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<p>To address the prognostic limitations in breast cancer (BRCA), we integrated transcriptomic profiles from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) to construct a novel 9-gene autophagy-related signature via Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression. The model demonstrated robust predictive accuracy for overall survival in the training cohort (HR = 2.28, <i>P &lt;</i> 0.001) and maintained stability in external validation (AUC = 0.740). Mechanistically, the risk score was significantly associated with selective autophagy pathways and an immune-exhausted microenvironment characterized by T-cell dysfunction. Furthermore, drug sensitivity profiling identified a positive correlation between the risk gene MTDH and sensitivity to Vincristine and Gemcitabine. This study presents a reliable risk-stratification tool that bridges autophagic mechanisms with personalized chemotherapy guidance.</p>

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Identification of a 9-gene autophagy-related signature for predicting prognosis and immune exhaustion features in breast cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月10日

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  • Jianan Zhang,
  • Yijun Wang,
  • Mengsha Zou

摘要

To address the prognostic limitations in breast cancer (BRCA), we integrated transcriptomic profiles from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) to construct a novel 9-gene autophagy-related signature via Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression. The model demonstrated robust predictive accuracy for overall survival in the training cohort (HR = 2.28, P < 0.001) and maintained stability in external validation (AUC = 0.740). Mechanistically, the risk score was significantly associated with selective autophagy pathways and an immune-exhausted microenvironment characterized by T-cell dysfunction. Furthermore, drug sensitivity profiling identified a positive correlation between the risk gene MTDH and sensitivity to Vincristine and Gemcitabine. This study presents a reliable risk-stratification tool that bridges autophagic mechanisms with personalized chemotherapy guidance.