Retraction: Cell membrane based biomimetic nanocomposites for targeted therapy of drug resistant EGFR-mutated lung cancer.

Retraction of 'Cell membrane based biomimetic nanocomposites for targeted therapy of drug resistant EGFR-mutated lung cancer' by Pengying Wu et al., Nanoscale, 2019, 11, 19520-19528, https://doi.org/10.1039/C9NR05791A.

Retraction: A solid ultrasonic coupling membrane for superficial vascular ultrasonography.

Retraction of 'A solid ultrasonic coupling membrane for superficial vascular ultrasonography' by Di Sun et al., Nanoscale, 2022, 14, 3545-3553, https://doi.org/10.1039/D1NR05353A.

A solid ultrasonic coupling membrane for superficial vascular ultrasonography.

Superficial thrombophlebitis is one of the most significant complications of superficial vein thrombosis. Rapid imaging and mapping with high resolution is particularly important for accurate diagnosis so as to carry out treatment as soon as possible. Ultrasound imaging technology has been used extensively because of the low-cost, minimal invasiveness, and convenient application in clinical practice. And the ultrasonic couplant is an essential component in ultrasound examination. However, when imaging superficial structures, traditional liquid ultrasonic couplants often produce inadequate results. In this study, we investigate whether a hydrogel membrane can be used to improve the imaging of superficial vessels. To this end, we generated a polyacrylamide-bacterial nanocellulose hydrogel membrane (PAM-BC) that efficiently forms at 60 °C in only 10 min by redox polymerization. With PAM-BC-2.5, it was possible to acquire high resolution intravascular ultrasound images to assess superficial vessels in humans and the superficial vasculature in rats and miniature pigs using various brands of ultrasound instruments. The PAM-BCs represent a new, solid ultrasonic membrane which is suitable for diagnosing disease in superficial vessels.

Cell membrane based biomimetic nanocomposites for targeted therapy of drug resistant EGFR-mutated lung cancer.

The therapeutic efficacy of anti-cancer nanomedicines is generally constrained due to limited accumulation in the solid tumors. In this study, we developed a biomimetic nano-carrier to enhance the chemo-therapeutic efficacy of doxorubicin and icotinib in a chemo-resistant non-small cell lung cancer (NSCLC) cell line harboring a mutation in the epidermal growth factor receptor (EGFR). The unique nanomedicine was prepared by coating with targeting cancer cell membrane proteins as highly specific ligands. The resulting biomimetic nanoparticles were highly stable and exhibited superior homologous targeting ability in vitro compared with control groups. In a mouse EGFR-mutated NSCLC xenograft model, intravenous injection of the biomimetic nanomedicine led to a high tumour inhibition rate (87.56%). Histopathological analysis demonstrated that the biomimetic nanomedicine had minimal side effects. Taken together, a cancer cell membrane-based biomimetic drug carrier can significantly enhance drug accumulation and improve therapeutic efficacy in cancers.

Precision Nanomedicine Development Based on Specific Opsonization of Human Cancer Patient-Personalized Protein Coronas.

When a nanomedicine is administrated into the human body, biomolecules in biological fluids, particularly proteins, form a layer on the surface of the nanoparticle known as a "personalized protein corona". An understanding of the formation and behavior of the personalized protein corona not only benefits the nanotherapy treatment efficacy but also can aid in disease diagnosis. Here we used Gd@C82(OH)22 nanoparticles, a nanomedicine effective against several types of cancer, as a model nanomedicine to investigate the natural protein fingerprint of the personalized protein corona formed in 10 human lung squamous cell carcinoma patients. Our analysis revealed a specific biomarker, complement component C1q, in lung cancer personalized protein coronas, abundantly bound to Gd@C82(OH)22 NPs. This binding altered the secondary structure of C1q protein and led to the activation of an innate immune response, which could be exploited for cancer immune therapy. On the basis of this finding, we provide a new strategy for the development of precision nanomedicine derived from opsonization of a unique protein fingerprint within patients. This approach overcomes the common pitfall of protein corona formation and exploits the corona proteins to generate a precision nanomedicine and diagnostic tool.

Comparison of perioperative characteristics and prognostic performance in patients with pulmonary lobectomy in early or later period after percutaneous coronary intervention.

BACKGROUND: In order to analyze the feasibility of pulmonary lobectomy for non-small cell lung cancer (NSCLC) in early period after percutaneous coronary intervention (PCI), the current study was designed to compare perioperative characteristics and prognostic performance of patients with pulmonary lobectomy within 3 months or 3 months later after PCI. METHODS: This study enrolled 349 patients simultaneously with NSCLC and coronary stenosis. There were 198 and 151 patients with pulmonary lobectomy within 3 months or 3 months later after PCI, respectively. RESULTS: Age of all patients was 62 [53-75] years. There was no difference in demographic characteristics, medical histories, cancer locations and stent numbers between two groups (P>0.05 for all). Operation time, blood loss and hospital stay after pulmonary lobectomy had no difference between two groups (P>0.05 for all). Compared with those with pulmonary lobectomy 3 months later after PCI, survival rate during 5 years after pulmonary lobectomy was significantly higher in patients with pulmonary lobectomy within 3 months after PCI (P<0.05 for all). CONCLUSIONS: Patients with pulmonary lobectomy within 3 months after PCI had similar perioperative characteristics and better prognostic performance, as compared to those with pulmonary lobectomy 3 months later after PCI. The current study could provide valuable information in patients simultaneously with NSCLC and coronary stenosis to decide the timing of pulmonary lobectomy, and it might be feasible to perform pulmonary lobectomy in early period after PCI.

