Hypotension from afatinib in epidermal growth factor receptor-mutated non-small cell lung cancer: a case report and literature review.

Side effects of afatinib are a problem in patients with advanced non-small cell lung cancer (NSCLC). However, little is known about the occurrence of afatinib-induced hypotension. An 81-year-old man with NSCLC had an epidermal growth factor receptor-positive genotype with the p.L861Q mutation in exon 21. He was administered afatinib (40 mg/day) as anticancer therapy. Hypotension occurred twice after afatinib initiation. He suffered from dizziness and nausea. Blood pressure gradually returned to normal after afatinib cessation. Clinicians should be aware of hypotension in patients with NSCLC after afatinib initiation.

TGF-ß-induced α-SMA expression is mediated by C/EBPß acetylation in human alveolar epithelial cells.

BACKGROUND: Although the morbidity and mortality rates associated with idiopathic pulmonary fibrosis (IPF) are high, there is still lack of powerful and precise therapeutic options for IPF. OBJECT: Through in vitro model, this study sought to determine whether binding of acetylated CCAAT/enhancer binding protein ß (C/EBPß) to alpha-smooth muscle actin (α-SMA) promoter could affect the activity of the latter as well as assess if it is essential for epithelial-to-mesenchymal transition (EMT) and extracellular matrix deposition in IPF. METHODS: The expression of EMT and C/EBPß in A549 cells treated with transforming growth factor-beta (TGF-ß) as pulmonary fibrotic model was detected by western blotting and qPCR. Collagen-I expression using ELISA was performed. The luciferase activity was used to examine the activity of C/EBPß. Knockdown of C/EBPß was performed by siRNA. We also investigated the effect of deacetylation of C/EBPß on EMT using sirtuin 1 (SIRT1). The binding ability of C/EBPß with α-SMA promoter was affirmed via chromatin immunoprecipitation (ChIP) and electrophoresis mobility shift assay (EMSA). The relationship between α-SMA and acetylated C/EBPß was determined with co-immunoprecipitation (Co-IP). SiRNA-mediated knockdown of C/EBPß in A549 cells attenuated TGF-ß1-induced myofibroblast differentiation and ECM deposition. The extent of association between acetylated C/EBPß and α-SMA promoter was dynamically monitored. RESULTS: It was confirmed that deacetylation of C/EBPß in A549 cells successfully ameliorated TGF-ß1-induced EMT, as shown by reduction in α-SMA expression and excessive collagen-I accumulation. CONCLUSION: The EMT and fibrotic effect of TGF-ß1 is dependent on acetylated C/EBPß-mediated regulation of α-SMA gene activity. Thus, C/EBPß acetylation may play a central role in pulmonary fibrosis.

The prognostic role of MAC30 in advanced gastric cancer patients receiving platinum-based chemotherapy.

AIM: We aimed to investigate a practical profile of MAC30 on chemotherapeutic response in gastric cancer (GC). PATIENTS & METHODS: We elected 87 GC patients receiving platinum-based chemotherapy in this study. MAC30 levels in tumor and adjuvant nontumor tissues were confirmed via reverse transcription-PCR to identify the clinical profile in GC and the correlation with therapeutic response. RESULTS: We found elevated MAC30 in GC compared with the matched adjacent nontumor tissues. GC with enhanced MAC30 exhibited poorer survival by Kaplan-Meier analysis and poor response to adjuvant platinum-based chemotherapy. A multivariate analysis showed that MAC30 was an independent prognostic factor of overall survival in GC receiving platinum-based chemotherapy. CONCLUSION: MAC30 could play as a potential biomarker for prognosis of GC with platinum-based chemotherapy.

Antifibrotic properties of receptor for advanced glycation end products in idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a progressive chronic interstitial lung disease with poor survival. Previous reports suggested the contributory effect of receptor for advanced glycation end products (RAGE) to the pathogenesis of IPF. But the findings are controversial. The present in vivo study with RAGE null mice, we further confirmed the evidence that lack of RAGE evolves worse bleomycin-induced pulmonary fibrosis compared with control mice. Moreover, RAGE null mice spontaneously developed similar pathogenesis of lung fibrosis via immunohistochemical staining. In addition, we investigated the negative roles of RAGE on epithelial-mesenchymal transition (EMT) indicated by elevated α-smooth muscle actin (α-SMA) and collagen-I (Col-I) deposition in A549 cell treated with transforming growth factor-ß (TGF-ß), all of which were blocked by sRAGE, a decoy receptor. Furthermore, interacting with the specific ligand as AGE, RAGE blocked TGF-ß-induced activation of Smad2, ERK and JNK signals in A549 cells, which were also challenged by sRAGE administration. This present study confirmed an important role of RAGE in vivo and vitro models of pulmonary fibrosis and suggested the therapeutic possibility for pulmonary fibrosis via RAGE regulation.

