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Updated: Jul 15, 2025

Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen
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Enhancement of Apoptotic and Autophagic Induction by a Novel Synthetic C-1 Analogue of 7-deoxypancratistatin in Human Breast Adenocarcinoma and Neuroblastoma Cells with Tamoxifen

Published on: May 30, 2012

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KRAS Inhibition Activates an Actionable CD24 "Don't Eat Me" Signal in Pancreatic Cancer

Yongkun Wei, Minghui Liu, Er-Yen Yen

    Biorxiv : the Preprint Server for Biology
    |October 4, 2023
    PubMed

    Insights

    Targeting KRAS G12C in pancreatic cancer shows modest benefit. Blocking CD24, a

    Area of Science:

    • Oncology
    • Cancer Biology
    • Immunology

    Background:

    • KRAS G12C inhibitors offer limited clinical benefit in pancreatic ductal adenocarcinoma (PDAC), necessitating research into resistance mechanisms.
    • Developing faithful preclinical models is essential for understanding PDAC tumor biology and identifying therapeutic vulnerabilities.
    • Oncogenic KRAS alleles exhibit distinct biology, impacting therapeutic strategies in PDAC.

    Conclusions:

    • CD24 is an actionable adaptive resistance mechanism in PDAC treated with KRAS G12C inhibitors.
    • Combining KRAS inhibitors with CD24 blockade represents a promising strategy to improve therapeutic efficacy in PDAC.
    • This study elucidates common and distinct KRAS allele-specific biology, offering insights into PDAC treatment.

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