Jianwei Wang

A ZnO sonosensitizer optimized by oxygen defect modulation is used to achieve cancer therapy with excellent sonodynamic activity. The antitumor efficacy is testified both in vitro and in vivo .

Sonodynamic therapy (SDT) typically suffers from compromised anticancer efficacy owing to the low reactive oxygen species (ROS) yield and complicated tumor microenvironment (TME) which can consume ROS and support the occurrence and development of tumors. Herein, ultrathin‐FeOOH‐coated MnO₂ nanospheres (denoted as MO@FHO) as sonosensitizers which can not only facilitate ultrasound (US)‐triggered ROS but also tune the TME by hypoxia alleviation, H₂O₂ consumption as well as glutathione (GSH) depletion are designed. The FeOOH coating will boost the production yield of singlet oxygen (¹O₂) and hydroxyl radicals (^•OH) by inhibiting the recombination of US‐initiated electron–hole pairs and Fenton‐like reaction, respectively. Additionally, the catalase‐like and GSH peroxidase‐like activities of MO@FHO nanospheres enable them to break the TME equilibrium via hypoxia alleviation and GSH depletion. The combination of high ROS yield and fundamental destruction of TME equilibrium results in satisfactory antitumor outcomes, as demonstrated by the high tumor suppression efficacy of MO@FHO on MDA‐MB‐231‐tumor‐bearing mice. No obvious toxicity is detected to normal tissues at therapeutic doses in vivo. The capability to modulate the ROS production and TME simultaneously can afford new probability for the development of advanced sonosensitizers for synergistic comprehensive cancer therapy.

Metal oxides hold great promise as robust sonosensitizers for sonodynamic therapy (SDT). However, they usually suffer from limited production yield of reactive oxygen species (ROS) due to the fast recombination of ultrasound‐triggered electrons and holes. Herein, porous lanthanum (La)‐doped MnO₂ (LMO) nanoparticles are firstly developed as promising sonosensitizers in SDT. The strategic introduction of La dopants greatly promotes the separation efficiency of ultrasound‐triggered electrons and holes of MnO₂, endowing them with significantly improved ROS yield. Consequently, the LMO with polyethylene glycol decoration exhibits good SDT activity toward breast cancer cells. This work highlights the doping strategy for the development of enhanced ROS production of metal oxide sonosensitizers for SDT.

: Considerable attention has been focused on aqueous supercapacitors (SCs), owing to their large power density and excellent cycling stability, which makes them more suitable for high power applications. However, the lower energy densities ( E ) of aqueous SCs as compared to batteries have impeded their range of commercial applications. To overcome this challenge, intensive studies have been devoted to the topic, in which surface engineering becomes critical to the high‐performance electrode design due to the efficient manipulation of a material surface to boost energy storage while maintaining the integrity of interior of the material. The purpose of this Minireview article is to highlight recent significant breakthroughs realized through surface engineering approaches such as surface functionalization, heterostructure design, and surface charge modulation. Current challenges, emerging trends, and opportunities for advanced SCs are discussed accordingly.

This study was aimed to assess whether ultrasonic spectrum analysis of radiofrequency (RF) time series using a clinical ultrasound system allows for early differentiating between the chemotherapy responders and nonresponders in human breast cancer xenografts that imitate clinical responding and nonresponding tumors. Clinically responding (n = 20; MCF-7) and nonresponding (n = 20; MBA-MD-231) breast cancer xenografts were established in 40 nude mice. Ten mice from each group received either chemotherapy (adriamycin, 4 mg/kg) or saline as controls. Each tumor was imaged longitudinally with a clinical ultrasound scanner at baseline (day 0) and subsequently on days 2, 4, 6, 8 and 12 following treatment, and the corresponding RF time-series data were collected. Changes in six RF time-series parameters (slope, intercept, S1, S2, S3 and S4) were compared with the measurement of the tumor cell density, and their differential performances of the treatment response were analyzed. Adriamycin significantly inhibited tumor growth and decreased the cancer cell density in responders (P < 0.001) but not in nonresponders (P > 0.05). Fold changes of slope were significantly increased in responders two days after adriamycin treatment (P = 0.002), but not in nonresponders (P > 0.05). Early changes in slope on day 2 could differentiate the treatment response in 100% of both responders (95% CI, 62.9–100.0%) and nonresponders (95% CI, 88.4–100%). Ultrasonic RF time series allowed for the monitoring of the tumor response to chemotherapy and could further serve as biomarkers for early differentiating between the treatment responders and nonresponders.

Background: Famitinib is a tyrosine kinase inhibitor against multiple targets, including vascular endothelial growth factor receptor 2/3, platelet‐derived growth factor receptor, and stem cell factor receptor (c‐kit). Previous studies have demonstrated anti‐tumour activities of famitinib against a wide variety of advanced‐stage solid cancers. We aimed to determine the safety and efficacy of famitinib with concurrent chemoradiotherapy (CCRT) in patients with locoregionally advanced nasopharyngeal carcinoma (NPC). We also evaluated the feasibility of contrast‐enhanced ultrasound (D‐CEUS) as a predictor of early tumour response to famitinib and to correlate functional parameters with clinical efficacy. Methods: The trial was conducted in subjects with stage III or IVa‐b NPC using a 3 + 3 design of escalating famitinib doses. Briefly, subjects received 2 weeks of famitinib monotherapy followed by 7 weeks of famitinib plus CCRT. D‐CEUS of the neck lymph nodes was performed at day 0, 8 and 15 after famitinib was administered before starting concurrent chemoradiotherapy. End points included safety, tolerability and anti‐tumour activity. Results: Twenty patients were enrolled (six each for 12.5, 16.5 and 20 mg and two for 25 mg). Two patients in the 25 mg cohort developed dose‐limiting toxicities, including grade 4 thrombocytopenia and grade 3 hypertension. The most common grade 3/4 adverse events were leukopenia, neutropenia and radiation mucositis. D‐CEUS tests showed that more than 60% of patients achieved a perfusion parameter response after 2 weeks taking famitinib alone, and the parameter response was associated with disease improvement. In the famitinib monotherapy stage, three patients (15%) showed partial responses. The complete response rate was 65% at the completion of treatment and 95% 3 months after the treatment ended. After a median follow‐up of 44 months, the 3‐year progression‐free survival (PFS) and distant metastasis‐free survival were 70% and 75%, respectively. Subjects with a decrease of perfusion parameter response, such as peak intensity decreased at least 30% after 1 week of famitinib treatment, had higher 3‐year PFS (90.9% vs. 44.4%, 95% CI 73.7%–100% vs. 11.9%–76.9%, P < 0.001) than those with an increase or a reduction of less than 30%. Conclusions: The recommended famitinib dose for phase II trial is 20 mg with CCRT for patients with local advanced NPC. D‐CEUS is a reliable and early measure of efficacy for famitinib therapies. Further investigation is required to confirm the effects of famitinib plus chemoradiotherapy.