ArticlePloS one2013
DOK2 inhibits EGFR-mutated lung adenocarcinoma.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 43 citations in OpenAlex.
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- Chromosome-level Asian elephant genome assembly and comparative genomics of long-lived mammals reveal the common substitutions for cancer resistance.Aging cell · 2023Article
- Genome-Wide Population Structure and Selection Signatures of Yunling Goat Based on RAD-seq.Animals : an open access journal from MDPI · 2022Article
- Review
- Introduction to DOK2 and its potential role in cancer.Physiological research · 2021Review
- Comprehensive network analysis of different subtypes of molecular disorders in lung cancer.American journal of translational research · 2021Article
- Article
- Compound haploinsufficiency of Dok2 and Dusp4 promotes lung tumorigenesis.The Journal of clinical investigation · 2019Article
- Region-Specific Dok2 Overexpression Associates with Poor Prognosis in Human Astrocytoma.Molecular neurobiology · 2018Article
- Co-expression and significance of Dok2 and Ras p21 protein activator 1 in breast cancer.Oncology letters · 2017Article
- Expression and significance of DOK2 in colorectal cancer.Oncology letters · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 1 country.
Funding
Abstract
Somatic mutations in the EGFR proto-oncogene occur in ~15% of human lung adenocarcinomas and the importance of EGFR mutations for the initiation and maintenance of lung cancer is well established from mouse models and cancer therapy trials in human lung cancer patients. Recently, we identified DOK2 as a lung adenocarcinoma tumor suppressor gene. Here we show that genomic loss of DOK2 is associated with EGFR mutations in human lung adenocarcinoma, and we hypothesized that loss of DOK2 might therefore cooperate with EGFR mutations to promote lung tumorigenesis. We tested this hypothesis using genetically engineered mouse models and find that loss of Dok2 in the mouse accelerates lung tumorigenesis initiated by oncogenic EGFR, but not that initiated by mutated Kras. Moreover, we find that DOK2 participates in a negative feedback loop that opposes mutated EGFR; EGFR mutation leads to recruitment of DOK2 to EGFR and DOK2-mediated inhibition of downstream activation of RAS. These data identify DOK2 as a tumor suppressor in EGFR-mutant lung adenocarcinoma.
Indexed as
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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.