Transarterial Chemoembolization (TACE) has been widely used for the treatment of intermediate-staged hepatocellular carcinoma. One of its intrinsic disadvantages is that the anticancer drug mixed with lipiodol is very easy to wash out from the tumor, not only alleviating its therapeutic effect but also leading to adverse reactions. Drug-eluting polymeric beads were introduced as a new embolic agent due to their unique characteristic of simultaneous embolization and release of anticancer drugs in a sustainable manner. This significantly reduces the occurrence of adverse events related to the systemic release of the anticancer drug. The rational design of the polymeric embolic is a critical issue. This review presents different frameworks of polymeric embolic as well as their loading and unloading of drugs for chemoembolization. Additionally, besides those inert polymeric beads, we will introduce more functional and active embolic polymers that disturb the tumor microenvironment after embolization, not just carrying the anticancer drugs. These rapidly advancing polymeric biomaterials are pushing vessel embolization techniques toward a more precise therapeutic strategy.

Hepatocellular carcinoma (HCC) frequently recurs after surgical treatment, necessitating effective postoperative recurrence management for improved long-term patient outcomes. Currently, no standardized treatment approach exists for recurrent unresectable HCC. This study aims to investigate the safety and efficacy of combining tyrosine kinase inhibitors (TKIs) and programmed cell death protein-1 (PD-1) inhibitors with hepatic arterial infusion chemotherapy (HAIC) or transarterial chemoembolization (TACE) in the treatment of recurrent unresectable HCC. A retrospective analysis was conducted on clinical data from 83 patients diagnosed with unresectable recurrent HCC. Patients were categorized into three groups based on their treatment regimens: HAIC combined with TKIs and PD-1 inhibitors (HTP), TACE combined with TKIs and PD-1 inhibitors (TTP), and TACE alone. Treatment efficacy and safety were compared among these groups, and potential risk factors were identified. The median progression-free survival (PFS) for patients in the HTP group, TTP group, and TACE alone group was found to be 13.7, 9.2, and 2.5 months (p = 0.001, p = 0.002). According to the mRECIST criteria, the disease control rates (DCR) in the HTP, TTP and TACE groups was 89.7

Renal fibrosis is a common feature of chronic kidney disease (CKD) and is characterized by interstitial fibrotic tissue deposition, impaired renal function, and interstitial inflammation. To date, there are no clinically effective therapeutic agents specifically approved for the treatment of renal fibrosis. Sevelamer, as a phosphate binder, was approved to treat hyperphosphatemia and was recently shown to have antifibrotic effects in preclinical studies. In this study, we established a folic acid (FA)-induced renal interstitial fibrosis mouse model and an in vitro model using human kidney-2 (HK-2) cells to evaluate the therapeutic effects and mechanisms of sevelamer in renal fibrosis. Our results revealed that sevelamer reduced serum phosphate levels in fibrotic mice and improved renal function by restoring serum creatinine (Scr), blood urea nitrogen (BUN), and uric acid (UA) levels. Sevelamer significantly alleviated tubular injury, reduced extracellular matrix (ECM) accumulation, decreased the expression of inflammatory cytokines (IL-1β, IL-6, and TNF-α) in the serum, and mitigated renal inflammation. In vitro, sevelamer-induced phosphate deprivation inhibited HK-2 cell migration and epithelial‒mesenchymal transition (EMT), reducing the expression of fibrosis-associated proteins. Mechanistic studies revealed that low-phosphate stress induced by sevelamer suppressed the phosphorylation of IκBα and NF-κB-p65, inhibiting nuclear factor kappa B (NF-κB) signaling both in vivo and in vitro. As a result, sevelamer-mediated low-phosphate stress improved renal function, reduced ECM deposition, suppressed the expression of EMT markers in mouse kidneys and HK-2 cells, decreased inflammatory cytokine release, and attenuated NF-κB pathway activation. Sevelamer may be a potential therapeutic agent for the treatment of renal fibrosis.