DNA damage in peripheral blood lymphocytes from patients with OSAHS.

PURPOSE: Obstructive sleep apnea hypopnea syndrome (OSAHS) is characterized by intermittent hypoxia during sleep time, followed by oxidative stress. Hypoxia-induced oxidative stress can lead to DNA damage, which is related to chromosome aberrations and micronuclei. The purpose of this study is to investigate the level of DNA damage in peripheral blood of patients with OSAHS. METHODS: Thirty patients with OSAHS diagnosed by polysomnography and 28 healthy volunteers were assessed by the Epworth sleepiness scale. The levels of DNA damage were investigated through the cytokinesis-blocked micronucleus assay. RESULTS: In the group of patients with OSAHS, the mean frequency of binucleated cells with micronuclei were significantly higher than that in the control group (P<0.01), and the frequency of micronuclei among the patients in mild, moderate, and severe stages differed significantly (P<0.05). The mean frequency of nucleoplasmic bridge in OSAHS group was also higher than that in the control group (P<0.05). Nasal continuous positive airway pressure treatment decreased the frequencies of binucleated cells with micronuclei, nucleoplasmic bridge, and nuclear buds. CONCLUSIONS: Oxidative DNA damage increased in peripheral blood lymphocytes of OSAHS patients. It may be related to oxidative stress induced by intermittent hypoxia and may be involved in the pathogenesis of cardiovascular and other target organ injuries.

Integrated analysis of purine metabolism assists in predicting prognosis and treatment decisions for patients with lung adenocarcinoma.

The incidence of lung cancer, especially lung adenocarcinoma (LUAD), has recently increased. Targeted therapy and immunotherapy combined with conventional treatment have shown surprising benefits in enhancing the LUAD patient's prognosis. For the purpose of guiding treatment planning and the prognosis of LUAD, more research is required. The particular aim of this work was to establish a purine metabolism scoring (PMS) model for the purpose of individually forecasting treatment outcomes and overall survival for patients who have LUAD. Clinical and whole genome data were obtained from the TCGA-LUAD cohort via "UCSC". The 25 driver purine metabolism-related prognostic genes were determined founded on univariate Cox regression. Then PMS was developed through stepwise LASSO Cox regression. Survival analysis indicated that patients who have PMS experienced worse outcomes. We validated the PGM2 effect on lung adenocarcinoma malignancy in in vitro experiments. Univariate as well as multivariate Cox regression suggested that PMS was an independent prognostic indicator for LUAD patients, which was confirmed in subgroup analysis. Functional assay demonstrated that immune response as well as cytotoxicity pathways have a connection with lower PMS, and patients who have low PMS possess an active immune microenvironment. Moreover, the LUAD patients who have low PMS showed greater sensitivity to immunotherapy, targeted therapy, as well as chemotherapy. Knockdown of PGM2 was discovered to decrease the proliferation, invasion, as well as migration of lung adenocarcinoma cells in an in vitro assay. Pertaining to this particular research, we created a PMS model and conducted a thorough analysis of purine metabolism in LUAD in order to determine prognosis and offer recommendations for treatment. This finding offered a fresh concept for the clinical management of LUAD and novel therapy protocols.

Promotion of Dentin Biomimetic Mineralization and Bonding Efficacy by Interfacial Control of an Experimental Citric Acid Dental Etching Agent.

