摘要
Cancer cells escape from growth cont rol by accumulating genetic and epig enetic alterations.In rare instances,epigenetic changes alone are oncogenic.Furthermore,a gents that modify DNA methylation or chromatin structure can restore a normal phenotype to cells harboring oncogenic mutations.How ever,it is unclear to what extent epi genetic reprogramming can reverse o ncogenesis.Using somatic nuclear transfer,we show that medul loblastomas arising in Ptc1+/-mice can direct preimplantation develop ment.Additionally,blastocysts derived from medullobl astoma nuclei form postimplantatio n embryos with typical cell layers.T hus,tumor cells can be epigenetically reprogrammed into n ormal cell types.This approach coul d lead to a general strategy for assessing genetic and epigenetic contributions to tumorigenesis.
Cancer cells escape from growth cont rol by accumulating genetic and epig enetic alterations.In rare instances,epigenetic changes alone are oncogenic.Furthermore,a gents that modify DNA methylation or chromatin structure can restore a normal phenotype to cells harboring oncogenic mutations.How ever,it is unclear to what extent epi genetic reprogramming can reverse o ncogenesis.Using somatic nuclear transfer,we show that medul loblastomas arising in Ptc1+/-mice can direct preimplantation develop ment.Additionally,blastocysts derived from medullobl astoma nuclei form postimplantatio n embryos with typical cell layers.T hus,tumor cells can be epigenetically reprogrammed into n ormal cell types.This approach coul d lead to a general strategy for assessing genetic and epigenetic contributions to tumorigenesis.
出处
《癌症》
SCIE
CAS
CSCD
北大核心
2003年第7期679-679,共1页
Chinese Journal of Cancer
