arsenic trioxide

Compared to free ATO, the nanomedicine exhibited significantly improved in vivo anti-tumor effects, achieving a 100% 45-day survival rate in mice with favorable biosafety profiles. This study offers novel insights into tumor chemotherapy sensitization and presents a promising strategy for ATO nanoformulation development.

A cigarette compound-formed tumor microenvironment resisted HCC to sorafenib by locking the adaptor protein 14-3-3η in a constitutively active state. This outcome provided a mechanistic rationale and a translational strategy to re-sensitize HCC patients exposed to cigarette to targeted therapy.

Differentiation syndrome (DS) is a serious complication with an unclear pathogenesis that arises following all-trans retinoic acid (ATRA) or arsenic trioxide induction therapy in acute promyelocytic leukemia (APL)...25(OH)D3 also inhibited the ATRA-induced production of cytokines (e.g., IL-8), including IL-1β, TNF-α, and MCP-1, associated with the "cytokine storm." Combined treatment with ATRA plus 25(OH)D3 reduced cellular phospho-p65 and transglutaminase 2 (TG2) levels and increased the level of inhibitor of Rel (IκB), thereby attenuating the cytokine storm. These findings provide a molecular interpretation for clinical DS and IHC observations and may support future exploration of ATRA plus 25(OH)D3 cotreatment as a therapy for APL.

Pro-oxidant therapies aim to overwhelm cellular defenses, with agents like high-dose vitamin C and arsenic trioxide (ATO) showing significant tumor-selective toxicity...Disruption of the GSH system by inhibiting cysteine uptake with sulfasalazine or erastin potently induces ferroptosis, a non-apoptotic cell death driven by lipid peroxidation...Moreover, novel therapeutic strategies, including the expanding field of redox-active metal complexes, such as manganese porphyrins, which strategically leverage the differential redox state of normal versus cancer cells through both pro-oxidant and indirect Nrf2-mediated antioxidative mechanisms (triggered by Keap1 oxidation), with several agents currently in advanced clinical trials, have also been discussed. Essentially, pharmacologically tipping the redox balance beyond the threshold of tolerance offers a rational and powerful approach to eliminate malignant cells, defining a novel frontier for targeted cancer therapy.

Significant differences were observed between the DIC and non-DIC groups in the proportion of patients with initial white blood cells (WBC) ≥5 × 109/L, initial platelets (PLT) ≤26 × 109/L and arsenic trioxide (ATO) use (p < 0.05)...Compared with ATO, RIF is a protective factor during induction therapy. Additionally, FLT3 mutation, PLT ≤26 × 109/L and initial bone marrow blasts ≥90% are independent risk factors for grade 4-5 DIC.

Most patients with APL presented with fever and bleeding. The bcr1 transcript of PML-RARα was the most commonly observed. ATRA and ATO-based treatment was associated with high remission rates, manageable toxicity, and a low relapse rate.

Strategies to mitigate the cardiotoxicity of anticancer therapies and identify patients who may require time-sensitive interventions or long-term follow-up represent promising opportunities to improve the quality and safety of care in the emerging field of cardio-oncology pharmacy.

The introduction of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) has dramatically improved outcomes in APL, making it a leading example of successful treatment through differentiation of cancer cells...Zinc also regulates key transcription factors involved in differentiation and proliferation, including RUNX2, KLF4, GFI1, and CREB. In this review, we examine how zinc may impact zinc-finger (ZnF) and non-ZnF transcription factors and differentiation therapy in APL, thereby identifying potential strategies to enhance treatment efficacy and minimize side effects.

Both ATO alone and the combination treatment markedly induced a significant elevation of ROS and ferroptosis, which was effectively blocked by the administration of ferrostatin-1 and deferoxamine mesylate. Additionally, ATO and the combination of Lenvatinib and ATO also decreased the expression of GPX4 protein both in vitro and in vivo. In conclusion, ATO enhances the antitumor activity of Lenvatinib against HCC by inducing ferroptosis through upregulation of HMOX1 and downregulation GPX4.

The antineoplastic drugs arsenic trioxide and fulvestrant stand out as examples for leveraging a SUMOylation-ubiquitylation cascade to inactivate the oncogenic fusion proteins PML-RARα and estrogen receptor α, respectively. Recent proof-of-concept studies indicate that proximity-inducing modalities can recruit aggregation-prone proteins to the StUbL machinery, potentially mitigating the formation of neurotoxic inclusions. We review new insights on StUbL-based therapeutics and reflect perspectives of reprogramming SUMO-StUbL signaling for use in oncology and neurology.

Here, we report a case with a single fusion of PML::RARA formed on der(17), without the RARA::PML fusion, and the patient responded well to all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO) therapy. To our knowledge, this represents only the fourth reported case of this type. Our findings indicate that the PML::RARA fusion is the primary driver of APL leukemogenesis and the main therapeutic target for ATRA and ATO, suggesting that the RARA::PML transcript may not be essential for APL development.

All-trans retinoic acid (ATRA) and arsenic trioxide (ATO)-based therapies render APL the most curable subtype of AML, yet approximately 1% of cases are resistant and 5% relapse...Notably, our data demonstrate that glycolytic impairment via AKT inhibition by PML::RARα renders APL cells reliant on OXPHOS. This dependency confers high sensitivity to the VTX-AZA combination, suggesting the therapeutic efficacy of targeted combination treatment in resistant or relapsed APLs.