ArticleMolecular cancer2008
Gene expression deregulation by KRAS G12D and G12V in a BRAF V600E context.
Article in Molecular cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 43 citations in OpenAlex.
- Ganetespib, a novel Hsp90 inhibitor in patients with KRAS mutated and wild type, refractory metastatic colorectal cancer.Clinical colorectal cancer · 2014Trial
- Colorectal cancer tumor phenotypes associated withWorld journal of gastrointestinal pathophysiology · 2025Article
- Mortality Outcome Associated with SpecificDiagnostics (Basel, Switzerland) · 2025Article
- Methylation-Based Characterization of a NewInternational journal of molecular sciences · 2024Article
- Brusatol attenuated proliferation and invasion induced by KRAS in differentiated thyroid cancer through inhibiting Nrf2.Journal of endocrinological investigation · 2024Article
- Article
- Small-Molecule RAS Inhibitors as Anticancer Agents: Discovery, Development, and Mechanistic Studies.International journal of molecular sciences · 2022Review
- Somatic mosaicism in the MAPK pathway in sporadic brain arteriovenous malformation and association with phenotype.Journal of neurosurgery · 2022Article
- eVIP2: Expression-based variant impact phenotyping to predict the function of gene variants.PLoS computational biology · 2021Article
- Metformin selectively inhibits metastatic colorectal cancer with theProceedings of the National Academy of Sciences of the United States of America · 2020Article
- The Frequency of EGFR and KRAS Mutations in the Turkish Population with Non-small Cell Lung Cancer and their Response to Erlotinib Therapy.Balkan journal of medical genetics : BJMG · 2018Article
- Review
- The co-regulatory networks of tumor suppressor genes, oncogenes, and miRNAs in colorectal cancer.Genes, chromosomes & cancer · 2017Article
- Cytotoxicity of allitinib, an irreversible anti-EGFR agent, in a large panel of human cancer-derived cell lines: KRAS mutation status as a predictive biomarker.Cellular oncology (Dordrecht, Netherlands) · 2016Article
- Oncogene-induced senescence underlies the mutual exclusive nature of oncogenic KRAS and BRAF.Oncogene · 2016Article
- Circulating Tumor Cells and Circulating Tumor DNA Provide New Insights into Pancreatic Cancer.International journal of medical sciences · 2016Review
- Efficacy of bevacizumab and chemotherapy in the first-line treatment of metastatic colorectal cancer: broadening KRAS-focused clinical view.BMC gastroenterology · 2015Observational
- Permissiveness of human cancer cells to oncolytic bovine herpesvirus 1 is mediated in part by KRAS activity.Journal of virology · 2014Article
- KRAS (but not BRAF) mutations in ovarian serous borderline tumour are associated with recurrent low-grade serous carcinoma.The Journal of pathology · 2013Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKRAS and BRAF mutations appear of relevance in the genesis and progression of several solid tumor types but the co-occurrence and interaction of these mutations have not yet been fully elucidated. Using a microsatellite stable (MSS) colorectal cancer (CRC) cell line (Colo741) having mutated BRAF and KRASWT, we also aimed to investigate the KRAS-BRAF interaction. Gene expression profiles for control KRASWT, KRAS G12V and KRAS G12D transfected cells were obtained after cell clone selection and RT-PCR screening. Extensive qPCR was performed to confirm microarray data.
resultsWe found that the KRAS G12V state deregulated several genes associated to cell cycle, apoptosis and nitrogen metabolism. These findings indicated a reduced survival and proliferation with respect to the KRASWT state. The KRAS G12D state was, instead, characterized by several other distinct functional changes as for example those related to chromatin organization and cell-cell adhesion without affecting apoptosis related genes.
conclusionThese data predict that the G12D mutation may be more likely selected in a BRAF mutated context. At the same time, the presence of the KRAS G12V mutation in the cells escaping apoptosis and inducing angiogenesis via IL8 may confer a more aggressive phenotype. The present results get along with the observations that CRCs with G12V are associated with a worse prognosis with respect to the WT and G12D states and may help identifying novel CRC pathways and biomarkers of clinical relevance.
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.