Purpose: To determine how low inorganic phosphate stress (LIPS) induced by sevelamer particle transarterial embolization (S-TAE) affects immune regulation and angiogenesis in hepatocellular carcinoma. Material and Methods: Transcatheter arterial embolization (TAE) using conventional ethiodized oil plus polyvinyl alcohol microspheres and S-TAE, which depletes intratumoral inorganic phosphate, were conducted on a McA-RH7777 orthotopic liver tumor model in rats, followed by the assessment of alterations in immunity-related and angiogenesis-related factors. The cells were cultured under hypoxic conditions and stimulated with LIPS to analyze the modulation of programmed cell death 1 ligand (PD-L1), vascular endothelial growth factor (VEGF)-alpha, and transforming growth factor-R1 expression using western blotting, quantitative real-time polymerase chain reaction, and immunofluorescence assays. Cell migratory capacity and angiogenesis were also evaluated. Results: TAE increased the expression of neoplastic PD-L1 and VEGF-alpha, and S-TAE downregulated the expression of PD- L1, VEGF-alpha, and transforming growth factor TGF-R1 and augmented the infiltration of CD8+ T cells, and thereby inhibited angiogenesis and activated anticancer immunity. In vitro, the study demonstrated that LIPS inhibited hypoxia-induced upregulation of PD-L1 expression and the hypoxia-inducible factor-1 alpha/VEGF-alpha axis. Moreover, LIPS inhibited the tube formation ability of human umbilical vein endothelial cells and the migration ability and epithelial-mesenchymal transition process of cancer cells under hypoxic conditions. Conclusions: S-TAE inhibited the expression of PD-L1 and VEGF-alpha, thereby activating antitumor immunity and suppressing tumor angiogenesis. The biology of tumors under LIPS suggests the potential therapeutic value of phosphate depletion using sevelamer for S-TAE.

BACKGROUND/AIM:Lung cancer bone metastasis significantly reduces the quality of life of advanced-stage patients, leading to cancer-related pain and pathological fractures. Currently, there is a lack of drugs simultaneously inhibiting the growth of metastatic lesions and reducing pain. Ibrutinib, a selective inhibitor of EGFR-mutated non-small cell lung cancer, has been shown to inhibit the proliferation and migration of lung cancer cells. This study aimed to investigate the effects of ibrutinib on tumor progression, pain, and bone protection. MATERIALS AND METHODS:Cell viability and migration of the murine Lewis lung carcinoma (LLC, FH0325) and human NSCLC (NCI-H1975, FH0086) cell lines were assessed using CCK-8, wound healing, and transwell assays after treatment with ibrutinib. Behavior tests, mechanical allodynia, flinches and pain scoring, micro-computed tomography and histological analysis were evaluated on the tumor-bearing C57BL/6 mice. RESULTS:CCK-8, wound healing, and transwell assays demonstrated that ibrutinib significantly suppressed the proliferation and migration of lung cancer cell lines. The efficacy of ibrutinib treatment was evaluated in a mouse model of lung cancer bone metastasis. Behavioral analysis validated the reduction in mechanical and spontaneous pain and the delay in the loss of motor function. Micro-CT revealed greater bone volume and density and less bone trabecular separation. Moreover, TRAP staining indicated a decrease in osteoclast numbers following ibrutinib treatment. Histopathological examination revealed fewer lung metastatic lesions, while TUNEL staining indicated more severe tumor cell apoptosis induced by ibrutinib. CONCLUSION:Ibrutinib effectively inhibited the proliferation and migration of lung cancer cells, and in a lung cancer bone metastasis model, this drug inhibited tumor growth, alleviated pain, and protected the tibial bone.

