High intensity nanosecond pulsed electric fields
(nsPEF) were applied on melanoma tumors to observe
functional and structural biological changes and to
investigate the possible molecular mechanisms
responsible. A treatment of 300 nanosecond pulses
were delivered to melanoma. The nsPEF
Tx caused tumor self-destruction with sharply
decreased cell volumes and shrunken nuclei. The
apoptotic biochemical tests confirmed nsPEF Tx
induced apoptosis in a time-dependent manner.
Examination of gross vessel and micro-vessel density
indicated direct vascular damage to pre-existing
vessels and anti-angiogenic consequence on
neovascular development concomitant with tumor self-
destruction. In contradistinction to ionization,
thermal or electroporation Tx, nsPEFs produced broad
impacts on the melanomas in vivo, ranging from DNA
fragmentation, caspase activation, nuclear damage,
apoptosis induction, damage to pre-existing intra-
tumoral vessels and neovascular inhibition. This
work was supported by National Natural Sciense
Fundation of China (Grant Number No. 3070078) and
Juliette Reidy Cancer Fellowship from Frank Reidy
Research Center in U.S.A.
(nsPEF) were applied on melanoma tumors to observe
functional and structural biological changes and to
investigate the possible molecular mechanisms
responsible. A treatment of 300 nanosecond pulses
were delivered to melanoma. The nsPEF
Tx caused tumor self-destruction with sharply
decreased cell volumes and shrunken nuclei. The
apoptotic biochemical tests confirmed nsPEF Tx
induced apoptosis in a time-dependent manner.
Examination of gross vessel and micro-vessel density
indicated direct vascular damage to pre-existing
vessels and anti-angiogenic consequence on
neovascular development concomitant with tumor self-
destruction. In contradistinction to ionization,
thermal or electroporation Tx, nsPEFs produced broad
impacts on the melanomas in vivo, ranging from DNA
fragmentation, caspase activation, nuclear damage,
apoptosis induction, damage to pre-existing intra-
tumoral vessels and neovascular inhibition. This
work was supported by National Natural Sciense
Fundation of China (Grant Number No. 3070078) and
Juliette Reidy Cancer Fellowship from Frank Reidy
Research Center in U.S.A.