Frequent somatic mutations of the transcription factor ATBF1 in human prostate cancer

Xiaodong Sun, Henry F. Frierson, Ceshi Chen, Changling Li, Qimei Ran, Kristen B. Otto, Brandi M. Cantarel, Robert L. Vessella, Allen C. Gao, John Petros, Yutaka Miura, Jonathan W. Simons, Jin Tang Dong

Research output: Contribution to journalArticlepeer-review

136 Scopus citations


Cancer often results from the accumulation of multiple genetic alterations. Although most malignancies are sporadic, only a small number of genes have been shown to undergo frequent mutations in sporadic cancers. The long arm of chromosome 16 is frequently deleted in human cancers, but the target gene for this deletion has not been identified1-4. Here we report that ATBF1, which encodes a transcription factor that negatively regulates AFP and MYB 5,6 but transactivates CDKN1A7, is a good candidate for the 16q22 tumor-suppressor gene. We narrowed the region of deletion at 16q22 to 861 kb containing ATBF1. ATBF1 mRNA was abundant in normal prostates but more scarce in approximately half of prostate cancers tested. In 24 of 66 (36%) cancers examined, we identified 22 unique somatic mutations, many of which impair ATBF1 function. Furthermore, ATBF1 inhibited cell proliferation. Hence, loss of ATBF1 is one mechanism that defines the absence of growth control in prostate cancer.

Original languageEnglish (US)
Pages (from-to)407-412
Number of pages6
JournalNature genetics
Issue number4
StatePublished - Apr 2005

ASJC Scopus subject areas

  • Genetics


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