Additionally, we critically assess the therapeutic potential of targeting this switch, emphasizing how drugs that either inhibit or promote autophagy can work together with arsenic trioxide (ATO) to combat drug resistance in solid tumors such as glioblastoma and ovarian cancer. By shifting from simple descriptions to a detailed mechanistic and contextual understanding, this review offers a valuable guide for future research aiming to harness the autophagy switch for cancer prevention and personalized treatment.

In vitro, ATO demonstrated superior cytotoxicity over doxorubicin against multiple HCC cells under hypoxia. Most importantly, in an orthotopic rat HCC model, the combined treatment exhibited powerful synergistic efficacy, attaining a remarkable 96% tumor suppression rate and significantly prolonging survival, with a favorable safety profile. This work presents a novel "embolization‑imaging‑targeted chemotherapy" strategy that simultaneously overcomes the key limitations of conventional TACE and ATO delivery, offering a promising and translatable nanoplatform for the effective treatment of advanced HCC.

Furthermore, we identify a synergistic antitumor effect between KPT-330 and translation inhibitors, including everolimus and homoharringtonine. Notably, the disruptive impact of KPT-330 on CRC homeostasis extends to other cancer cell lineages, underscoring its broad mechanistic relevance. Collectively, our findings elucidate a novel mechanism through which KPT-330 destabilizes CRC via translational dysregulation and highlight its potential therapeutic utility in combination regimens for DDLPS.

Both agents mitigate ATO‑induced neurotoxicity through antioxidant, anti‑inflammatory, and anti‑apoptotic mechanisms, with their co‑administration surpassing individual efficacy. The Keap‑1/Nrf2/HO‑1 axis emerges as a critical therapeutic node, underscoring the translational potential of combined intervention.

P2, N=95, Recruiting, TaiRx, Inc. | Trial completion date: Mar 2026 --> Dec 2026 | Trial primary completion date: Mar 2026 --> Dec 2026

P2, N=40, Recruiting, TaiRx, Inc.

Multidisciplinary supportive care with continuation of ATRA-ATO therapy resulted in complete hematologic and molecular remission. This case highlights the importance of recognizing and managing complex complications in APL while maintaining curative therapy.

P1, N=24, Not yet recruiting, Celtic Biotech Ltd | Trial completion date: Dec 2025 --> Nov 2027 | Trial primary completion date: Aug 2025 --> Oct 2027

P1, N=94, Not yet recruiting, Zhongda Hospital

P2, N=40, Enrolling by invitation, Guangdong Second Provincial General Hospital

PLD1-inhibitor remodeled phospholipid metabolism, induced ferroptosis and restored QUIZOM response in LSC. Our findings provided the therapeutic and resistant mechanisms of QUIZOM and paved the way for targeted interventions in this AML subtype.

In this study, we demonstrate that IDH1-mutant AML cells are markedly more sensitive to cuproptosis induced by the copper ionophore elesclomol (ES), compared to their wild-type counterparts...In vivo experiments confirm that ES more effectively suppresses tumor growth in IDH1-mutant xenografts. These findings uncover a copper-dependent metabolic vulnerability and provide a rationale for exploiting cuproptosis as a therapeutic strategy in IDH1-mutant AML.