NDLI: Reprogramming of a melanoma genome by nuclear transplantation.

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Reprogramming of a melanoma genome by nuclear transplantation.

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Reprogramming of a melanoma genome by nuclear transplantation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Hochedlinger, Konrad Blelloch, Robert Brennan, Cameron Yamada, Yasuhiro Kim, Minjung Chin, Lynda Jaenisch, Rudolf
Description	Country affiliation: United States Author Affiliation: Hochedlinger K ( Whitehead Institute for Biomedical Research, and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02142, USA.)
Abstract	We have used nuclear transplantation to test whether the reprogramming activity of oocytes can reestablish developmental pluripotency of malignant cancer cells. We show here that the nuclei of leukemia, lymphoma, and breast cancer cells could support normal preimplantation development to the blastocyst stage but failed to produce embryonic stem (ES) cells. However, a blastocyst cloned from a RAS-inducible melanoma nucleus gave rise to ES cells with the potential to differentiate into multiple cell types in vivo including melanocytes, lymphocytes, and fibroblasts. Chimeras produced from these ES cells developed cancer with higher penetrance, shorter latency, and an expanded tumor spectrum when compared with the donor mouse model. These results demonstrate that the secondary changes of a melanoma nucleus are compatible with a broad developmental potential but predispose mice to melanomas and other malignant tumors on reactivation of RAS. Our findings serve as a paradigm for studying the tumorigenic effect of a given cancer genome in the context of a whole animal.
File Format	HTM / HTML
ISSN	08909369
e-ISSN	15495477
Journal	Genes & Development
Issue Number	15
Volume Number	18
Language	English
Publisher	Cold Spring Harbor Laboratory Press
Publisher Date	2004-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Molecular Discipline Biology__semicolon__developmental Discipline Biology__semicolon__genetics__semicolon__cell Discipline Biology Genome Melanoma Pathology Nuclear Transfer Techniques Animals Blastocyst Cytology Metabolism Breast Neoplasms Cell Differentiation Chimera Dna-binding Proteins Genetics Physiology Embryo, Mammalian Fibroblasts Genes, Ras Leukemia Lymphocytes Lymphoma Melanocytes Mice Mice, Inbred C57bl Mice, Scid Oocytes Stem Cells Tumor Cells, Cultured Research Support, Non-u.s. Gov't Research Support, U.s. Gov't, P.h.s.
Content Type	Text
Resource Type	Article
Subject	Genetics Developmental Biology

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Alternative lengthening of telomeres in normal mammalian somatic cells.

De novo DNA methylation by Dnmt3a and Dnmt3b is dispensable for nuclear reprogramming of somatic cells to a pluripotent state.

Aberrant cell cycle checkpoint function and early embryonic death in Chk1(-/-) mice.

FoxO transcription factors suppress Myc-driven lymphomagenesis via direct activation of Arf.

Kindlin-2 controls bidirectional signaling of integrins.

DNA methylation dynamics during epigenetic reprogramming in the germline and preimplantation embryos.

Ku acts in a unique way at the mammalian telomere to prevent end joining.

Large-scale gene trapping in C57BL/6N mouse embryonic stem cells.

Beta-catenin induces immortalization of melanocytes by suppressing p16INK4a expression and cooperates with N-Ras in melanoma development.

Reprogramming of a melanoma genome by nuclear transplantation.

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De novo DNA methylation by Dnmt3a and Dnmt3b is dispensable for nuclear reprogramming of somatic cells to a pluripotent state.

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FoxO transcription factors suppress Myc-driven lymphomagenesis via direct activation of Arf.

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Beta-catenin induces immortalization of melanocytes by suppressing p16INK4a expression and cooperates with N-Ras in melanoma development.

Reprogramming of a melanoma genome by nuclear transplantation.