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sk-co-1  (CancerTools Org)


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    Structured Review

    CancerTools Org sk-co-1
    Sk Co 1, supplied by CancerTools Org, used in various techniques. Bioz Stars score: 99/100, based on 290 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/sk-co-1/SK-CO-1/custom%40161933%4042640371
    Average 99 stars, based on 290 article reviews
    sk-co-1 - by Bioz Stars, 2026-09
    99/100 stars

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    Related Articles

    Activity Assay:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Mutagenesis:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Invasion Assay:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Enzyme-linked Immunosorbent Assay:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Migration:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Expressing:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Inhibition:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Cell Isolation:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Cell Culture:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Drug discovery:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Isolation:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Reverse Transcription Polymerase Chain Reaction:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the

    Quantitative RT-PCR:

    Article Title: Exceptional treatment responses and molecular markers among 103 colorectal cancer cell lines.
    Article Snippet: alidity of the approach. This included FGFR inhibitors in the cell line NCI-H716, an ALK inhibitor in C10, and a PORCN inhibitor in SNU-1411 (Fig. S5a-c) [20, 24]. Furthermore, the cell lines KM12 and SK-CO-1 had outlier sensitivity to TRK and PARP inhibitors, respectively, which has previously been proposed to be associated with a TPM3-NTRK1 fusion and biallelic ATM mutation [25, 26]. However, the



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