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<p><i>KRAS</i> mutations drive pancreatic adenocarcinoma (PDAC) progression. This study investigates molecular heterogeneity among <i>KRAS</i> subtypes and their prognostic implications. This study explores <i>KRAS</i> mutations in PDAC, analyzing molecular heterogeneity and prognosis across our hospital cohort (SDFM, <i>n</i> = 113) with TCGA cohort (<i>n</i> = 183) and QCMG cohort (<i>n</i> = 383). <i>KRAS</i>, <i>TP53</i>, <i>CDKN2A</i>, and <i>SMAD4</i> were the main mutated genes. Co-mutations of <i>KRAS</i> with <i>TP53</i>, and <i>TP53</i> with <i>CDKN2A</i>, correlated with higher tumor mutation burden and poorer outcomes. <i>KRAS</i> subtypes G12D and Q16&amp;others had worse prognosis than G12V and G12R. Combining <i>TP53</i> status with <i>KRAS</i> subtypes improved risk stratification: high-risk patients had shorter survival (<i>P</i> ≤ 0.001), higher PD-L1 expression, P53 pathway alterations, fewer CD4+/CD8 + T cells and macrophages (<i>p</i> &lt; 0.05), but more neutrophils (<i>p</i> &lt; 0.001). These findings underscore the prognostic impact of <i>KRAS</i> and <i>TP53</i> mutations, guiding personalized treatment.</p>

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Molecular characterization and prognostic implications of KRAS mutations in pancreatic cancer patients: insights from multi-cohort analysis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月22日

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  • Yubo Jiang,
  • Gang Mai,
  • Xiaokai Zhao,
  • Meng Tang,
  • Pengmin Yang,
  • Qian Cheng,
  • He Tian,
  • Zuoxing Niu,
  • Xintao Wang,
  • Jiao Wang,
  • Yudong Zhu,
  • Jieyi Li,
  • Ziying Gong,
  • Daoyun Zhang,
  • Huirong Xu

摘要

KRAS mutations drive pancreatic adenocarcinoma (PDAC) progression. This study investigates molecular heterogeneity among KRAS subtypes and their prognostic implications. This study explores KRAS mutations in PDAC, analyzing molecular heterogeneity and prognosis across our hospital cohort (SDFM, n = 113) with TCGA cohort (n = 183) and QCMG cohort (n = 383). KRAS, TP53, CDKN2A, and SMAD4 were the main mutated genes. Co-mutations of KRAS with TP53, and TP53 with CDKN2A, correlated with higher tumor mutation burden and poorer outcomes. KRAS subtypes G12D and Q16&others had worse prognosis than G12V and G12R. Combining TP53 status with KRAS subtypes improved risk stratification: high-risk patients had shorter survival (P ≤ 0.001), higher PD-L1 expression, P53 pathway alterations, fewer CD4+/CD8 + T cells and macrophages (p < 0.05), but more neutrophils (p < 0.001). These findings underscore the prognostic impact of KRAS and TP53 mutations, guiding personalized treatment.