15 research outputs found

    Observational Prospective Study to Determine the Evolution of the Symptomatic Profile of Metastatic Non-Small Cell Lung Cancer (NSCLC) Patients and Its Relation to the Control of the Disease

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    Full copyright for enhanced digital features is owned by the authors. Article full text The full text of this article can be found here. Provide enhanced digital features for this article If you are an author of this publication and would like to provide additional enhanced digital features for your article then please contact [email protected]. The journal offers a range of additional features designed to increase visibility and readership. All features will be thoroughly peer reviewed to ensure the content is of the highest scientific standard and all features are marked as ‘peer reviewed’ to ensure readers are aware that the content has been reviewed to the same level as the articles they are being presented alongside. Moreover, all sponsorship and disclosure information is included to provide complete transparency and adherence to good publication practices. This ensures that however the content is reached the reader has a full understanding of its origin. No fees are charged for hosting additional open access content. Other enhanced features include, but are not limited to: • Slide decks • Videos and animations • Audio abstracts • Audio slides</p

    Supplementary Figures 1 - 10, Tables 1 - 11 from Nondisruptive p53 Mutations Are Associated with Shorter Survival in Patients with Advanced Non–Small Cell Lung Cancer

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    PDF file - 280KB, Supplementary Table S1. Primers for TP53 genotyping. Supplementary Table S2. Cell lines used as controls for TP53, KRAS, BRAF and PIK3CA genotyping. Supplementary Table S3. Amplification conditions for TP53 genotyping. Supplementary Table S4. Primers for k-RAS, BRAF and PIK3CA genotyping. Supplementary Table S5. Amplification conditions for KRAS, BRAF and PIK3CA genotyping. Supplementary Table S6: Additional clinical and biological characteristics of the patients in the training and validation cohorts, according to EGFR status. Supplementary Table S7: Characteristics of the patients in the training cohort, classified according to EGFR and TP53 status. Supplementary Table S8: List of observed TP53 mutations (training and validation cohorts). Supplementary Table S9: Univariate Cox regression analysis of selected factors for overall survival in the EGFR-wt and EGFR-mut populations of the training cohort. Supplementary Table S10: Results of multivariate analysis of selected factors for overall survival in the EGFR-wt and EGFR-mut groups of the training cohort. Supplementary Table S11: GOF activities in cell line models of some nondisruptive TP53 mutations found in this study. Supplementary Figure S1: Structure of the TP53 protein representing the location of the mutations found in the training cohort. Supplementary Figure S2: Types of TP53 mutations in the training and validation cohorts. Supplementary Figure S3: Distribution of KRAS, BRAF and PIK3CA mutations in the training cohort. Supplementary Figure S4. Kaplan-Meier plots of overall and progression-free survival of the 318 patients in the training cohort, according to EGFR mutational status. Supplementary Figure S5. Kaplan-Meier plots of overall survival of the 125 EGFR-wt patients in the training cohort, according to G12C mutations in K-RAS. Supplementary Figure S6: Kaplan-Meier plots of overall and progression-free survival of the 318 patients in the training cohort, according to TP53 status. Supplementary Figure S7. Kaplan-Meier plots of overall survival of the 110 EGFR-wt patients in the training cohort not carrying G12C mutations in K-RAS. Supplementary Figure S8: Kaplan-Meier plots of progression-free survival of the 318 patients in the training cohort, according to TP53 mutational status. Supplementary Figure S9: Kaplan-Meier plots of progression-free survival in the training cohort, according to EGFR and TP53 mutational status. Supplementary Figure S10: Kaplan-Meier plots of progression-free survival in the training cohort, according to type of treatment.</p

    Supplementary Tables 1 - 9, Figures 1 - 5 from The Impact of <i>EGFR</i> T790M Mutations and <i>BIM</i> mRNA Expression on Outcome in Patients with <i>EGFR</i>-Mutant NSCLC Treated with Erlotinib or Chemotherapy in the Randomized Phase III EURTAC Trial

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    PDF file - 934K, Table S1. Quantification of T790M allele in our samples Table S2. Percentage of EGFR T790M mutation in each sample. Table S3. Results of the analysis of the T790M mutation in 705 paraffin-embedded lung tumor samples using our PNA method. Table S4. Primers for TP53 genotyping. Table S5. Cell lines used as controls for TP53 genotyping Table S6. Annealing conditions for TP53 genotyping. Table S7. Comparison of studies detecting the T790M mutation by different methods. Table S8. Summary of all systemic treatments after discontinuation of randomly assigned treatment in 95 patients included in the EURTAC study. Table S9. Response according to T790M status in both arms. Figure S1. Representation of deltaCt (mean) versus the ratio of the T790M allele in our in-house assay in (A, B) two separate dilution banks where the total amount of mutated DNA was 50 pg/microL and (C) in a dilution bank where the total amount of mutated DNA was 5 pg/microL. Figure S2. Progression-free survival according to T790M mutation status in (S1A) 50 patients treated with erlotinib and (S1B) 45 patients treated with chemotherapy. Figure S3. Progression-free survival according to T790M mutation status as determined by the TMDA in the entire cohort of 95 patients. Figure S4. Overall survival of 173 patients in the EURTAC trial at January 24, 2013. Figure S5. Overall survival of 83 patients with BIM expression data according to treatment arm and BIM mRNA expression levels.</p
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