Pancreatic Cancer

P=N/A, N=107, Active, not recruiting, Weill Medical College of Cornell University | Trial completion date: Aug 2025 --> Jun 2026 | Trial primary completion date: Aug 2025 --> Jun 2026

P=N/A, N=36, Suspended, Cedars-Sinai Medical Center | Recruiting --> Suspended

P1/2, N=252, Recruiting, Bristol-Myers Squibb | Not yet recruiting --> Recruiting

P1, N=24, Active, not recruiting, University of Nebraska | Trial primary completion date: Oct 2025 --> May 2026

P2, N=40, Recruiting, Mayo Clinic | Trial completion date: May 2027 --> Jul 2029 | Trial primary completion date: May 2026 --> Jul 2029

P1, N=171, Recruiting, Boehringer Ingelheim | N=94 --> 171 | Trial primary completion date: Jun 2028 --> Feb 2029

P2, N=23, Completed, Emory University | Active, not recruiting --> Completed

Our findings reveal a novel mechanism whereby CUL2 promotes PC progression and ferroptosis resistance through regulation of the KEAP1-NRF2 axis. CUL2 overexpression enhances cellular antioxidant capacity and maintains mitochondrial integrity, thereby conferring broad resistance to ferroptosis-inducing conditions. This study suggests that targeting the CUL2-NRF2 axis to enhance ferroptosis sensitivity might represent a promising therapeutic strategy for PC treatment.

Our findings highlight the functional heterogeneity of myCAFs and identify TAGLN-expressing myCAFs as critical mediators of tumour progression, providing evidence that targeting stromal TAGLN may represent a promising therapeutic strategy for PDAC.

Impaired ER-phagy triggers protein aggregation, inflammation, and acinar-to-ductal metaplasia, promoting tumorigenesis. These findings highlight selective autophagy's role in cancer, with possible therapeutic implications.

The findings justify consideration of assessments of EBV status and tumor mutation burdens for patient stratification. Also, EBV-targeted immunotherapy for pancreatic adenocarcinoma may be considered for clinical trials.

P2, N=60, Not yet recruiting, M.D. Anderson Cancer Center