Abstract
The cyclin D1 (PRAD1, CCND1) gene is affected by translocations and amplification in the genomes of a number of human tumors, suggesting that these changes confer growth advantage on developing tumor cell clones. We show here that in cultured cells, a cDNA clone of the cyclin D1 gene can contribute to cell transformation by complementing a defective adenovirus E1A oncogene. In such cells, this candidate oncogene indeed functions like an oncogene, suggesting a similar role in tumor progression in vivo.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Adenovirus E1A Proteins / genetics
-
Alleles
-
Amino Acid Sequence
-
Animals
-
Cell Line, Transformed
-
Cell Transformation, Neoplastic / genetics
-
Cells, Cultured
-
Cyclin D1
-
Cyclins / genetics*
-
Defective Viruses / genetics
-
Genes, Viral
-
Genetic Complementation Test
-
Humans
-
Molecular Sequence Data
-
Mutation
-
Oncogene Proteins / genetics*
-
Oncogenes*
-
Rats
-
Transfection
Substances
-
Adenovirus E1A Proteins
-
Cyclins
-
Oncogene Proteins
-
Cyclin D1