Table II. Genes more expressed in post-chemotherapy samples (pFDR<0.01 and Fc ò2).

FIG. 4a. Patterns of gene expression in TDPS vs panc-1 cells.

FIG. 4b. Patterns of gene expression in panc-1 cells vs TDPS .

Table 4—Deregulated genes in Pre-eclampsia (PE) versus control samples

Table 1: Candidates for sequencing analysis in the LNCaP and 22Rv1 selected using GINI

Refinement of a previously published signature called the Gene expression Grade Index (GGI; PMID: 16478745); The original GGI is composed of 128 affy probes (97 unique genes) and was translated to qRT-PCR technology

Table 2. Changes in cell cycle-related genes after PU.1 induction

Supplementary Table S1. Thirty genes showing the highest up-regulation at 3 days after PU.1 induction

Supplementary Table S2. Thirty genes showing the most down-regulation 1 day after PU.1 induction

Supplementary Table S3. Thirty genes showing the most down-regulation at 3 days after PU.1 induction

Table 1. Thirty genes showing the highest upregulation at day 1 after PU.1 induction

Table 1. Aberrantly expressed genes earlier identified in HCC that are also aberrantly regulated by the HCC–TR mutants

Table 2. Partial list of cancer-implicated genes aberrantly regulated by the HCC–TR mutants

Supplementary Table S2 List of the 174 genes that are specifically modified by the pazopanib/lapatinib combination in A549 cells

Table 2. Selected examples (see complete list in Supplementary Table S2) of the differential transcriptional effects in A549 cells promoted by single or combined treatments of pazopanib and lapatinib

Supplementary Table S3 List of the 58 genes from suppl. Table S2 which are modified specifically by the pazopanib/lapatinib combination in all the 5 cell lines studied.

Table S6. 418 differentially expressed genes  39 which overlapped with the 62 classification markers we identified

Table 3. P-value and q-value for the 28 genes constituting the gene signature

Table 4. Details of the 28 genes contained in discriminating profile

Table 1. Selected transcriptional markers associated with virulence of Mycobacterium tuberculosis. Differential gene regulation in response to virulent  H37Rv or attenuated H37Ra Mycobacterium tuberculosis infection of lungs at 2 time points (d14 versus d30 p.i) in WT mice and iNOS knockout mice. Both hosts exhibited highly similar resistance to infection with H37Ra. In contrast, iNOS ko mice rapidly succumbed to H37Rv, whereas WT mice developed chronic course of disease. By differential analyses, virulence-specific changes in global host gene expression were analyzed to identify molecular markers characteristic for chronic versus acute infection