PT  - JOURNAL ARTICLE
AU  - Rogulski, Kenneth R.
AU  - Freytag, Svend O.
AU  - Zhang, Kang
AU  - Gilbert, Jeff D.
AU  - Paielli, Dell L.
AU  - Kim, Jae Ho
AU  - Heise, Carla C.
AU  - Kirn, David H.
TI  - <em>In Vivo</em> Antitumor Activity of ONYX-015 Is Influenced by <em>p53</em> Status and Is Augmented by Radiotherapy
DP  - 2000 Mar 01
TA  - Cancer Research
PG  - 1193--1196
VI  - 60
IP  - 5
4099  - http://cancerres.aacrjournals.org/content/60/5/1193.short
4100  - http://cancerres.aacrjournals.org/content/60/5/1193.full
SO  - Cancer Res2000 Mar 01; 60
AB  - The E1B-deleted, replication-competent ONYX-015 (dl1520) adenovirus was originally described as being able to selectively kill p53-deficient cells due to a requirement of p53 inactivation for efficient viral replication. This hypothesis has become controversial because subsequent in vitro studies have demonstrated that the host range specificity of ONYX-015 is independent of p53 gene status. Using a pair of isogenic cell lines that differ only in their p53 status, we demonstrate here that although ONYX-015 can replicate in both p53 wild-type and mutant cells in vitro, the virus demonstrates significantly greater antitumor activity against mutant p53 tumors in vivo. Moreover, ONYX-015 viral therapy can be combined with radiation to improve tumor control beyond that of either monotherapy. The results demonstrate that ONYX-015 can discern in vivo between tumors having a different p53 status and that it may be an effective neoadjuvant to radiation therapy.