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Dysregulated splicing factor SF3B1 unveils a dual therapeutic vulnerability to target pancreatic cancer cells and cancer stem cells with an anti-splicing drug.

Emilia Alors-PerezRicardo Blázquez-EncinasSonia AlcaláCristina Viyuela-GarcíaSergio Pedraza-ArevaloVicente Herrero-AguayoJuan M Jiménez-VacasAndrea MafficiniMarina E Sánchez-FríasMaría T CanoFernando Abollo-JiménezJuan A Marín-SanzPablo Cabezas-SainzRita T LawlorClaudio LuchiniLaura SánchezJuan M Sánchez-HidalgoSebastián VenturaLaura Martin-HijanoManuel D GaheteAldo ScarpaÁlvaro Arjona-SánchezAlejandro Ibáñez-CostaBruno SainzRaúl M LuqueJusto P. Castaño
Published in: Journal of experimental & clinical cancer research : CR (2021)
SF3B1 overexpression represents a therapeutic vulnerability in PDAC, as altered splicing can be targeted with Pladienolide-B both in cancer cells and CSCs, paving the way for novel therapies for this lethal cancer.
Keyphrases
  • cancer stem cells
  • climate change
  • papillary thyroid
  • cell proliferation
  • squamous cell
  • transcription factor
  • adverse drug