ArticleThe Journal of clinical investigation2011
The adaptive stroma joining the antiangiogenic resistance front.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 14 citations in OpenAlex.
- Sox17 promotes tumor angiogenesis and destabilizes tumor vessels in mice.The Journal of clinical investigation · 2013Trial
- Angiocrine endothelium: from physiology to cancer.Journal of translational medicine · 2020Review
- Necrosis in the Tumor Microenvironment and Its Role in Cancer Recurrence.Advances in experimental medicine and biology · 2020Review
- The HGF/c-MET Pathway Is a Driver and Biomarker of VEGFR-inhibitor Resistance and Vascular Remodeling in Non-Small Cell Lung Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Article
- Systems pharmacology approaches for optimization of antiangiogenic therapies: challenges and opportunities.Frontiers in pharmacology · 2015Article
- Activation of alternate prosurvival pathways accounts for acquired sunitinib resistance in U87MG glioma xenografts.The Journal of pharmacology and experimental therapeutics · 2012Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to antiangiogenic therapies in cancer involves both tumor cells and stromal components, but their relative contributions differ in each cancer subtype. In this issue of the JCI, Cascone et al. describe a stromal adaptation to antiangiogenic therapy in non-small cell lung carcinoma (NSCLC) models that include EGFR-driven vascular remodeling promoting resistance to VEGF inhibition. Their results suggest that the added benefit of dual VEGF/R and EGFR targeting in these models could be clinically relevant to fight resistance in NSCLC patients.
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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.