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tcga gistic2 gene-level copy number and somatic mutation data  (Broad Institute Inc)

 
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    Broad Institute Inc tcga gistic2 gene-level copy number and somatic mutation data
    Tcga Gistic2 Gene Level Copy Number And Somatic Mutation Data, supplied by Broad Institute Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 90 stars, based on 1 article reviews
    tcga gistic2 gene-level copy number and somatic mutation data - by Bioz Stars, 2026-07
    90/100 stars

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    KRAS G13D CRC cells are sensitive to NF1-mediated GTP hydrolysis. (A) Total number of mutations per sample in KRAS G12- and G13-mutated COAD from <t>TCGA</t> cancer samples (P = 0.018). (B) Mutational burden comparing KRAS codon 12 and codon 13 mutations with mismatch repair mutations and microsatellite instability (MSI-H, MSI high; MSI-L, MSI low; MSS, MS stable) in TCGA COAD samples. (C) Comparison of NF1 mutations and KRAS mutation status in CCLE cell lines. Category sample sizes are indicated above each bar. (D) NF1 overexpression in HCT-116, a KRAS G13D/NF1-mutated cell line, leads to reduced KRAS-GTP levels.
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    Image Search Results


    Boxplot for the unexplained variations between TCGA pseudo-bulk and real-bulk RNA data for evaluation of the Scaden-CA model The definition of the boxplot (box range, whiskers, and outliers) is the same as described in <xref ref-type=Figure 1 . " width="100%" height="100%">

    Journal: Patterns

    Article Title: Predicting drug response through tumor deconvolution by cancer cell lines

    doi: 10.1016/j.patter.2024.100949

    Figure Lengend Snippet: Boxplot for the unexplained variations between TCGA pseudo-bulk and real-bulk RNA data for evaluation of the Scaden-CA model The definition of the boxplot (box range, whiskers, and outliers) is the same as described in Figure 1 .

    Article Snippet: TCGA RNA, somatic mutation, and phenotypic data were downloaded from the University of California, Santa Cruz (UCSC) Xena browser ( https://xenabrowser.net/datapages/ ).

    Techniques:

    Validation of the drug response prediction algorithm by clinical drug treatment data (A) Boxplot for the predicted cell viability in patients with lung squamous cell carcinoma (LUSC) who did or did not respond to gemcitabine. (B) Boxplot for the predicted cell viability in patients with esophageal carcinoma (ESCA) among those who did or did not respond to cisplatin. Samples used were from TCGA. The definition of boxplots (box range, whiskers, and outliers) is the same as described in <xref ref-type=Figure 1 , and the definition of p values are the same as . " width="100%" height="100%">

    Journal: Patterns

    Article Title: Predicting drug response through tumor deconvolution by cancer cell lines

    doi: 10.1016/j.patter.2024.100949

    Figure Lengend Snippet: Validation of the drug response prediction algorithm by clinical drug treatment data (A) Boxplot for the predicted cell viability in patients with lung squamous cell carcinoma (LUSC) who did or did not respond to gemcitabine. (B) Boxplot for the predicted cell viability in patients with esophageal carcinoma (ESCA) among those who did or did not respond to cisplatin. Samples used were from TCGA. The definition of boxplots (box range, whiskers, and outliers) is the same as described in Figure 1 , and the definition of p values are the same as .

    Article Snippet: TCGA RNA, somatic mutation, and phenotypic data were downloaded from the University of California, Santa Cruz (UCSC) Xena browser ( https://xenabrowser.net/datapages/ ).

    Techniques: Biomarker Discovery

    Interactive analyses of molecular pathways in bladder cancer development from field effects with their validation in the TCGA cohort (A) Combined selected monotonically dysregulated pathways in field effects of both luminal and basal maps (One-sided Fisher exact test p value). (B) Differential enrichment scores for the regulons controlling immunity, inflammation, signal transduction/differentiation, and oncogenesis in molecular subtypes of bladder cancer in the TCGA cohort (n = 408). (C) Expression pattern for selected genes in the regulons of ILs, epidermal growth factor, and ovarian cancer signaling in the molecular subtypes of bladder cancer in the TCGA cohort (n = 408).

    Journal: iScience

    Article Title: The origin of bladder cancer from mucosal field effects

    doi: 10.1016/j.isci.2022.104551

    Figure Lengend Snippet: Interactive analyses of molecular pathways in bladder cancer development from field effects with their validation in the TCGA cohort (A) Combined selected monotonically dysregulated pathways in field effects of both luminal and basal maps (One-sided Fisher exact test p value). (B) Differential enrichment scores for the regulons controlling immunity, inflammation, signal transduction/differentiation, and oncogenesis in molecular subtypes of bladder cancer in the TCGA cohort (n = 408). (C) Expression pattern for selected genes in the regulons of ILs, epidermal growth factor, and ovarian cancer signaling in the molecular subtypes of bladder cancer in the TCGA cohort (n = 408).

    Article Snippet: TCGA mutational data , Broad Institute Genome Data Analysis Centers TCGA , http://gdac.broadinstitute.org/.

    Techniques: Biomarker Discovery, Transduction, Expressing

    KRAS G13D CRC cells are sensitive to NF1-mediated GTP hydrolysis. (A) Total number of mutations per sample in KRAS G12- and G13-mutated COAD from TCGA cancer samples (P = 0.018). (B) Mutational burden comparing KRAS codon 12 and codon 13 mutations with mismatch repair mutations and microsatellite instability (MSI-H, MSI high; MSI-L, MSI low; MSS, MS stable) in TCGA COAD samples. (C) Comparison of NF1 mutations and KRAS mutation status in CCLE cell lines. Category sample sizes are indicated above each bar. (D) NF1 overexpression in HCT-116, a KRAS G13D/NF1-mutated cell line, leads to reduced KRAS-GTP levels.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: KRAS G13D sensitivity to neurofibromin-mediated GTP hydrolysis

    doi: 10.1073/pnas.1908353116

    Figure Lengend Snippet: KRAS G13D CRC cells are sensitive to NF1-mediated GTP hydrolysis. (A) Total number of mutations per sample in KRAS G12- and G13-mutated COAD from TCGA cancer samples (P = 0.018). (B) Mutational burden comparing KRAS codon 12 and codon 13 mutations with mismatch repair mutations and microsatellite instability (MSI-H, MSI high; MSI-L, MSI low; MSS, MS stable) in TCGA COAD samples. (C) Comparison of NF1 mutations and KRAS mutation status in CCLE cell lines. Category sample sizes are indicated above each bar. (D) NF1 overexpression in HCT-116, a KRAS G13D/NF1-mutated cell line, leads to reduced KRAS-GTP levels.

    Article Snippet: TCGA mutation and clinical data were downloaded from the Broad Institute GDAC firehose website ( https://gdac.broadinstitute.org/ ).

    Techniques: Comparison, Mutagenesis, Over Expression