Liver fibrosis is a chronic liver disease characterized by a progressive wound healing response caused by chronic liver injury. Currently, there are no approved clinical treatments for liver fibrosis. Sevelamer is used clinically to treat hyperphosphatemia and has shown potential therapeutic effects on liver diseases. However, there have been few studies evaluating the therapeutic effects of sevelamer on liver fibrosis, and the specific mechanisms are still unclear. In this study, we investigated the antifibrotic effects of sevelamer-induced low inorganic phosphate (Pi) stress in vitro and in vivo and analyzed the detailed mechanisms. We found that low Pi stress could inhibit the proliferation of activated hepatic stellate cells (HSCs) by promoting apoptosis, effectively suppressing the migration and epithelial-mesenchymal transition (EMT) of hepatic stellate cells. Additionally, low Pi stress significantly increased the antioxidant stress response. It is worth noting that low Pi stress indirectly inhibited the activation and migration of HSCs by suppressing transforming growth factor β (TGF-β) expression in macrophages. In a rat model of liver fibrosis, oral administration of sevelamer significantly decreased blood phosphorus levels, improved liver function, reduced liver inflammation, and increased the antioxidant stress response in the liver. Our study revealed that the key mechanism by which sevelamer inhibited liver fibrosis involved binding to gastrointestinal phosphate, resulting in a decrease in blood phosphorus levels, the downregulation of TGF-β expression in macrophages, and the inhibition of HSC migration and fibrosis-related protein expression. Therefore, our results suggest that sevelamer-induced low Pi stress can attenuate hepatic stellate cell activation and inhibit the progression of liver fibrosis, making it a potential option for the treatment of liver fibrosis and other refractory chronic liver diseases.

To develop and validate the nomogram by combining MRI-derived radiomics and clinical features for preoperatively predicting massive intraoperative blood loss (IBL) in high-risk placenta accreta spectrum (PAS) patients. A total of 152 high-risk PAS patients from Hospital A were enrolled and constituted the training cohort, and 64 patients from Hospital B constituted the validation cohort. Clinical features were analyzed retrospectively. Placental regions of interest were manually positioned on sagittal T2-weighted HASTE images for each patient to extract quantitative radiomics features. Clinical model, radiomics model, and nomogram were built to predict the risk of massive IBL. The diagnostic performance was assessed using the area under the receiver operating characteristic curve (AUC) and the DeLong test. Decision curve analysis (DCA) was performed to determine the performance of the best predictive model. The nomogram (AUC = 0.866 and 0.876, respectively) and radiomics model (AUC = 0.821 and 0.855, respectively) outperformed the clinical model (AUC = 0.685 and 0.619, respectively) both in the training and validation cohorts (Delong test, P < 0.05). Furthermore, the nomogram performed best with an accuracy of 0.844, sensitivity of 0.882, and specificity of 0.830 for differentiating massive IBL in the validation cohort. DCA confirmed the clinical utility of the nomogram. The nomogram can be used to noninvasively predict massive IBL patients and guide obstetricians to make reasonable preoperative treatment plans.

To determine the hemostatic values of internal iliac artery balloon (IIABO) occlusion and abdominal aorta balloon occlusion (AABO), 142 patients with pernicious placenta previa were divided into three groups: control (45), IIABO (40), and AABO (57) groups, respectively. The blood loss, operative duration, time-averaged hemorrhage velocity (TAHV), blood transfusion, time-averaged transfusion velocity (TATV), and hospitalization days of these groups were compared. Angiographies and a circulatory simulation were used to unveil the bleeding mechanisms. Although the AABO group's operative duration and hospitalization days are longer (p < 0.001) than those of the other groups, the AABO group has considerably reduced blood loss (p < 0.05) and TAHV (p < 0.001) than the other groups. No obvious difference in blood transfusion and TATV between these groups can be observed. Angiographies showed that there was a large amount of blood flow in the pelvic cavity during IIABO, but AABO did not. In our modeling, the cumulative blood loss is about 2000 ml without using the balloon, which is the same as that when IIABO is used with collateral pressure of 75 mm Hg. The main source of blood loss is uterine arterioles. However, the blood loss during AABO is about 300 ml, which is mainly from uterine venules. These results suggested that IIABO failed to control bleeding, which may be related to collateral circulation, while AABO has a better prospect and may be more effective if the blood pressure of uterine venules is also isolated. These findings may guide technology selections for obstetricians and the improvement of hemostasis technology.

