ArticleCancers2013
The Molecular Crosstalk between the MET Receptor Tyrosine Kinase and the DNA Damage Response-Biological and Clinical Aspects.
Article in Cancers, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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
14 citing papers in PubMed, 40 citations in OpenAlex.
- Expression of HGF, pMet, and pAkt is related to benefit of radiotherapy after breast-conserving surgery: a long-term follow-up of the SweBCG91-RT randomised trial.Molecular oncology · 2020Trial
- Lipolysis gone rogue: the HSL connection in feeding cancer.Cell biology and toxicology · 2025Review
- E2F1-Associated Purine Synthesis Pathway Is a Major Component of the MET-DNA Damage Response Network.Cancer research communications · 2024Article
- A DNA-PK phosphorylation site on MET regulates its signaling interface with the DNA damage response.Oncogene · 2023Article
- An oncogene addiction phosphorylation signature and its derived scores inform tumor responsiveness to targeted therapies.Cellular and molecular life sciences : CMLS · 2022Article
- Budding yeast Rad51: a paradigm for how phosphorylation and intrinsic structural disorder regulate homologous recombination and protein homeostasis.Current genetics · 2021Review
- Long Noncoding RNA HCG9 Promotes Osteosarcoma Progression through RAD51 by Acting as a ceRNA of miR-34b-3p.Mediators of inflammation · 2021Article
- Inhibition of c-MET increases the antitumour activity of PARP inhibitors in gastric cancer models.Journal of cellular and molecular medicine · 2020Article
- Deciphering MET-dependent modulation of global cellular responses to DNA damage by quantitative phosphoproteomics.Molecular oncology · 2020Article
- Integrative genomic analysis identifies associations of molecular alterations to APOBEC and BRCA1/2 mutational signatures in breast cancer.Molecular genetics & genomic medicine · 2019Article
- Article
- Preclinical rationale for combination of crizotinib with mitomycin C for the treatment of advanced colorectal cancer.Cancer biology & therapy · 2017Article
- Is cancer a severe delayed hypersensitivity reaction and histamine a blueprint?Clinical and translational medicine · 2016Article
- Regulation of therapeutic resistance in cancers by receptor tyrosine kinases.American journal of cancer research · 2016Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiation therapy remains an imperative treatment modality for numerous malignancies. Enduring significant technical achievements both on the levels of treatment planning and radiation delivery have led to improvements in local control of tumor growth and reduction in healthy tissue toxicity. Nevertheless, resistance mechanisms, which presumably also involve activation of DNA damage response signaling pathways that eventually may account for loco-regional relapse and consequent tumor progression, still remain a critical problem. Accumulating data suggest that signaling via growth factor receptor tyrosine kinases, which are aberrantly expressed in many tumors, may interfere with the cytotoxic impact of ionizing radiation via the direct activation of the DNA damage response, leading eventually to so-called tumor radioresistance. The aim of this review is to overview the current known data that support a molecular crosstalk between the hepatocyte growth factor receptor tyrosine kinase MET and the DNA damage response. Apart of extending well established concepts over MET biology beyond its function as a growth factor receptor, these observations directly relate to the role of its aberrant activity in resistance to DNA damaging agents, such as ionizing radiation, which are routinely used in cancer therapy and advocate tumor sensitization towards DNA damaging agents in combination with MET targeting.
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.