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Updated: May 23, 2026
07:32
Screening and Identification of Small Peptides Targeting Fibroblast Growth Factor Receptor2 using a Phage Display Peptide Library
Published on: September 30, 2019
Targeting the insulin growth factor receptor 1
Fernanda I Arnaldez1, Lee J Helman
1Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 10 CRC Room 1-3816, Bethesda, MD 20892, USA. arnaldezf@mail.nih.gov
Hematology/Oncology Clinics of North America
|April 24, 2012
Summary
The Insulin-like Growth Factor (IGF) axis regulates cell growth and impacts cancer development. Inhibiting this axis shows promise as a targeted cancer therapy, offering new treatment strategies.
Area of Science:
- Endocrinology
- Cancer Biology
- Oncology
Background:
- The Insulin-like Growth Factor (IGF) axis is crucial for cell growth and development.
- This axis plays a significant role in cancer biology, influencing tumor progression.
- Alterations in the IGF system are frequently observed in various cancers.
Purpose of the Study:
- To review the role of the IGF axis in cancer initiation and progression.
- To describe recent advances in IGF inhibition as a therapeutic strategy for cancer.
Main Methods:
- Review of existing literature on the IGF axis in cancer.
- Analysis of alterations in IGF ligands, receptors, and signaling pathways in neoplasias.
- Examination of targeted therapeutic approaches, including monoclonal antibodies and small molecule inhibitors.
Main Results:
- IGF1 and IGF2 promote cancer growth via paracrine and autocrine mechanisms.
- The IGF axis can confer resistance to chemotherapy and radiation.
- Aberrations like increased ligand/receptor expression and altered gene copy numbers are common in cancers.
Conclusions:
- The IGF axis is a key player in cancer development and progression.
- Targeted inhibition of the IGF network, particularly IGF1R, represents a promising therapeutic avenue.
- Further research into IGF inhibition is crucial for advancing cancer treatment options.
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