ReviewSeminars in cell & developmental biology2016
The role of wild type RAS isoforms in cancer.
Review in Seminars in cell & developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.
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Who cites it
93 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.
- The prognostic value of KRAS mutation by cell-free DNA in cancer patients: A systematic review and meta-analysis.PloS one · 2017Pooled it
- Enhancer Remodeling during Adaptive Bypass to MEK Inhibition Is Attenuated by Pharmacologic Targeting of the P-TEFb Complex.Cancer discovery · 2017Trial
- Targeting Oncogenic KRAS Using Peptide Nucleic Acid Oligomers Attached to Cell-Penetrating Peptides.International journal of molecular sciences · 2026Article
- HPV-18-Immortalised Cells Require the Downregulation of the SncmtRNA-2/Hsa-miR-620 Axis During Cell Transformation.Medicina (Kaunas, Lithuania) · 2026Article
- Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- The role of inflammation in the immune evasion of KRas.Frontiers in immunology · 2026Review
- Research Progress on Copper Metabolism, Cuprotosis, and Their Regulatory Mechanism in Tumor Diagnosis and Treatment.Cancer management and research · 2026Review
- A Novel NRAS Variant Near the Splice Junction in Moroccan Childhood Acute Lymphoblastic Leukemia: A Molecular Dynamics Study.Biochemical genetics · 2025Article
- Proteomic Perspectives on KRAS-Driven Cancers and Emerging Therapeutic Approaches.Current oncology (Toronto, Ont.) · 2025Review
- A first-in-class EGFR-directed KRAS G12V selective inhibitor.Cancer cell · 2025Article
- Pancreatic Cells Are Resistant to KRASQ61L Expression due to Hyperactive ERK/MAPK Signaling and Apoptosis Induction.Cancer research communications · 2025Article
- Wild-type RAS signaling is an essential therapeutic target inScience signaling · 2025Article
- Elevated KRAS protein level is associated with better survival in pancreatic cancer.BMC cancer · 2025Article
- LZTR1 expression as a novel predictive biomarker for early recurrence of hepatocellular carcinoma.European journal of medical research · 2025Article
- The Role of RAS in CNS Tumors: A Key Player or an Overlooked Oncogene?International journal of molecular sciences · 2025Review
- Advancements in gene therapies targeting mutant KRAS in cancers.Cancer metastasis reviews · 2025Review
- A stromal inflammasome Ras safeguard against Myc-driven lymphomagenesis.Nature immunology · 2025Article
- MAPK/ERK signaling pathway in rheumatoid arthritis: mechanisms and therapeutic potential.PeerJ · 2025Review
- Review
- Cooperative genomic lesions in HRAS-mutant cancers predict resistance to farnesyltransferase inhibitors.Oncogene · 2024Article
33 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
3 authors at 1 institution in 1 country.
Funding
Abstract
Mutationally activated RAS proteins are critical oncogenic drivers in nearly 30% of all human cancers. As with mutant RAS, the role of wild type RAS proteins in oncogenesis, tumour maintenance and metastasis is context-dependent. Complexity is introduced by the existence of multiple RAS genes (HRAS, KRAS, NRAS) and protein "isoforms" (KRAS4A, KRAS4B), by the ever more complicated network of RAS signaling, and by the increasing identification of numerous genetic aberrations in cancers that do and do not harbour mutant RAS. Numerous mouse model carcinogenesis studies and examination of patient tumours reveal that, in RAS-mutant cancers, wild type RAS proteins are likely to serve as tumour suppressors when the mutant RAS is of the same isoform. This evidence is particularly robust in KRAS mutant cancers, which often display suppression or loss of wild type KRAS, but is not as strong for NRAS. In contrast, although not yet fully elucidated, the preponderance of evidence indicates that wild type RAS proteins play a tumour promoting role when the mutant RAS is of a different isoform. In non-RAS mutant cancers, wild type RAS is recognized as a mediator of oncogenic signaling due to chronic activation of upstream receptor tyrosine kinases that feed through RAS. Additionally, in the absence of mutant RAS, activation of wild type RAS may drive cancer upon the loss of negative RAS regulators such as NF1 GAP or SPRY proteins. Here we explore the current state of knowledge with respect to the roles of wild type RAS proteins in human cancers.
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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.