ArticleNeoplasia (New York, N.Y.)2007
Oncogenic K-Ras signals through epidermal growth factor receptor and wild-type H-Ras to promote radiation survival in pancreatic and colorectal carcinoma cells.
Article in Neoplasia (New York, N.Y.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 88 citations in OpenAlex.
- Emerging Applications of Stereotactic Ablative Radiotherapy in Oligometastatic Colorectal Cancer.International journal of molecular sciences · 2025Review
- Multifaceted roles of Galectins: from carbohydrate binding to targeted cancer therapy.Biomarker research · 2025Review
- Role of non-canonical post-translational modifications in gastrointestinal tumors.Cancer cell international · 2023Review
- Targeting K-Ras-mediated DNA damage response in radiation oncology: Current status, challenges and future perspectives.Clinical and translational radiation oncology · 2023Review
- How to Improve SBRT Outcomes in NSCLC: From Pre-Clinical Modeling to Successful Clinical Translation.Cancers · 2022Review
- Targeting the DNA replication stress phenotype of KRAS mutant cancer cells.Scientific reports · 2021Article
- Clinical and Preclinical Outcomes of Combining Targeted Therapy With Radiotherapy.Frontiers in oncology · 2021Review
- The Cellular Origins of Cancer-Associated Fibroblasts and Their Opposing Contributions to Pancreatic Cancer Growth.Frontiers in cell and developmental biology · 2021Review
- KRAS Codon 12 Mutation is Associated with More Aggressive Invasiveness in Synchronous Metastatic Colorectal Cancer (mCRC): Retrospective Research.OncoTargets and therapy · 2020Article
- Combination Therapy With Charged Particles and Molecular Targeting: A Promising Avenue to Overcome Radioresistance.Frontiers in oncology · 2020Review
- MIIP gene expression is associated with radiosensitivity in human nasopharyngeal carcinoma cells.Oncology letters · 2018Article
- Ferroptosis: A Novel Anti-tumor Action for Cisplatin.Cancer research and treatment · 2018Article
- The Role of Galectins in Cervical Cancer Biology and Progression.BioMed research international · 2018Review
- Radiation Resistance in KRAS-Mutated Lung Cancer Is Enabled by Stem-like Properties Mediated by an Osteopontin-EGFR Pathway.Cancer research · 2017Article
- The role of wild type RAS isoforms in cancer.Seminars in cell & developmental biology · 2016Review
- Dual targeting of PI3K and MEK enhances the radiation response of K-RAS mutated non-small cell lung cancer.Oncotarget · 2016Article
- Cellular Pathways in Response to Ionizing Radiation and Their Targetability for Tumor Radiosensitization.International journal of molecular sciences · 2016Review
- EGFR-mediated chromatin condensation protects KRAS-mutant cancer cells against ionizing radiation.Cancer research · 2014Article
- ERK2-dependent reactivation of Akt mediates the limited response of tumor cells with constitutive K-RAS activity to PI3K inhibition.Cancer biology & therapy · 2014Article
- MEK1/2 inhibition enhances the radiosensitivity of cancer cells by downregulating survival and growth signals mediated by EGFR ligands.International journal of oncology · 2013Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 4 countries.
Funding
Abstract
Pancreatic and colorectal carcinomas frequently express oncogenic/mutant K-Ras that contributes to both tumorigenesis and clinically observed resistance to radiation treatment. We have previously shown that farnesyltransferase inhibitors (FTI) radiosensitize many pancreatic and colorectal cancer cell lines that express oncogenic K-ras at doses that inhibit the prenylation and activation of H-Ras but not K-Ras. In the present study, we have examined the mechanism of FTI-mediated radiosensitization in cell lines that express oncogenic K-Ras and found that wild-type H-Ras is a contributor to radiation survival in tumor cells that express oncogenic K-Ras. In these experiments, inhibiting the expression of oncogenic K-Ras, wild-type H-Ras, or epidermal growth factor receptor (EGFR) led to similar levels of radiosensitization as treatment with the FTI tipifarnib. Treatment with the EGFR inhibitor gefitinib led to similar levels of radiosensitization, and the combinations of tipifarnib or gefitinib plus inhibition of K-Ras, H-Ras, or EGFR expression did not provide additional radiosensitization compared with tipifarnib or gefitinib alone. Finally, supplementing culture medium with the EGFR ligand transforming growth factor alpha was able to reverse the radiosensitizing effect of inhibiting K-ras expression. Taken together, these findings suggest that EGFR-activated H-Ras signaling is initiated by oncogenic K-Ras to promote radiation survival in pancreatic and colorectal 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.