The Plastic Surgery Foundation
Log In Donate Now

Grants We Funded

Grant applicants for the 2023 cycle requested a total of nearly $4 million dollars. The PSF Study Section Subcommittees of Basic & Translational Research and Clinical Research evaluated nearly 140 grant applications on the following topics:

The PSF awarded research grants totaling over $1 million dollars to support nearly 30 plastic surgery research proposals.

ASPS/PSF leadership is committed to continuing to provide high levels of investigator-initiated research support to ensure that plastic surgeons have the needed research resources to be pioneers and innovators in advancing the practice of medicine.

Research Abstracts

Search The PSF database to have easy access to full-text grant abstracts from past PSF-funded research projects 2003 to present. All abstracts are the work of the Principal Investigators and were retrieved from their PSF grant applications. Several different filters may be applied to locate abstracts specific to a particular focus area or PSF funding mechanism.

Effects of an Fgfr2c Mutation on Palatal and Craniofacial Development

Principal Investigator
Chad Perlyn MD


Washington University

Funding Mechanism
Research Fellowship

Focus Area
Cranio/Maxillofacial/Head and Neck

Activating mutations in FGFR2 have been identified as the cause of several craniofacial anomalies, including Crouzon, Pfeiffer, and Apert syndromes (Cohen 2000, Wilkie and Morriss-Kay 2(01). Most mutations underlying Crouzon and Pfeiffer syndromes involve gain or loss of a cysteine residue in the alternatively spliced domain of the FGFR2c protein; the most common of these mutations is FGFR2C342Y (Wilkie and Morriss-Kay 2001, Ornitz and Itoh 2(01). Recently a mouse model with an Fgfr2c342Y mutation has been constructed (Eswarakumar et al., 2004), and my project involves an in depth analysis of craniofacial development in this mouse. Like the human cases, Fgfr2c342Y mice are viable and have premature fusion of the cranial sutures, proptotic eyes, shortened midface, and high arched or cleft palate. Fgfr2c342YIC342Y mice, which die shortly after birth, show a more severe Crouzon-like phenotype with rounder cranium, shorter nasomaxillary region, and cleft palate. Anomalies of the trachea, lungs, axial skeleton, and joints are found. The aim of my research is to understand the role of Fgfr2c in craniofacial development through investigating 3 developmental processes in the Fgfr2c342Y mouse model: (1) Palatogenesis and the etiology of cleft palate; (2) Tracheal ring development and etiology of the cartilaginous sleeve anomaly; (3) Skull growth and cranial suture development.