Resin-bonded restorations are the most important caries treatment method in clinical practice. Thus, improving the durability of dentin bonding remains a pressing issue. As a promising solution, guided tissue remineralization can induce the formation of apatite nanocrystals to repair defects in the dentin bonding interface. In this study, we present an experimental 20 wt % citric acid (CA) dental etching agent that removes the smear layer. After CA-etching, approximately 3.55 wt % residual CA formed a strong bond with collagen fibrils, reducing the interfacial energy between the remineralizing solution and dentin. CA helped achieve almost complete intrafibrillar and extrafibrillar mineralization after 24 h of mineralization. CA also significantly promoted poly(amidoamine)-induced dentin biomimetic mineralization. The elastic modulus and microhardness of remineralized dentin were restored to that of sound dentin. The remineralized interface reduced microleakage and provided a stronger, longer-lasting bond than conventional phosphate acid-etching. The newly developed CA dental etching agents promoted rapid dentin biomimetic mineralization and improved bonding efficacy through interfacial control, representing a new approach with clinical practice implications.

Synergistic effect of ion-releasing fillers on the remineralization and mechanical properties of resin-dentin bonding interfaces.

In modern restorative dentistry, adhesive resin materials are vital for achieving minimally invasive, esthetic, and tooth-preserving restorations. However, exposed collagen fibers are found in the hybrid layer of the resin-dentin bonding interface due to incomplete resin penetration. As a result, the hybrid layer is susceptible to attack by internal and external factors such as hydrolysis and enzymatic degradation, and the durability of dentin bonding remains limited. Therefore, efforts have been made to improve the stability of the resin-dentin interface and achieve long-term clinical success. New ion-releasing adhesive resin materials are synthesized by introducing remineralizing ions such as calcium and phosphorus, which continuously release mineral ions into the bonding interface in resin-bonded restorations to achieve dentin biomimetic remineralization and improve bond durability. As an adhesive resin material capable of biomimetic mineralization, maintaining excellent bond strength and restoring the mechanical properties of demineralized dentin is the key to its function. This paper reviews whether ion-releasing dental adhesive materials can maintain the mechanical properties of the resin-dentin bonding interface by supplementing the various active ingredients required for dentin remineralization from three aspects: phosphate, silicate, and bioactive glass.

Elevated serum Activin A in chronic obstructive pulmonary disease with skeletal muscle wasting.

OBJECTIVE: Muscle wasting contributes to the reduced quality of life and increased mortality in chronic obstructive pulmonary disease (COPD). Muscle atrophy in mice with cachexia was caused by Activin A binding to ActRIIB. The role of circulating Activin A leading to muscle atrophy in COPD remains elusive. METHODS: In the present study, we evaluated the relationship between serum levels of Activin A and skeletal muscle wasting in COPD patients. The expression levels of serum Activin A were measured in 78 stable COPD patients and in 60 healthy controls via ELISA, which was also used to determine the expression of circulating TNF-α levels. Total skeletal muscle mass (SMM) was calculated according to a validated formula by age and anthropometric measurements. The fat-free mass index (FFMI) was determined as the fat-free mass (FFM) corrected for body surface area. RESULTS: Compared to the healthy controls, COPD patients had upregulated Activin A expression. The elevated levels of Activin A were correlated with TNF-α expression, while total SMM and FFMI were significantly decreased in COPD patients. Furthermore, serum Activin A expression in COPD patients was negatively associated with both FFMI and BMI. CONCLUSION: The above results showed an association between increased circulating Activin A in COPD patients and the presence of muscle atrophy. Given our previous knowledge, we speculate that Activin A contributes to skeletal muscle wasting in COPD.

Diagnostic role of Wnt pathway gene promoter methylation in non small cell lung cancer.

Wnt signal pathway genes are known to be involved with cancer development. Here we tested the hypothesis whether DNA methylation of genes part of the Wnt signaling pathway could help the diagnosis of non-small cell lung cancer (NSCLC). The methylation levels of SFRP1, SFRP2, WIF1 and PRKCB in 111 NSCLC patients were evaluated by quantitative methylation-specific PCR (qMSP). Promoter methylation levels of four candidate genes were significantly higher in tumor tissues compared with the adjacent tissues. SFRP1, SFRP2 and PRKCB genes were all shown to be good predictors of NSCLC risk (SFRP1: AUC = 0.711; SFRP2: AUC = 0.631; PRKCB: AUC = 0.650). The combined analysis showed that the methylation status of the four genes had a sensitivity of 70.3% and a specificity of 73.9% in the prediction of NSCLC risk for study cohort. A higher diagnostic value with an AUC of 0.945 (95% CI: 0.923-0.967, sensitivity: 90.6%, specificity: 93.0%) was found in TCGA cohort. In addition, SFRP1 and SFRP2 hypermethylation events were specific to male patients. Further TCGA data mining analysis suggested that SFRP1_cg15839448, SFRP2_cg05774801, and WIF1_cg21383810 were inversely associated with the host gene expression. Moreover, GEO database analysis showed that 5'-Aza-deoxycytidine was able to upregulate gene expression in several lung cancer cell lines. Subsequent dual-luciferase reporter assay showed a crucial regulatory function of PRKCB promoter. In summary, our study showed that a panel of Wnt signal pathway genes (SFRP1, SFRP2, WIF1 and PRKCB) had the potential as methylation biomarkers in the diagnosis of NSCLC.

