Validation of bevacizumab assay (n = 15).

<p>The coefficient of variation (CV) was calculated for each concentration point by dividing the mean by the standard deviation. The assay was validated for CVs under 20% (bold). Inaccuracy (bias) was calculated (mean minus value divided by value) only over the validated range.</p><p>NA: not applicable.</p

Patient characteristics.

<p>Serum bevacizumab concentrations were determined at the plateau (70 days; values labeled with an asterisk correspond to 56 days). M: Male; F: Female.</p

Bevacizumab assay calibration.

<p>Fluorescence intensity was measured on 15 independent assays over a large bevacizumab range (0–6 mg/mL).</p

Serum bevacizumab levels as a function of treatment efficacy.

<p>(▪) mean value for patients with side effects (n = 5); (▴)mean value for patients with residual angiogenesis (n = 4); (♦) mean value for patients responding favorably to treatment (n = 4).</p

Evolution of blood bevacizumab concentrations over the first 3 months of treatment.

<p>Points represent the mean bevacizumab concentrations for the 17 patients (+/− SD).The dotted line corresponds to the theoretical bevacizumab concentration in a 70-kg patient, with treatment by 7 repeat administrations of 10 mg/kg every other week. The theoretical value was calculated using the bevacizumab half-life reported by Roche-Genentech (20 days).</p

Additional file 1 of Aberrant activation of five embryonic stem cell-specific genes robustly predicts a high risk of relapse in breast cancers

Additional file 1: Fig. S1. (A) Heatmap showing the expression of 1882 genes in normal adult tissues with predominant expression in testis (male germinal), embryonic stem cells (ES cells) or placenta, and not expressed in normal breast (female genital). The expression levels of all genes are normalized by scaling each feature to a range between zero and one. The genes are ordered according their normalized expression levels in the tissues of interest (testis, placenta and ES cells, respectively). (B) Venn diagram showing the distribution of 1882 genes according the tissue of predominance: testis, embryonic stem cells and/or placenta. Fig. S2. Flow chart representing the main steps of the biomarker discovery pipeline. Fig. S3. Expression profiles in normal tissues of the five genes in the GEC panel DNMT3B, EXO1, MCM10, CENPF and CENPE based on RNA-seq data from GTEX and NCBI Sequence Read Archive. All five genes have a predominant expression profile in embryonic stem cells. They are also expressed in testis (male germinal) at lower levels. These genes are not expressed in normal breast and female genital tissues. Fig. S4. Kaplan-Meier individual survival curves of the genes DNMT3B, EXO1, MCM10, CENPF and CENPE in the training (TCGA-BRCA) and validation (GSE25066, GSE21653, GSE42568) datasets

Additional file 2 of Aberrant activation of five embryonic stem cell-specific genes robustly predicts a high risk of relapse in breast cancers

Additional file 2: Table S1. List of genes with predominant expression in testis, placenta and/or embryonic stem cells. Table S2. Frequencies of ectopic activations of the tissue-specific genes. Table S3. Results of the validation step in the biomarker discovery pipeline. Table S4. Datasets of normal tissues and breast cancers with corresponding sample sizes. Table S5. List of normal tissues and the corresponding sample sizes

Description of <i>DPYD</i> variations along with <i>in silico</i> / <i>in vitro</i> functionality.

<p>Description of <i>DPYD</i> variations along with <i>in silico</i> / <i>in vitro</i> functionality.</p

Association of variant combinations and/or DPD phenotype with capecitabine-related toxicity (maximum toxicity grade considering hematotoxicity, digestive and neurotoxicity).

<p>Association of variant combinations and/or DPD phenotype with capecitabine-related toxicity (maximum toxicity grade considering hematotoxicity, digestive and neurotoxicity).</p

CONSORT diagram.

<p>CONSORT diagram.</p