Correlation of simultaneous differential gene expression in the blood and heart with known mechanisms of XXXX -induced @entity296 in the rat.

@entity1 @entity632 @entity137 @entity296 @entity6211 @entity5 @entity299 @entity1370
As the genomes of @entity1 species become sequenced and gene functions are ascribed, the use of differential gene expression (DGE) to evaluate organ function will become common in the experimental evaluation of new drug therapies. The ability to translate this technology into useful information for @entity1 exposures depends on tissue sampling that is impractical or generally not possible in @entity1 . The possibility that the DGE of nucleated cells, reticulocytes, or platelets in blood may present the necessary link with target organ @entity137 provides an opportunity to correlate preclinical with clinical outcomes. @entity632 is highly effective alone and more frequently in combination with other chemotherapeutic agents in the treatment of a variety of susceptible @entity5 . @entity632 -induced @entity296 was examined as an endpoint to measure the utility of DOE on whole blood as a predictor of @entity1370 . Statistically significant gene changes were observed between relevant blood and cardiac gene profiles that corroborated the accepted mechanisms of @entity137 (oxidative stress, effects on @entity6211 transport, DNA intercalation). There were, however, clear indications that other target organs (bone marrow and intestinal tract) were affected. The divergent expression of some genes between the blood and the heart on day 7 may also indicate the timing and mechanism of development of the @entity296 and confirm current therapeutic approaches for its prevention. The data demonstrate that whole blood gene expression particularly in relation to oxidative stress, in conjunction with standard hematology and clinical chemistry, may be useful in monitoring and predicting @entity299 secondary to @entity632 administration. Appendices A _ B, referenced in this paper, are not printed in this issue of Toxicologic Pathology. They are available as downloadable text files at http://taylorandfrancis.metapress.com/openurl.asp?genre=journal_issn=0192-6233. To access them, click on the issue link for 30(4), then select this article. A download option appears at the bottom of this abstract. In order to access the full article online, you must either have an individual subscription or a member subscription accessed through www.toxpath.org.
