PTEN Oxidation Promotes Constitutive PI3K Signaling and Inducible Macropinocytosis in Pancreatic Cancer
PTEN inactivation by intramolecular disulfide bond formation and elevated expression of PI3K isoforms in pancreatic cancer leads to unchecked KRAS-independent PI3K signaling, highlighting the need for therapeutic approaches targeting constitutive PI3K signaling.
Authors
- Hannah S. Coalson (ORCID: https://orcid.org/0000-0001-7791-3180)
- Cameron Bumbleburg (ORCID: https://orcid.org/0009-0000-3895-4270)
- Amanda J. Linke (ORCID: https://orcid.org/0000-0001-5719-9696)
- Kamala Sundararaj (ORCID: https://orcid.org/0009-0004-5049-9767)
- David F. Kashatus (ORCID: https://orcid.org/0000-0001-8007-0612)
- Sara J. Adair (ORCID: https://orcid.org/0000-0002-9973-4252)
- Lucas Bialousow (ORCID: https://orcid.org/0000-0003-1126-8670)
- Rachel A. Burge (ORCID: https://orcid.org/0000-0001-9363-4333)
- G. Aaron Hobbs (ORCID: https://orcid.org/0000-0002-4751-9681)
- Todd W. Bauer (ORCID: https://orcid.org/0000-0002-9516-1848)
- Merissa Smith
Institutions
- Medical University of South Carolina (US)
- University of Virginia Health System (US)
- MUSC Hollings Cancer Center (US)
- University of Virginia (US)
Publication Details
- Journal
- Cancer Research
- Published
- 2025-10-24
- DOI
- https://doi.org/10.1158/0008-5472.can-24-4501
- Citations
- 1
- Primary Topic
- Pancreatic and Hepatic Oncology Research
- Type
- article
- Field-Weighted Citation Impact
- 1.05