ReviewCancers2016
KRAS Mutant Pancreatic Cancer: No Lone Path to an Effective Treatment.
Review in Cancers, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 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
91 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Non-coding RNAs underlying the pathophysiological links between type 2 diabetes and pancreatic cancer: A systematic review.Journal of diabetes investigation · 2022Pooled it
- The prognostic value of KRAS mutation by cell-free DNA in cancer patients: A systematic review and meta-analysis.PloS one · 2017Pooled it
- Trial
- Crosstalk between KRAS and miRNAs in pancreatic cancer: Opportunities for its diagnosis, prognosis and therapeutic intervention (Review).International journal of oncology · 2026Review
- Tumor microenvironment in breast cancer: cellular crosstalk, pathways, and therapeutic insights.Molecular biology reports · 2025Review
- Review
- Tetraspanins in digestive‑system cancers: Expression, function and therapeutic potential (Review).Molecular medicine reports · 2024Review
- Cytokine CCL9 Mediates Oncogenic KRAS-Induced Pancreatic Acinar-to-Ductal Metaplasia by Promoting Reactive Oxygen Species and Metalloproteinases.International journal of molecular sciences · 2024Article
- Exploring somatic mutations inFrontiers in pharmacology · 2024Article
- Challenges and Opportunities in Targeting the Complex Pancreatic Tumor Microenvironment.JCO oncology advances · 2024Review
- CASPER: A Phase I trial combining calaspargase pegol-mnkl and cobimetinib in pancreatic cancer.Future oncology (London, England) · 2024Article
- Synergistic effect of antagonists to KRas4B/PDE6 molecular complex in pancreatic cancer.Life science alliance · 2023Article
- Oncogenic KRAS triggers metabolic reprogramming in pancreatic ductal adenocarcinoma.Journal of translational internal medicine · 2023Article
- Article
- A super-enhancer-regulated RNA-binding protein cascade drives pancreatic cancer.Nature communications · 2023Article
- Reverse vaccinology and immunoinformatics approaches to design multi-epitope based vaccine against oncogenic KRAS.Medical oncology (Northwood, London, England) · 2023Article
- An integrated model for predicting KRAS dependency.PLoS computational biology · 2023Article
- Recent advances in targeted therapy for pancreatic adenocarcinoma.World journal of gastrointestinal oncology · 2023Review
- A novel protein RASON encoded by a lncRNA controls oncogenic RAS signaling in KRAS mutant cancers.Cell research · 2023Article
- Article
31 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
4 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is among the deadliest cancers with a dismal 7% 5-year survival rate and is projected to become the second leading cause of cancer-related deaths by 2020. KRAS is mutated in 95% of PDACs and is a well-validated driver of PDAC growth and maintenance. However, despite comprehensive efforts, an effective anti-RAS drug has yet to reach the clinic. Different paths to inhibiting RAS signaling are currently under investigation in the hope of finding a successful treatment. Recently, direct RAS binding molecules have been discovered, challenging the perception that RAS is an "undruggable" protein. Other strategies currently being pursued take an indirect approach, targeting proteins that facilitate RAS membrane association or downstream effector signaling. Unbiased genetic screens have identified synthetic lethal interactors of mutant RAS. Most recently, metabolic targets in pathways related to glycolytic signaling, glutamine utilization, autophagy, and macropinocytosis are also being explored. Harnessing the patient's immune system to fight their cancer is an additional exciting route that is being considered. The "best" path to inhibiting KRAS has yet to be determined, with each having promise as well as potential pitfalls. We will summarize the state-of-the-art for each direction, focusing on efforts directed toward the development of therapeutics for pancreatic cancer patients with mutated KRAS.
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.