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        <datestamp>2026-09-22T09:22:31Z</datestamp>
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          <dc:title>Supporting data for Genetic Alterations and Age-Dependent Precision Treatment of Liver Cancer</dc:title>
          <dc:creator>Helen Do Gai Xue (13269171)</dc:creator>
          <dc:subject>Cancer cell biology</dc:subject>
          <dc:subject>Molecular targets</dc:subject>
          <dc:subject>Solid tumours</dc:subject>
          <dc:subject>Cancer therapy (excl. chemotherapy and radiation therapy)</dc:subject>
          <dc:subject>Liver Cancer Combination therapy</dc:subject>
          <dc:subject>Therapeutic resistance</dc:subject>
          <dc:subject>Targeted therapy.</dc:subject>
          <dc:description>&lt;p dir="ltr"&gt;This study explores the underlying mechanism by which mitochondrial translation supports therapeutic resistance to ivosidenib, which is the targeted therapy for IDH1-mutated intrahepatic cholangiocarcinoma. Using a genome-wide CRISPR library screen in iCCA cells, we identified MTFMT and MTRF1L, mitochondrial translation regulators, as key resistance mechanisms. MTFMT and MTRF1L knockdown combined with ivosidenib treatment suppressed cell proliferation and enhanced apoptosis. In the dataset, normalized sgRNA read counts from the genome-wide CRISPR library screen were analysed, and mRNA expression of MTFMT and MTRF1L in TCGA patient tumor and non-tumor were analysed. qRT-PCR analysis was performed to study MTFMT and MTRF1L mRNA after knockdown. Cell proliferation and Annexin-V assays were used to study cell proliferation and apoptosis under the combination of KD-MTFMT/MTRF1L and ivsosidenib. &lt;/p&gt;</dc:description>
          <dc:date>2026-09-22T09:22:31Z</dc:date>
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          <dc:identifier>10.25442/hku.33348066.v1</dc:identifier>
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          <dc:rights>Open Access after 2030-08-31</dc:rights>
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