Antimetastatic gene expression profiles mediated by retinoic acid receptor beta 2 in MDA-MB-435 breast cancer cells-2

<p><b>Copyright information:</b></p><p>Taken from "Antimetastatic gene expression profiles mediated by retinoic acid receptor beta 2 in MDA-MB-435 breast cancer cells"</p><p>BMC Cancer 2005;5():140-140.</p><p>Published online 28 Oct 2005</p><p>PMCID:PMC1283145.</p><p>Copyright © 2005 Wallden et al; licensee BioMed Central Ltd.</p>on of cancer antigens, tumor suppressors, and genes involved in interferon signalling. Other gene activities are suppressed through RARβ2 action: AP1, cell adhesion, and nutrient processes. All gene activities in this diagram have been confirmed by cell culture qRT-PCR. Gene names in italics (red), have also been confirmed using randomly selected xenograft primary tumors, comparing two pairs of vector control- and RARβ2-resected tumors

Antimetastatic gene expression profiles mediated by retinoic acid receptor beta 2 in MDA-MB-435 breast cancer cells-0

<p><b>Copyright information:</b></p><p>Taken from "Antimetastatic gene expression profiles mediated by retinoic acid receptor beta 2 in MDA-MB-435 breast cancer cells"</p><p>BMC Cancer 2005;5():140-140.</p><p>Published online 28 Oct 2005</p><p>PMCID:PMC1283145.</p><p>Copyright © 2005 Wallden et al; licensee BioMed Central Ltd.</p>Using total RNA used in the arrays, Northern blots were probed with P-dCTP labelled RARβ2 or CTAG1 cDNA. The RARβ2 probe consists of ~1.2 kb KpnI-BamH1 digest fragment of pSG RARβ2 ([75], from Pierre Chambon). The CTAG1 probe was generated from a 463 bp reverse transcriptase PCR product that encompasses the Agilent 60-mer. Blots were sequentially probed with a cDNA for RPLP0 (36B4) as a loading and transfer control. Quantitation of relative transcript levels was normalized to RPLP0 by phosphorimaging using exposure levels within the linear range of detection, avoiding saturation. The RARβ2 mRNA includes elements transcribed from the retroviral vector [8]

Antimetastatic gene expression profiles mediated by retinoic acid receptor beta 2 in MDA-MB-435 breast cancer cells-1

<p><b>Copyright information:</b></p><p>Taken from "Antimetastatic gene expression profiles mediated by retinoic acid receptor beta 2 in MDA-MB-435 breast cancer cells"</p><p>BMC Cancer 2005;5():140-140.</p><p>Published online 28 Oct 2005</p><p>PMCID:PMC1283145.</p><p>Copyright © 2005 Wallden et al; licensee BioMed Central Ltd.</p> were probed with a 1384 bp fragment of SPP1 (see methods) or 800 bp, fragment of RPLP0 (36B4). Phosphorimaging was used for detection and quantitation. B. Western immunoblot analysis. Two independent preparations of each clonal cell line were used. Three mL of serum free-media from 3 × 10cell equivalents was immunoblotted, using a goat anti-SPP1/osteopontin polyclonal antibody (antibody and recombinant protein were a gift from Dr. CM Giachelli) and a secondary rabbit anti-goat antibody (Pierce)

Additional file 1: of Pan-cancer adaptive immune resistance as defined by the Tumor Inflammation Signature (TIS): results from The Cancer Genome Atlas (TCGA)

Figure S7. Distribution of TIS scores in stage IV disease. TIS scores are shown for all TCGA patients with stage 4 disease. Cancer types are ordered by median TIS score in all patients, identical to Fig. 1. (PDF 30 kb

Additional file 2: of Pan-cancer adaptive immune resistance as defined by the Tumor Inflammation Signature (TIS): results from The Cancer Genome Atlas (TCGA)

Figure S1. Meta-analysis of TIS score with objective response rates. [21, 50, 57–106]. (PDF 6 kb

Additional file 3: of Pan-cancer adaptive immune resistance as defined by the Tumor Inflammation Signature (TIS): results from The Cancer Genome Atlas (TCGA)

Figure S6. Distribution of TIS scores within two MSI status categories and three cancer types. Points show individual samples’ TIS scores. (PDF 31 kb

Additional file 5: of Pan-cancer adaptive immune resistance as defined by the Tumor Inflammation Signature (TIS): results from The Cancer Genome Atlas (TCGA)

Figure S4. GO terms with the strongest negative association with TIS. Color shows GSA score. (PDF 16 kb

Additional file 9: of Pan-cancer adaptive immune resistance as defined by the Tumor Inflammation Signature (TIS): results from The Cancer Genome Atlas (TCGA)

Figure S5. Association between TIS score and breast cancer survival. Breast cancers were divided in 4 subsets based on their TIS scores. Kaplan-Meier curves and confidence intervals are shown for each subset. (PDF 17 kb

Additional file 4: of Pan-cancer adaptive immune resistance as defined by the Tumor Inflammation Signature (TIS): results from The Cancer Genome Atlas (TCGA)

Figure S2. In order to assess whether/how cancer cell of origin could directly affect the expression of TIS genes, the observed expression level for each gene versus the expected expression level based on total TIS score was evaluated. Specifically, for each algorithm gene, a linear mixed model (LMM) was fit predicting the gene’s log2 expression from TIS score and cancer type, with cancer type modelled as a random effect. The LMM’s variance term for cancer type was compared to each gene’s marginal variance across TCGA datasets. (PDF 4 kb

Additional file 6: of Pan-cancer adaptive immune resistance as defined by the Tumor Inflammation Signature (TIS): results from The Cancer Genome Atlas (TCGA)

Table S1. For each cancer type, GO terms with negative associations with TIS, defined as a GSA score below − 1. (CSV 48 kb