A gene signature induced by activated TGF-beta type I receptor (Alk5 with the mutation T204D [Alk5(T204D)]) in HER2-overexpressing cells which correlated with poor clinical outcomes in patients with invasive breast cancer. Supplementary Table 1 Genes were filtered for expression changes greater than twofold in triplicate arrays with a t test P value of  0.01; 271 unique genes passed the criteria

Additional File 3. list of genes responsive to each of the eight different MCF7 treatment conditions in a study of the effect of oxidative stress on  ER-positive/PR-positive MCF7 breast cancer cells.  Cells were harvested 72 hours after estrogen deprivation  small-interfering RNA knockdown of ER-alpha  short-term (8 hours) exposure to various oxidant stresses (diamide  hydrogen peroxide  and menadione)  or simultaneous ER-alpha knockdown and oxidant stress

Table 3  Oxidant-sensitive estrogen/ER-responsive gene signature oxidant-sensitive estrogen/ER-responsive gene signature Ox-E/ER gene signature; Pathway analysis was performed using Ingenuity Pathway Systems  which identified three top networks represented within the 62-gene Ox-E/ER signature including those related to cancer  cell growth  and death  as well as cancer and cellular development

SuppTable1 Genes 1-50 Up-Regulated in MSCs when Compared to Fibroblasts

SuppTable2 Genes 51-100 Up-Regulated in MSCs when Compared to Fibroblasts

SuppTable3 Genes 1-50 Down-Regulated in MSCs when Compared to Fibroblasts

SuppTable4 Genes 51-100 Down-Regulated in MSCs when Compared to Fibroblasts

Table 2. Genes showing higher levels in OSCC (oral squamous cell carcinoma) with lymph node metastasis

Table 3. Genes showing lower levels in OSCC (oral squamous cell carcinoma) with lymph node metastasis

Supplementary Table 3-ERBB2 Gene Module; HER2 -phenotype gene module; the module was populated by genes being significantly correlated to ERBB2  as determined in a multivariate linear  model from which the corresponding z-scores were combined in a meta-analytical framework