Among ER positive tumors, a higher dormancy score is significantly associated with lower hazard of metastasis. Models of in vivo tumor dormancy driven by tumor cell quiescence or angiogenic failure have identified gene signatures associated with these phenotypes. We hypothesized that these signatures would be helpful in identifying tumors whose disseminated cells would be more prone to undergo dormancy. Based on these expression profiles, we generated a 49-gene signature for tumor cell dormancy, in which we consider genes upregulated in dormant cells as positive dormancy genes and genes downregulated in dormant cells as negative dormancy genes. For each gene, we scaled the expression intensities by dividing them by their average intensity across samples. Then we defined the dormancy score as the difference between the sum of log intensities of the positive dormancy genes and the sum of the log intensities of the negative dormancy genes. All genes were equally weighted in their contributions to the dormancy score. Thus, we set out to determine Cetylpyridinium Chloride whether tumors or cell lines that have a higher dormancy score showed any association with clinico-pathological parameters. We first applied the dormancy score to published microarray data of 51 breast Protopanaxtriol cancer cell lines grown in tissue culture. We found that ER positive breast cancer cell lines have significantly higher dormancy scores than ER negative ones. To test if the in vivo conditions in patients reveal a similar or better relationship between the dormancy scores and breast cancer progression, we evaluated the dormancy signatures of clinical breast cancer samples. We used four published microarray data sets that included well annotated invasive breast cancers with at least seven years of follow-up. We performed an analysis of all the samples in the four studies, stratified by study, and found that the dormancy scores were significantly higher in ER+ tumors compared to ER- tumors. This is consistent with our analysis of the breast cancer cell lines. Analysis of the individual studies also showed a significantly higher dormancy score in ER+ vs. ERtumors in three out of four while one study showed a weak trend in the same direction. Thus, although the genes selected for the dormancy score were identified from gene expression patterns of cell lines grown in tissue culture, their predictive value for an in vivo phenotype in the experimental models could be extended to differentiating between primary tumors with different ER status. Examination of the clustering of the clinical samples revealed a difference between the positive and negative dormancy genes. The set of negative dormancy genes that was upregulated in the tumors with low dormancy scores was similar to the set that we observed in the cell lines;