Independent long-term result of robotic thymectomy for myasthenia gravis, a single center experience.

BACKGROUND: Robotic thymectomy has been suggested a feasible and safe approach for myasthenia gravis (MG). Few investigations have revealed the independent effect of robotic thymectomy without the confounding impact of immunosuppressive (IM) therapy. METHODS: Between May 2009 and December 2012, robotic extended thymectomy was carried out for patients with diagnosis of MG. The clinical data, subsequent neurological therapy and postintervention status were collected. RESULTS: Data of 37 cases was available for analysis. The mean follow-up was 70.0±13.3 months. The median age was 40 years. Twelve (32.4%) patients kept free of IM therapy, and 25 (67.6%) patients accepted postoperatively. The overall 5-year complete stable remission (CSR) rate was 40.6% and improvement rate was 81.6%. The young (age ≤40) displayed a significant better CSR rate (P=0.015) and a trend of better improvement rate (P=0.050) compared to the old (age >40). Patients without usage of IM therapy showed significant higher CSR rate (P=0.014) and improvement rate (P=0.024) compared to those with usage of IM therapy. Patients with Myasthenia Gravis Foundation of America (MGFA) classes I showed a trend of higher remission rate by multivariate analysis. No significant differences were found for the remission rate according to gender, pathology, and the duration of symptoms. CONCLUSIONS: The mono-therapy of robotic thymectomy may bring with a satisfactory long-term result for part of MG patients. Precision selection and individualized therapy are of the most importance.

Methylation of CHFR sensitizes esophageal squamous cell cancer to docetaxel and paclitaxel.

Esophageal squamous cell carcinoma (ESCC) is one of the most common malignancies worldwide. Both genetic and epigenetic changes are involved in esophageal carcinogenesis. CHFR methylation has been found frequently in different cancers and is regarded as a marker of taxane sensitivity. CHFR methylation was found in 0% (0/16) of normal mucosa, 2.9% (1/34) of grade I dysplasia, 0% (0/8) of grade II dysplasia, 12.5% (1/8) of grade III dysplasia and 45% (49/109) of invasive cancer. When treated with docetaxel or paclitaxel, cell viability was lower in CHFR methylated esophageal cancer cells than in unmethylated cells (p<0.05). No difference was found with either cisplatin or VP16 treatment in either group (p>0.05). In CHFR methylated cells, treatment with docetaxel or paclitaxel resulted in almost all cells being suspended in G0/G1 phase of the cell cycle. After 5-AZ treatment, there was an increased fraction of CHFR-methylated cells in S and G2/M phases (p<0.05). In conclusion, CHFR is frequently methylated in ESCC and the expression of CHFR is regulated by promoter region methylation. CHFR methylation is a late stage event in ESCC. Methylation of CHFR sensitized ESCC cells to taxanes. 5-AZ may re-sensitize chemotherapy resistant in refractory tumors by inducing cell cycle phase re-distribution.

SOX17 methylation inhibits its antagonism of Wnt signaling pathway in lung cancer.

The purpose of this study was to explore epigenetic changes and functions of SOX17 in human lung cancer. Five lung cancer cell lines and 88 primary lung cancer samples were examined in this study. Methylation-specific polymerase chain reaction (MSP), semi-quantitative reverse-transcription PCR, immunohistochemistry, luciferase reporter assays, colony-formation assays, and western blotting were used to analyze methylation changes and functions of SOX17 in lung cancer. SOX17 methylation was found in 60.2% of primary human lung cancer samples, and promoter region methylation of SOX17 silenced its expression. SOX17 methylation was associated with female patients and lung cancer differentiation. Colony-formation assays revealed that SOX17 suppressed lung cancer cell proliferation. Re-expression of SOX17 inhibited Wnt signaling in H23 lung cancer cell line. SOX17 acts as a Wnt signaling inhibitor.

AKT signaling pathway activated by HIN-1 methylation in non-small cell lung cancer.

The purpose of this study is to determine the epigenetic changes and function of High in Normal-1 (HIN-1) in non-small cell lung cancer (NSCLC). HIN-1 expression was examined by semiquantitative RT-PCR before and after 5-aza-2'-deoxycytidine (5-aza) treatment in NSCLC cell lines. Promoter methylation status of HIN-1 was tested by methylation-specific PCR (MSP). Effect of forced expression of HIN-1 on different key molecules of AKT signaling pathway was tested by Western Blot analysis in H157 and H23 cell lines. Promoter methylations are inversely correlated with expression of HIN-1 in eight (H23, H157, 95D, H1299, H358, H1752, H460, A549) of ten NSCLC cell lines and re-expression was observed by 5-aza treatment. We then tested promoter methylation of HIN-1 in primary NSCLC tissues. Methylation was detected in 73 out of 152 (48%) NSCLC cases. Forced expression of HIN-1 in NSCLC cell lines inhibited colony formation and induce apoptosis. Furthermore, overexpression of HIN-1 reduces the expression of phosphorated-AKT (p-AKT), c-myc, Bcl-2 and cyclinD1 while Bax was increased. Our data suggest that HIN-1 is a potential tumor suppressor gene in NSCLC, silenced by promoter hypermethylation and negatively regulate AKT signaling pathway.