目的:探究中医辨证施治结合正念减压疗法对中晚期肝癌介入治疗患者生存率及生存质量的影响.方法:选取南昌大学第一附属医院 2021 年 1-7 月收治的 58 例中晚期肝癌介入治疗患者作为研究对象,将其按随机数字表法分为两组,各 29 例.对照组患者接受常规治疗,研究组患者在对照组基础上接受中医辨证施治结合正念减压疗法.对比两组中医症候积分、心理韧性、癌因性疲乏、生存质量及治疗后 3、6 个月的生存率.结果:治疗前两组焦虑自评量表(SAS)、抑郁自评量表(SDS)及癌因性疲乏量表评分比较,差异均无统计学意义(P>0.05);治疗后,研究组以上各项指标评分相较于对照组均更低(P<0.05).治疗后,研究组中医症候积分均较对照组更低,生存质量各项评分均高于对照组,差异均有统计学意义(P<0.05).研究组治疗后 3、6 个月的生存率相较于对照组均更高,差异均有统计学意义(P<0.05).结论:为中晚期肝癌介入治疗患者应用中医辨证施治结合正念减压疗法,能够缓解患者的不适症状,提高患者的心理韧性,改善生存质量,提高生存率.

MiR-1283 has been identified as a tumor suppressor in some malignancies. Whereas, the role of miR-1283 in HER2-positive (HER2+) breast cancer, particularly its role in regulating cell proliferation, one of the most significant features of tumor progression, is unclear. The related microRNA screened by the breast cancer sample GSE131599 dataset were detected in HER2+ breast cancer tissues and cell lines. Then, the obtained miR-1283 was overexpressed in SKBR3 and BT-474 cells followed by relevant functional assays concerning cell proliferation and apoptosis. The xenograft mouse model was induced and the effect of miR-1283 on tumor growth and cell proliferation was examined. The target of miR-1283 and the transcription factor regulating miR-1283 were predicted and identified. Finally, the influence of transcription factor KLF14 on cell proliferation and apoptosis was investigated. An integrated analysis confirmed that miR-1283 expression was significantly decreased in HER2+ breast cancer tissues. Also, by q-RT-PCR detection, miR-1283 expression was markedly reduced in HER2+ breast cancer tissues and cell lines. The miR-1283 overexpression prevented the proliferation and enhanced apoptosis of HER2+ breast cancer cells, as well as inhibited tumor growth. Mechanistically, miR-1283 inhibited TFAP2C expression by targeting the 3'-untranslated regions of TFAP2C messenger RNA, and the KLF14 enhanced miR-1283 level via binding to its promoter. The result subsequently confirmed the KLF14/miR-1283 signaling suppressed cell proliferation in HER2+ breast cancer. Our results suggested that the KLF14/miR-1283/TFAP2C axis inhibited HER2+ breast cancer progression, which might provide novel insight into mechanical exploration for this disease.

Previous clinic models for patients with hepatocellular carcinoma (HCC) receiving transarterial chemoembolization (TACE) mainly focused on the overall survival, whereas a simple-to-use tool for predicting the response to the first TACE and the management of risk classification before TACE are lacking. Our aim was to develop a scoring system calculated manually for these patients. A total of 437 patients with hepatocellular carcinoma (HCC) who underwent TACE treatment were carefully selected for analysis. They were then randomly divided into two groups: a training group comprising 350 patients and a validation group comprising 77 patients. Furthermore, 45 HCC patients who had recently undergone TACE treatment been included in the study to validate the model's efficacy and applicability. The factors selected for the predictive model were comprehensively based on the results of the LASSO, univariate and multivariate logistic regression analyses. The discrimination, calibration ability and clinic utility of models were evaluated in both the training and validation groups. A prediction model incorporated 3 objective imaging characteristics and 2 indicators of liver function. The model showed good discrimination, with AUROCs of 0.735, 0.706 and 0.884 and in the training group and validation groups, and good calibration. The model classified the patients into three groups based on the calculated score, including low risk, median risk and high-risk groups, with rates of no response to TACE of 26.3%, 40.2% and 76.8%, respectively. We derived and validated a model for predicting the response of patients with HCC before receiving the first TACE that had adequate performance and utility. This model may be a useful and layered management tool for patients with HCC undergoing TACE.

