arsenic trioxide

In therapy-sensitive wild-type ER cells with low basal PML1 levels and PI3K/MAPK activity, fulvestrant's ER-suppressive effects overcome drug-induced elevated PML1 and PI3K/MAPK activity, thereby maintaining therapeutic efficacy...Notably, reducing PML1 levels through knockdown or arsenic trioxide (ATO), an FDA-approved PML1 degrader, disrupts this resistance circuit and restores endocrine sensitivity. Treatment of ATO resensitizes ER Y537S-bearing resistant tumors to endocrine therapy in xenograft models. These findings establish PML1 as a central hub of resistance, linking ER signaling to the activation of the PI3K/MAPK survival pathway.

These results indicate that ATO suppresses the malignant phenotype of A549 cells by inhibiting mTOR phosphorylation, downregulating key BER components, and activating the extrinsic and intrinsic apoptotic pathways, providing experimental evidence for further studies of ATO in lung adenocarcinoma therapy.

Z2-A-Z2 is a promising organic arsenical with superior efficacy and safety over ATO. Its unique dual-action strategy of simultaneously inducing oxidative stress and critically inhibiting the NF-κB/IκBα signaling axis, positioning it as a strong clinical candidate for effectively treating DLBCL.

The combination of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) has significantly improved outcomes in patients with APL. The patient achieved molecular complete remission within two months of initiating isotretinoin-based consolidation therapy and continues to have negative PML::RARA reverse transcriptase polymerase chain reaction (RT-PCR) results, with sustained remission at 18 months of follow-up with ongoing molecular monitoring every three months. Although the concurrent use of ATO and prior ATRA-based induction are important confounders, this case highlights the potential role of isotretinoin as a cost-effective alternative retinoid for consolidation therapy in APL when ATRA is inaccessible, although ATRA remains the recommended standard treatment.

P2/3, N=12, Not yet recruiting, Quetzal Therapeutics LLC

These transcriptional changes paralleled a transient inflammatory response, including early Tnf-α induction and female-specific Il-6 elevation. Collectively, these findings highlight sex-dependent modulation of hepatic ATO handling and drug metabolizing capacity, with important implications for risk assessment and individualized ATO containing regimens.

Acute promyelocytic leukemia (APML) is characterized by promyelocytic leukemia retinoic acid receptor alpha (PML-RARA) fusion gene resulting from at (15;17) translocation. While, TLC significantly decreased from baseline in high risk cases to last follow-up (24 × 109/L vs. 9 × 109/L; P = 0.016). Patients with APML can be successfully treated with a combination of ATO and ATRA.

RTS exhibited superior selectivity compared with inorganic arsenic trioxide (ATO) and paclitaxel, significantly reducing the viability of TNBC cells (MDA-MB-231, BT-549, and MDA-MB-468) while sparing non-malignant MCF-10 A cells.. Collectively, these in vitro findings establish a "lysosome-mitochondria" signaling axis in which early pH perturbation represents a potential vulnerability in TNBC. While the multicomponent nature of RTS requires further characterization, this study provides preliminary insights into targeting organelle-specific Ca2+ hubs as a complementary strategy for refractory solid tumors.

P=N/A, N=110, Beijing Chao-Yang Hospital, Capital Medical University; Beijing Chao-Yang Hospital, Capital Medical University

Moreover, the combination therapy resulted in a marked increase in anti-proliferative effects. These findings provide new insights into the potential use of ATO and atorvastatin as a combined therapeutic strategy, highlighting their promise as a novel approach in the treatment of ALL.

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.