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 struct...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.展开更多
Medulloblastoma is the most common malignant pediatric brain tumor. In mice, Ptcl haploinsufficiency and disruption of DNA repair (DNA ligase IV inactivation) or cell cycle regulation (Kipl, Ink4d, or Inkd.c inactivat...Medulloblastoma is the most common malignant pediatric brain tumor. In mice, Ptcl haploinsufficiency and disruption of DNA repair (DNA ligase IV inactivation) or cell cycle regulation (Kipl, Ink4d, or Inkd.c inactivation), in conjunction with p53 dysfunction, predispose to medulloblastoma. To identify genes important for this tumor, we evaluated gene expression profiles in medulloblastomas from these mice. Unexpectedly, medulloblastoma展开更多
文摘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.
文摘Medulloblastoma is the most common malignant pediatric brain tumor. In mice, Ptcl haploinsufficiency and disruption of DNA repair (DNA ligase IV inactivation) or cell cycle regulation (Kipl, Ink4d, or Inkd.c inactivation), in conjunction with p53 dysfunction, predispose to medulloblastoma. To identify genes important for this tumor, we evaluated gene expression profiles in medulloblastomas from these mice. Unexpectedly, medulloblastoma