As the most efficient method to treat hepatocellular carcinoma in the immediate or advanced stage, transarterial chemoembolization (TACE) is coming into the era of microsphere (MP). Drug-eluting beads have shown their huge potential as an embolic agent and drug carrier for chemoembolization, but their sizes are strictly limited to be above 40 μm, which was considered to occlude vessels in a safe mode. microsphere smaller than 40 µm is easy to be washed out and transported to the normal liver lobe or other organs, causing severe adverse events and failed embolization. To determine whether sevelamer ultrafine particle (0.2–0.5 µm) is qualified as a safe and efficient embolic agent, we investigated the safety and therapeutic efficiency of transarterial sevelamer embolization (TASE) in the VX2 rabbit liver cancer model, aiming to challenge the “40 µm” rule on the selection criteria of the MP. In a four-arm study, blank bead (Callisphere, 100–300 µm), luminescent polystyrene microsphere (10, 100 µm), and sevelamer particle were transarterially administered to evaluate the threshold size of the MP size for intrahepatic or extrahepatic permeability. Another four-arm study was designed to clarify the safety and efficiency of preclinical transarterial sevelamer embolizationTASE tests over other techniques. Sham (saline), TASE, C-TACE, and D-TACE (n = 6) were compared in terms of serum chemistry, histopathology, and tumor necrosis ratio. In the first trials, the “40 µm” rule was detectable on the VX2 cancer model, but the regulation has no application to the new embolic agent as sevelamer ultrafine particles have not been found to leak out from the VX2 lesions, only found in the embolized vessels. Pathology proves that less viable tumor residue was found 2 weeks after the procedure, evidencing a better therapeutic outcome. No adverse events were found except for a short stress response. These results indicate that sevelamer is a safe and efficient embolic as an alternative to the current MP-based embolization therapy techniques.

Decades have witnessed rapid progress of polymeric materials for vascular embolic or chemoembolic applications. Commercially available polymeric embolics range from gelatin foam to synthetic polymers such as poly(vinyl alcohol). Current systems under investigation include tunable, bioresorbable microspheres composed of chitosan or poly(ethylene glycol) derivatives,in situgelling liquid embolics with improved safety profiles, and radiopaque embolics that are trackablein vivo. In this paper, we proposed a concept of 'responsive embolization'. Sevelamer, clinically proved as an inorganic phosphate binder, was ground into nanoparticles. Sevelamer nanoparticle is highly mobile and capable of swelling and aggregating in the presence of endogenous inorganic phosphate, thereby effectively occluding blood flow in the vessel as it was administered as an embolic agent for interventional therapy. Moreover, citrated sevelamer nanoparticles delayed the aggregation, preferable to penetrate deeply into the capillary system. On the rabbit VX2 liver cancer model, both sevelamer particles aggregates occlude the tumor feeding artery, but backflow was found for the pristine one, thereby citrate passivation of sevelamer nanoparticles endows it have potential from 'bench to bedside' as a new type of vascular embolic.

It is a decade-long controversy that transarterial chemoembolization (TACE) has definite priority over transarterial embolization (TAE) in treating patients with hepatocellular carcinoma (HCC), since HCC cells are regularly resistant to chemotherapy by enhanced expression of proteins that confer drug resistance, and ABC transporters pump the intracellular drug out of the cell. We addressed this issue by modulating the chemo-environment. In an animal model, sevelamer, a polymeric phosphate binder, was introduced as an embolic agent to induce intratumoral inorganic phosphate (Pi) starvation, and trans-arterially co-delivered with doxorubicin (DOX). The new type of TACE was named as DOX-TASE. This Pi-starved environment enhanced DOX tumoral accumulation and retention, and DOX-TASE thereby induced more severe tumor necrosis than that induced by conventional TACE (C-TACE) and drug-eluting bead TACE (D-TACE) at the same dose. In vitro tests showed that Pi starvation increased the cellular accumulation of DOX in an irreversible manner and enhanced cytotoxicity and cell apoptosis by suppressing the expression of ABC transporters (P-glycoprotein (P-gp), BCRP, and MRP1) and the production of intracellular ATP. Our results are indicative of an alternative interventional therapy combining chemotherapy with embolization more effectively.

