10 research outputs found

    Supplementary Tables 1 - 3 from <i>BRAF</i> V600E Is a Determinant of Sensitivity to Proteasome Inhibitors

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    XLSX file - 144K, Supplementary table S1. List of compounds employed in the present work. Supplementary Table S2. List of t-tests p values comparing the responses of the different mutant cell lines to a given drug concentration with the response of the WT Scramble control cells. Supplementary Table S3. List of the drugs included in the library and tested on HME-1 cell lines.</p

    Supplementary Material from BCAM and LAMA5 Mediate the Recognition between Tumor Cells and the Endothelium in the Metastatic Spreading of KRAS-Mutant Colorectal Cancer

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    The supplementary material includes Supplementary Methods, two Supplementary Tables, and six Supplementary Figures Table S1. Complete set of BCAM-mimic peptides. Table S2. Characterization of human CRC cell lines in animal models. Figure S1. Quality control of the phage display experiments: sequencing readout. Figure S2. BCAM protein expression in the complete panel of human hepatic metastases. Figure S3. BCAM protein expression in human primary CRCs. Figure S4. BCAM protein and mRNA expression in all cell lines. Figure S5. Photographic documentation of the experimental hepatic metastasis models. Figure S6. HT-55, DLD-1, LIM1215 and SW-48 cells cannot be reduced to adhesion-functional monocellular suspensions.</p

    Supplementary Methods, Figure Legends, Table Legends, Figures S1 - S4, Tables S1 - S5 from Acquired Resistance to the TRK Inhibitor Entrectinib in Colorectal Cancer

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    Supplementary Figure S1. LMNA-NTRK1 genetic rearrangement detected in patient's plasma and xeno. Supplementary Figure S2. Acquisition of mutations in the TRKA kinase domain drives secondary resistance to entrectinib in Ba/F3 TRKA WT cells. Supplementary Figure S3. NTRK1 mutations confer resistance to TRKA inhibition. Supplementary Figure S4. Homology alignment of NTRK1 p.G595 and p.G667 variants. Supplementary Table S1. NGS analysis of NTRK1 gene in patient's plasma and xeno. Supplementary Table S2. NGS analysis of patient's derived samples. Supplementary Table S3. Summary of serial ctDNA analyses. Supplementary Table S4. The p.G595R and p.G667C mutations confer resistance to multiple TRK inhibitors. Supplementary Table S5. NTRK1 p. G595R, p.G667C and LMNA-NTRK1 fusion probes for ddPCR.</p

    Supplementary Figures and Tables from Molecular Landscape of Acquired Resistance to Targeted Therapy Combinations in <i>BRAF</i>-Mutant Colorectal Cancer

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    Supplementary Tables S1-S3 - List of drug concentrations to generate resistant cell lines (S1); Drug concentrations applied in the screening depicted in Figure 6 (S2); Primers for gene amplification and sequencing (S3). Supplementary Figure S1. Synergistic activity of targeted therapy combinations in BRAF mutant colorectal cancer cells. Supplementary Figure S2. Amplification of mutant BRAF V600E confers resistance to combined EGFR and MEK targeting in colorectal cancer cells. Supplemental Figure S3. Cytotoxicity induced by ERK inhibition in VACO432 resistant to BRAF combination therapies.</p
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