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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.
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Hinds et al. (1994) studied this question.
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