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Updated: Jun 4, 2026

Screening and Identification of Small Peptides Targeting Fibroblast Growth Factor Receptor2 using a Phage Display Peptide Library
Published on: September 30, 2019
Targeting mutant fibroblast growth factor receptors in cancer
Heidi Greulich1, Pamela M Pollock
1Dana-Farber Cancer Institute, Boston, MA 02115, USA. heidig@broadinstitute.org
Abstract:
Fibroblast growth factor receptors (FGFRs) play diverse roles in the control of cell proliferation, cell differentiation, angiogenesis and development. Activating the mutations of FGFRs in the germline has long been known to cause a variety of skeletal developmental disorders, but it is only recently that a similar spectrum of somatic FGFR mutations has been associated with human cancers. Many of these somatic mutations are gain-of-function and oncogenic and create dependencies in tumor cell lines harboring such mutations. A combination of knockdown studies and pharmaceutical inhibition in preclinical models has further substantiated genomically altered FGFR as a therapeutic target in cancer, and the oncology community is responding with clinical trials evaluating multikinase inhibitors with anti-FGFR activity and a new generation of specific pan-FGFR inhibitors.
Insights
Activating mutations in Fibroblast Growth Factor Receptors (FGFRs) cause skeletal disorders and are increasingly linked to cancer. Targeting FGFRs shows promise as a cancer therapy, with ongoing clinical trials.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Fibroblast Growth Factor Receptors (FGFRs) are crucial for cell functions including proliferation, differentiation, and development.
- Germline mutations in FGFRs are known to cause skeletal developmental disorders.
- Somatic mutations in FGFRs are increasingly recognized in human cancers, often acting as oncogenic drivers.
Purpose of the Study:
- To review the role of FGFR mutations in cancer.
- To highlight the therapeutic potential of targeting FGFRs in oncology.
- To discuss the development of FGFR-targeted therapies.
Main Methods:
- Review of existing literature on FGFR mutations in development and cancer.
- Analysis of preclinical studies using knockdown and pharmaceutical inhibition of FGFRs.
- Examination of ongoing clinical trials for FGFR-targeted cancer therapies.
Main Results:
- Gain-of-function FGFR mutations are oncogenic and create dependencies in cancer cells.
- Preclinical models confirm FGFRs as viable therapeutic targets in cancer.
- Clinical trials are evaluating both multi-kinase inhibitors and specific pan-FGFR inhibitors.
Conclusions:
- FGFRs represent a significant therapeutic target in oncology due to their role in cancer development and progression.
- Targeting FGFRs, through various inhibitors, offers a promising avenue for cancer treatment.
- The development of specific FGFR inhibitors is advancing cancer therapy research.
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