ArticleNature biotechnology2010
Chimeric mouse tumor models reveal differences in pathway activation between ERBB family- and KRAS-dependent lung adenocarcinomas.
Article in Nature biotechnology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 86 citations in OpenAlex.
- Spatiotemporal lineage tracing reveals the dynamic spatial architecture of tumor growth and metastasis.Nature genetics · 2026Article
- The application of experimental models for the drug discovery for digestive tumors.Molecular cancer · 2026Review
- Modeling CIC::DUX4 sarcoma reveals oncogene-mediated MHCI-dependent immune evasion.Molecular cancer · 2025Article
- Comprehensive review of drug resistance in mammalian cancer stem cells: implications for cancer therapy.Cancer cell international · 2024Review
- Advances in Making Cancer Mouse Models More Accessible and Informative through Non-Germline Genetic Engineering.Cold Spring Harbor perspectives in medicine · 2024Review
- The Possible Connection of Two Dual Function Processes: The Relationship of Ferroptosis and the JNK Pathway.International journal of molecular sciences · 2022Article
- Article
- A Versatile ES Cell-Based Melanoma Mouse Modeling Platform.Cancer research · 2020Article
- Using Mouse andInternational journal of molecular sciences · 2018Review
- Transgenic Mouse Models in Cancer Research.Frontiers in oncology · 2018Review
- Influence of node abundance on signaling network state and dynamics analyzed by mass cytometry.Nature biotechnology · 2017Article
- Targeting the VEGF-C/VEGFR3 axis suppresses Slug-mediated cancer metastasis and stemness via inhibition of KRAS/YAP1 signaling.Oncotarget · 2017Review
- MEK inhibitors against MET-amplified non-small cell lung cancer.International journal of oncology · 2016Article
- Review
- Translational value of mouse models in oncology drug development.Nature medicine · 2015Article
- Preclinical Murine Models for Lung Cancer: Clinical Trial Applications.BioMed research international · 2015Review
- BRAF vs RAS oncogenes: are mutations of the same pathway equal? Differential signalling and therapeutic implications.Oncotarget · 2014Review
- Scrib heterozygosity predisposes to lung cancer and cooperates with KRas hyperactivation to accelerate lung cancer progression in vivo.Oncogene · 2014Article
- Foxm1 transcription factor is required for the initiation of lung tumorigenesis by oncogenic Kras(G12D.).Oncogene · 2014Article
- Targeting the K-Ras--JNK axis eliminates cancer stem-like cells and prevents pancreatic tumor formation.Oncotarget · 2014Article
Corrections and comments
- Commented on by
Authors and funding
16 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To recapitulate the stochastic nature of human cancer development, we have devised a strategy for generating mouse tumor models that involves stepwise genetic manipulation of embryonic stem (ES) cells and chimera generation. Tumors in the chimeric animals develop from engineered cells in the context of normal tissue. Adenocarcinomas arising in an allelic series of lung cancer models containing HER2 (also known as ERBB2), KRAS or EGFR oncogenes exhibit features of advanced malignancies. Treatment of EGFR(L858R) and KRAS(G12V) chimeric models with an EGFR inhibitor resulted in near complete tumor regression and no response to the treatment, respectively, accurately reflecting previous clinical observations. Transcriptome and immunohistochemical analyses reveal that PI3K pathway activation is unique to ERBB family tumors whereas KRAS-driven tumors show activation of the JNK/SAP pathway, suggesting points of therapeutic intervention for this difficult-to-treat tumor category.
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.