Arsenic trioxide (As2O3, ATO) has limited therapeutic benefit to treat solid tumors, whether used alone or in combination. Nanoscale drug delivery vehicles have great potential to overcome the limitation of the utility of ATO by rapid renal clearance and dose-limiting toxicity. Polymeric materials ranging from gelatin foam to synthetic polymers such as poly(vinyl alcohol) were developed for vascular embolic or chemoembolic applications. Recently, we have introduced sevelamer, an oral phosphate binder, as a new polymeric embolic for vascular interventional therapy. In this paper, sevelamer arsenite nanoparticle with a polygonal shape and a size of 50–300 nm, synthesized by anionic exchange from sevelamer chloride, was developed as a Pi-responsive bifunctional drug carrier and embolic agent for chemoembolization therapy. At the same arsenic dosage, sevelamer arsenite-induced severer tumor necrosis than ATO on the VX2 cancer model. In vitro tests evidenced that Pi deprivation by sevelamer could enhance ATO's anticancer effect. The results showed that ATO in Pi starvation reduced cell viability, induced more apoptosis, and diminished the mitochondrial membrane potential (Δψm) of cells since Pi starvation helps ATO to further down-regulate Bcl-2 expression, up-regulate Bax expression, enhance the activation of caspase-3 and increase the release of cytochrome c, and the production of excessive reactive oxygen species (ROS). Sevelamer arsenite not only plays a Pi-activated nano-drug delivery system but also integrated anticancer drug with embolic for interventional therapy. Therefore, our results presented a new administration route of ATO as well as an alternative chemoembolization therapy.

Metabolic stress (for example, low pO 2 , low pH) stimulates cancer progression in a complex and largely unresolved manner. Excessive inorganic phosphate burden is being considered as another stimulator, until now there is no well‐designed study to examine the potential benefits of reducing phosphate burden on cancer progression. Sevelamer microspheres, a polymeric phosphate binder, are introduced as embolic material for interventional treatment of rabbit VX2 liver cancer model. This technique is named as “transarterial sevelamer embolization (TASE).” The microspheres prove to be highly biocompatible, and TASE is found to be a safe local‐regional technique. Compared with conventional transarterial chemoembolization (TACE), TASE is found to not only occlude the tumor‐feeding vessel, but simultaneously deplete intratumoral inorganic phosphate (Pi), thereby inducing severe necrosis as well reducing metastasis and recurrence. Reduced Pi stress inhibits tumor vascularity, invasion, and metastasis by downregulating the angiogenic factors and oncoprotein expression. Energy metabolomics indicate that Pi stress also suppresses tumor anaerobic glycolysis and glutaminolysis. This systemic anti‐cancer effect indicates a promising new application for sevelamer and TASE as a potential alternative to conventional TACE for liver cancer treatment.

