Overcome Drug Resistance in Colorectal Cancer.International journal of molecular sciences · 2025Review
- EGFR-targeting RNase A-cetuximab antibody-drug conjugate induces ROS-mediated apoptosis to overcome drug resistance in KRAS mutant cancer cells.Scientific reports · 2025Article
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 3 institutions in 1 country.
Funding
Abstract
Colorectal cancer is one of the world's most prevalent and lethal cancers. Mutations of the KRAS gene occur in ~40% of metastatic colorectal cancers. While this cohort has historically been difficult to manage, the last few years have shown exponential growth in the development of selective inhibitors targeting KRAS mutations. Their foremost mechanism of action utilizes the Switch II binding pocket and Cys12 residue of GDP-bound KRAS proteins in G12C mutants, confining them to their inactive state. Sotorasib and Adagrasib, both FDA-approved for the treatment of non-small cell lung cancer (NSCLC), have been pivotal in paving the way for KRAS G12C inhibitors in the clinical setting. Other KRAS inhibitors in development include a multi-targeting KRAS-mutant drug and a G12D mutant drug. Treatment resistance remains an issue with combination treatment regimens including indirect pathway inhibition and immunotherapy providing possible ways to combat this. While KRAS-mutant selective therapy has come a long way, more work is required to make this an effective and viable option for patients with colorectal cancer.
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.