Inhibition of the insulin-like growth factor receptor-1 tyrosine kinase activity as a therapeutic strategy for multiple myeloma, other hematologic malignancies, and solid tumors.
By C. Mitsiades, N. Mitsiades, C. McMullan, V. Poulaki, R. Shringarpure, M. Akiyama, T. Hideshima, D. Chauhan, Marie G. Joseph, T. Libermann and 5 more. Cancer Cell, 2004
651 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Hematology
View Paper: https://www.semanticscholar.org/paper/5d5760f94adfbd21d8138b3facffe9ba056298ab
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In Endocrinology, Diabetes and Metabolism
In Epidemiology
Citations in the corpus
- New signals from the invasive front (2006, background): “Indeed, both NVP-AEW541, a small chemical IGF-1R inhibitor, and neutralizing antibodies against IGF-1R prevent the growth of tumour cells by blocking proliferation and inducing apoptosis in culture and in animal model”
- Insulin-like growth factors and neoplasia (2004, background): “; use of small-molecule IGF1R-specific tyrosine kinase inhibitor”
- ERBB receptors and cancer: the complexity of targeted inhibitors (2005, background): “Turning to combination strategies, the importance of IGF1R in maintaining strong activation of the PI3K–AKT pathway, and its potential to interfere with ERBB-targeted inhibitors, indicates that it is logical to consider combining anti-ERBB agents with an IGF1R inhibito”
- BET bromodomain inhibition as a therapeutic strategy to target c-Myc (2011, neutral): “1S-luc), which recapitulates the clinical sequelae, anatomic distribution of MM lesions, and hallmark bone pathophysiology observed in MM patients (Mitsiades et al., 2004).”
- Cancer prevention by tea: animal studies, molecular mechanisms and human relevance (2009, background): “IGF1R activation can induce cell proliferation and survival, as well as inhibit apoptosis, transformation, metastasis and angiogenesis in different types of cance”