Use of Restriction Fragment Length Polymorphisms to Determine the Clonal Origin of Human Tumors
- 8 February 1985
- journal article
- research article
- Published by American Association for the Advancement of Science (AAAS) in Science
- Vol. 227 (4687) , 642-645
- https://doi.org/10.1126/science.2982210
Abstract
A novel strategy to determine the clonal origin of human tumors has been devised. The strategy involves the use of a cloned polymorphic X-chromosomal gene and two restriction endonucleases. The first endonuclease distinguishes the paternal and maternal copies of the gene through a DNA polymorphism of restriction fragment length. The second endonuclease distinguishes active from inactive copies of this gene through changes in DNA methylation. As illustrations of this strategy, three human cancers were each shown to be monoclonal. The analysis described should have a wide variety of clinical and experimental applications.This publication has 32 references indexed in Scilit:
- Detection of specific sequences among DNA fragments separated by gel electrophoresisPublished by Elsevier ,2006
- Biclonal B-Cell LymphomaNew England Journal of Medicine, 1984
- A Clonal Complete Remission in a Patient with Acute Nonlymphocytic Leukemia Originating in a Multipotent Stem CellNew England Journal of Medicine, 1984
- Monoclonality of Lymphoproliferative Lesions in Cardiac-Transplant RecipientsNew England Journal of Medicine, 1984
- Fatal Lymphoma after Transplantation of Cultured Thymus in Children with Combined Immunodeficiency DiseaseNew England Journal of Medicine, 1979
- Use of restriction enzymes to study eukaryotic DNA methylationJournal of Molecular Biology, 1978
- Enhanced autoradiographic detection of 32P and 125I using intensifying screens and hypersensitized filmFEBS Letters, 1977
- Multicellular Origin of Parathyroid “Adenomas”New England Journal of Medicine, 1977
- Labeling deoxyribonucleic acid to high specific activity in vitro by nick translation with DNA polymerase IJournal of Molecular Biology, 1977
- Stability of X Chromosomal Inactivation in Human Somatic CellsNature, 1972