Background Circular RNAs (circRNAs) are pivotal regulators of various human cancers and circ-ERBB2 is abnormally expressed in breast cancer cells. However, the role and mechanism of circ-ERBB2 in HER2-positive breast cancer are still unknown. Methods The circ-ERBB2 expressions in the tumor tissues of HER2-positive breast cancer patients were tested using quantitative real-time PCR. The circ-ERBB2 function was investigated by cell counting kit 8 assay, Transwell, flow cytometry and Western blot. Mechanistically, fluorescence in situ hybridization, RNA immunoprecipitation, RNA pull-down and dual-luciferase reporter gene assays were conducted to confirm the interaction between circ-ERBB2 and miR-136-5p or miR-198 in HER2-positive breast cancer cells. Results Circ-ERBB2 was elevated in the tumor tissues of HER2-positive breast cancer patients. Functionally, the interference with circ-ERBB2 repressed HER2-positive breast cancer cell proliferation, migration, invasion and accelerated cell apoptosis. Furthermore, the mechanistic analysis corroborated that circ-ERBB2 acted as a competing endogenous RNA for miR-136-5p or miR-198 to relieve the repressive influence of miR-136-5p or miR-198 on its target transcription factor activator protein 2C (TFAP2C). Meanwhile, in vivo assays further corroborated the oncogenic function of circ-ERBB2 in HER2-positive breast cancer. Conclusions Circ-ERBB2 accelerated HER2-positive breast cancer progression through the circ-ERBB2/miR-136-5p/TFAP2C axis or the circ-ERBB2/miR-198/TFAP2C axis.

凶险性前置胎盘剖宫产术中可能发生灾难性大出血,导致子宫切除等不良妊娠结局,严重者危及孕产妇生命.近20年来,介入放射学技术,特别是动脉内球囊阻断技术应用于产科出血的救治越来越广泛,受到产科医师的青睐.现就各种介入技术在凶险性前置胎盘剖宫产术中的应用及进展进行综述.

Commercially available drug-eluting embolization beads (100-500 μm) reduced the occurrence of adverse events related to an anticancer drug, but were unascertained to remarkably benefit the transcatheter arterial chemoembolization (TACE) treatment of intermediate-stage liver cancer. Dextran-coated arsenite nanoparticles with the size ranging from 400 to 600 nm were developed as a nanosized drug-eluting bead (NDEB) for chemoembolization therapy of the rabbit VX2 liver tumor. We fully characterized their relevant physicochemistry and drug release properties. Their hemolysis was investigated before vessel embolization. The introduction of the NDEB allowed continuous embolization of tumor feeding vessels and sustained release of arsenic trioxide, thereby causing severe tumor necrosis and reduced vascularity. Sonography including B mode ultrasound, color Doppler flow imaging (CDFI) and dynamic contrast-enhanced ultrasound (CEUS) were performed to evaluate the tumor vascularity and viability. Additionally, its hepatotoxicity was tolerable at a medium dose. NDEB-TACE might be an effective therapeutic strategy for interventional therapy.

Arsenic trioxide (ATO) has remarkably enhanced therapeutic efficacy in treating both newly diagnosed and relapsed patients suffering from Acute Promyelocytic Leukemia (APL). Unfortunately, whether as a single agent, component of combined chemotherapy, or as a chemosensitizer or radiosensitizer combined with interventional therapy/radiotherapy, it did not benefit treatment of solid tumor (liver cancer, bladder cancer, glioma, breast cancer, cervical cancer, colorectal cancer, lung cancer, and melanoma) as seen from the clinical trials reported from the published journals or FDA-approved trials in the past decades. The clinical outcome failed to live up to our expectations, which was attributed to severe systemic toxicity and inappropriate pharmacokinetic such as low delivery efficiency and rapid renal elimination. Nanomedicine is designed to fuel up pharmaceuticals and polish off adverse effects by the moderation of their absorption, distribution, metabolism, and excretion. Nevertheless, quite a few nanodrugs (such as Doxil, Abraxane) were approved to be used clinically, and "from bench to bedside" it seems to be no easy way for most of them, such as nano-ATO. Encapsulating ATO into several types of nano-vehicles (liposome, polymer micelle, porous silicon, etc.), nano-TO can improve pharmacokinetic and become a prominent candidate to penetrate into tumor tissue, but so far no nanoATO clinical trials have been approved around the world. On summarizing the clinical trials of ATO on solid tumor and preclinical study of nano-ATO, it is believed there is still a chance for ATO to play a critical co-helper in a comprehensive therapy to fight with solid tumor.