Irreversible electroporation (IRE) is a novel tumor ablation technique using a non-thermal energy to create innumerable permanent nanopores in the cell membrane to disrupt cellular homeostasis. This disruption of cellular homeostasis initiates apoptosis which leads to permanent cell death. In our translational research, we have demonstrated that IRE can be a safe, fast and powerful method of tumor treatment. In this review, we present an overview of IRE ablation including a brief history of IRE, advantages and disadvantages of IRE and clinical and research implications of IRE.
Ablation Techniques ; Apoptosis ; Cell Death ; Cell Membrane ; Electroporation ; Homeostasis ; Nanopores ; Translational Medical Research

OBJECTIVE: Activating mutations in the fibroblast growth factor receptor-2 (FGFR2) have been shown to cause syndromic craniosynostosis such as Apert and Crouzon syndromes. The purpose of this pilot study was to investigate the resultant phenotypes induced by the two distinctive bone-targeted gene constructs of FGFR2, Pro253Arg and Cys278Phe, corresponding to human Apert and Crouzon syndromes respectively. METHODS: Wild type and a transgenic mouse model with normal FGFR2 were used as controls to examine the validity of the microinjection. Micro-CT and morphometric analysis on the skull revealed the following results. RESULTS: Both Apert and Crouzon mutants of FGFR2 induced fusion of calvarial sutures and anteroposteriorly constricted facial dimension, with anterior crossbite present only in Apert mice. Apert mice differed from Crouzon mice and transgenic mice with normal FGFR2 in the anterior cranial base flexure and calvarial flexure angle which implies a possible difference in the pathogenesis of the two mutations. In contrast, the transgenic mice with normal FGFR2 displayed normal craniofacial phenotype. CONCLUSION: Apert and Crouzon mutations appear to lead to genotype-specific phenotypes, possibly causing the distinctive sites and sequence of synostosis in the calvaria and cranial base. The exact function of the altered FGFR2 at each suture needs further investigation.
Acrocephalosyndactylia ; Animals ; Craniofacial Dysostosis* ; Craniosynostoses ; Fibroblast Growth Factors ; Humans ; Malocclusion ; Mice ; Mice, Transgenic ; Microinjections ; Phenotype ; Pilot Projects ; Skull ; Skull Base ; Sutures ; Synostosis