The Stem Cell Podcast

Ep. 87: “Cancer Stem Cell Evasion” Featuring Dr. Justin Lathia

Mar 14, 2017
Dr. Justin Lathia, an assistant professor studying how stem cell programs drive tumor progression and therapy resistance, discusses cancer stem cell heterogeneity and why some tumors stay lethal. He explains how treatment shapes more aggressive cells. He describes how cancer stem cells suppress TLR4 to evade immune signals and outlines therapeutic strategies to restore or target that pathway.
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INSIGHT

Stem Cell State Drives Post-Therapy Tumor Evolution

  • Tumor cellular heterogeneity is driven in part by a persistent cancer stem cell state that survives therapy and fuels recurrence.
  • Justin Lathia explains therapy enriches stem-like cells which inherit more survival receptors into daughter cells, promoting aggressive post-treatment tumors.
INSIGHT

Glioblastoma Stem Cells Silence TLR4 To Evade Damage Signals

  • Cancer stem cells in glioblastoma downregulate TLR4 to avoid damage signals that would suppress their self-renewal.
  • Restoring TLR4 expression or activating its pathway engages RBBP5 and shuts down self-renewal via stem transcription factor control.
INSIGHT

TLR4 Signals Can Promote Or Inhibit Stemness Depending On Context

  • TLR4 signaling outcomes are tissue-specific and depend on adapter usage such as MyD88, producing opposite effects in different cancers.
  • Lathia notes liver cancer uses MyD88-dependent TLR4 to support stemness, whereas glioblastoma uses a MyD88-independent pathway.
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