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.