In conclusion, our findings demonstrate that trapping cells in a state of high autophagic flux through simultaneous induction and late stage inhibition, is a potent strategy to trigger non-apoptotic cell death in leukemia. This approach represents a promising therapeutic strategy to overcome apoptosis-resistant leukemia.

While CD8+ T cells were critical to the anti-tumor immune response to autophagy inhibition in PDAC, they were not directly involved in cytotoxicity but played a critical role in stimulating macrophage phagocytosis of tumor cells. Taken together, this study strongly supports the implementation of autophagy inhibition in pancreatic cancer and highlights a crucial link between PDAC biology and the TME-macrophage crosstalk that effectively promotes tumor cell killing.

Diminished radiation-induced autophagy was observed by the knockdown of PINK1, a key regulator of mitophagy. These findings highlight that inhibition of autophagy can improve the efficacy of HNSCC treatments and suggest that targeting specific autophagy subtypes may be crucial for developing personalized treatment combinations for HNSCC patients.

ADAR1 inhibits the LUAD-associated autophagy by modifying INPP5J to activate the PI3K/AKT/mTOR pathway, providing a novel adjuvant therapeutic target for LUAD.

P1/2, N=31, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: May 2026 --> May 2027 | Trial primary completion date: May 2026 --> May 2027

P=N/A, N=14, Shulan (Hangzhou) Hospital; Shulan (Hangzhou) Hospital

P1/2, N=31, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Jan 2026 --> May 2026 | Trial primary completion date: Jan 2026 --> May 2026

Co-treatment with alpelisib and chloroquine (CQ) further suppressed tumor cell growth, viability, migration, and colony formation more effectively than alpelisib alone, owing to increased apoptosis, elevated early and late apoptotic populations, and increased levels of cleaved PARP and caspase-3. These findings suggest that combining alpelisib with autophagy inhibition significantly enhances its antitumor activity in PI3K-mutated NSCLC, highlighting a promising therapeutic strategy to address unmet clinical needs in this molecular subset. This discovery opens new possibilities for developing innovative targeted therapies for challenging NSCLC.

This study demonstrates that SIP1 is effective in inducing apoptosis and promotes cisplatin-induced apoptosis by repressing cisplatin-induced autophagy in MDA-MB-231 cells.

Our data suggests that one of the possible mechanisms by which PV-10 triggers ICD is by inducing endoplasmic reticulum stress, autophagy, and apoptosis. Our findings contribute to further understanding of the underlying mechanisms of PV-10 induced cytotoxicity and to develop future clinical trials in locally recurrent HNSCC.

Our findings reveal a mechanism by which TNFα disrupts hemostasis through autophagy inhibition, highlighting TNFα as a critical regulator of platelet metabolism and function. This study provides new insights into inflammation-associated pathologies and suggests autophagy-targeting strategies as potential therapeutic avenues to restore hemostatic balance.

P=N/A, N=40, Completed, Sichuan Provincial People's Hospital; Sichuan Provincial People's Hospital