ArticleThe Journal of clinical investigation2008
Mechanisms of resistance to ErbB-targeted cancer therapeutics.
Article in The Journal of clinical investigation, 2008. 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
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
12 citing papers in PubMed, 31 citations in OpenAlex.
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- Somatic USP8 Gene Mutations Are a Common Cause of Pediatric Cushing Disease.The Journal of clinical endocrinology and metabolism · 2017Article
- Systems biology of cancer: entropy, disorder, and selection-driven evolution to independence, invasion and "swarm intelligence".Cancer metastasis reviews · 2013Review
- A fluorescent reporter of ATP binding-competent receptor kinases.Bioorganic & medicinal chemistry letters · 2012Article
- EGFR as a therapeutic target for human, canine, and mouse ACTH-secreting pituitary adenomas.The Journal of clinical investigation · 2011Article
- A new medical therapy for Cushing disease?The Journal of clinical investigation · 2011Article
- Article
- HER2/ErbB2 receptor signaling in rat and human prolactinoma cells: strategy for targeted prolactinoma therapy.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Selective disruption of insulin-like growth factor-1 (IGF-1) signaling via phosphoinositide-dependent kinase-1 prevents the protective effect of IGF-1 on human cancer cell death.The Journal of biological chemistry · 2010Article
- Reversal of oncogene transformation and suppression of tumor growth by the novel IGF1R kinase inhibitor A-928605.BMC cancer · 2009Article
- The role of HER2 in early breast cancer metastasis and the origins of resistance to HER2-targeted therapies.Experimental and molecular pathology · 2009Review
Corrections and comments
- Comment on
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ErbB receptors, such as EGFR, have been intensely pursued as targets for cancer therapeutics. However, a large percentage of patients who are initially responsive to ErbB-targeted therapies experience tumor recurrence and become refractory to therapy. In this issue of the JCI, Guix et al. demonstrate that downregulation of IGF-binding protein 3 (IGFBP-3) and -4, the negative regulators of IGF-I receptor signaling, contributes to the resistance of human squamous cell carcinomas to the EGFR inhibitor gefitinib (see the related article beginning on page 2609). Understanding the mechanisms involved in the resistance of some tumors to ErbB-targeted molecules may provide guidelines for developing more efficient therapeutic approaches.
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.