ArticleOncoscience2015
Retrospective Review of MET Gene Mutations.
Article in Oncoscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 31 citations in OpenAlex.
- Recent progress in non-clear cell renal cell carcinoma: biology and therapeutic strategies.Therapeutic advances in medical oncology · 2025Review
- Translational pharmacokinetic-pharmacodynamic modeling of preclinical and clinical data of the oral MET inhibitor tepotinib to determine the recommended phase II dose.CPT: pharmacometrics & systems pharmacology · 2021Article
- Comprehensive Immune Profiling of Medullary Thyroid Cancer.Thyroid : official journal of the American Thyroid Association · 2020Article
- Gene mutation profile and risk stratification in AML1‑ETO‑positive acute myeloid leukemia based on next‑generation sequencing.Oncology reports · 2019Article
- A Review of Papillary Renal Cell Carcinoma and MET Inhibitors.Kidney cancer (Clifton, Va.) · 2019Review
- Rapid Deep Responses With Nivolumab Plus Ipilimumab in Papillary Renal Cell Carcinoma With Sarcomatoid Dedifferentiation.Clinical genitourinary cancer · 2019Article
- Cooperative Effect of OncogenicMolecular cancer therapeutics · 2019Article
- Gefitinib or lapatinib with foretinib synergistically induce a cytotoxic effect in melanoma cell lines.Oncotarget · 2018Article
- Role of the HGF/c-MET tyrosine kinase inhibitors in metastasic melanoma.Molecular cancer · 2018Review
- Have Clinical Trials Properly Assessed c-Met Inhibitors?Trends in cancer · 2018Review
- Genomic abnormalities in invasive endocervical adenocarcinoma correlate with pattern of invasion: biologic and clinical implications.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017Article
- Preclinical rationale for combination of crizotinib with mitomycin C for the treatment of advanced colorectal cancer.Cancer biology & therapy · 2017Article
- PIK3CA hotspot mutations differentially impact responses to MET targeting in MET-driven and non-driven preclinical cancer models.Molecular cancer · 2017Article
- A Concise Atlas of Thyroid Cancer Next-Generation Sequencing Panel ThyroSeq v.2.Molecular imaging and radionuclide therapy · 2017Article
- Cell-free DNA and next-generation sequencing in the service of personalized medicine for lung cancer.Oncotarget · 2016Review
- Targeted molecular profiling of rare genetic alterations in colorectal cancer using next-generation sequencing.Medical oncology (Northwood, London, England) · 2016Article
- Hepatocyte growth factor and alternative splice variants - expression, regulation and implications in osteogenesis and bone health and repair.Expert opinion on therapeutic targets · 2016Review
- 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
9 authors at 3 institutions in 1 country.
Funding
Abstract
C-MET proto-oncogene is a tyrosine kinase situated on chromosome 7. C-MET and its ligand hepatocyte growth factor/scatter factor (HGF/SF) play a role in proliferation, differentiation and organ development. C-MET genetic aberrations are found associated with driving tumorigenesis. In this retrospective study, we reviewed molecular analysis data gathered from a cancer institute during a two-year period (2010-2012). Upon detection of tumors harboring c-MET mutations, we determined the status of the other mutations tested and evaluated c-MET expression by fluorescent in-situ hybridization (FISH). Our search resulted in identification of 134 c-MET mutations, 44% of which had mutations of at least one of the other genes tested. No c-MET expression aberrancy was detected in this subset by FISH. Survival amongst the patients with surgically resected metastatic colorectal cancers (CRC) was slightly better in those with only a c-MET mutation compared to those with no mutation detected, although the difference was not statistically significant. When c-MET inhibition becomes an integrated part of chemotherapy practice, our observed frequency of co-mutations will be an argument for utilizing c-MET targeted treatment in combination with other targeted drugs and therapeutic strategies. Larger studies can aid to further parse out c-MET prognostic and therapeutic significance.
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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.