AGTR1 promoter hypermethylation in lung squamous cell carcinoma but not in lung adenocarcinoma.

Aberrant DNA methylation is associated with non-small cell lung cancer (NSCLC), suggesting that gene promoter methylation may be a potential biomarker for the detection or risk prediction of NSCLC. The present study aimed to evaluate the potential usage of angiotensin II receptor type 1 (AGTR1) methylation in two major pathologic subtypes: Lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC). Quantitative methylation-specific polymerase chain reaction was used to investigate the effect of AGTR1 promoter methylation in the tumor and the paired adjacent non-tumor tissue samples from 42 patients with LUSC, and 69 with LUAD. The percentage of methylated reference was calculated and presented as the median (interquartile range 25th-75th percentile). The results of the current study revealed that there was significantly increased AGTR1 promoter methylation in the tumor tissues compared with the paired adjacent non-tumor tissue [97.4 (57.22-130.5) vs. 85 (48.25-123); P=0.024]. Furthermore, higher AGTR1 promoter methylation was observed in patients with LUSC compared with LUAD (odds ratio=2.483; 95% confidence interval=1.125-5.480; P=0.023). Significant differences were identified in AGTR1 methylation between non-tumor and the tumor tissues in LUSC [113.5 (68.33-148.73) vs. 93.04 (45.94-140); P=0.008]. In addition, the Cancer Genome Atlas data of 378 patients with LUSC and 477 with LUAD revealed an inverse correlation between gene expression and the methylation status of AGTR1 promoter.. These data suggest that AGTR1 hypermethylation is a promising biomarker to assist in LUSC detection and diagnosis.

The Prognostic Effect of MAC30 Expression on Patients With Non-Small Cell Lung Cancer Receiving Adjuvant Chemotherapy.

The purpose of this study was to examine the MAC30 expression in non-small cell lung cancer and to evaluate its prognostic value on therapeutic response in patients with non-small cell lung cancer receiving postoperative chemotherapy. Among a total of 218 retrospective Chinese patients with non-small cell lung cancer, 164 patients receiving adjuvant chemotherapy were enrolled in this study. Real-time polymerase chain reaction was performed to confirm the expression of MAC30 messenger RNA in 32 cases of non-small cell lung cancer tumors with the corresponding nontumor lung tissues. The MAC30 protein expression in all specimens was analyzed by immunohistochemical staining. Moreover, we assessed the correlation of MAC30 expression with clinicopathological features, therapeutic response, and survival of patients. Here, we observed the increased expression of MAC30 messenger RNA in patients with non-small cell lung cancer compared to those in control samples. The overexpression of MAC30 was strongly associated with poor tumor differentiation, high tumor-node-metastasis stage, and lymph node metastasis. In addition, we observed that patients with increased MAC30 expression showed gloomy overall survival and disease-free survival. A multivariate analysis explicated that higher MAC30 expression was a valuable independent prognostic factor of poorer tumor differentiation, shorter overall survival, and disease-free survival in patients receiving chemotherapy. MAC30 could be a useful biomarker of tumor differentiation and outcome of patients with non-small cell lung cancer. Overexpression of MAC30 predicts a worse tumor differentiated stage and prognosis in patients with non-small cell lung cancer receiving adjuvant chemotherapy.

Synthesis, characterization and anticancer activities of transition metal complexes with a nicotinohydrazone ligand.

The reaction of divalent transition metal salts and (E)-N'-(1-(pyridin-2-yl)ethylidene)nicotinohydrazide (penh) led to the formation of [Mn(penh)2] (complex 1), [Co(penh)2] (complex 2), [Cu(penh)2] (complex 3) and [Cd (penh)2] (complex 4) complexes. The four complexes were characterized using elemental analyses, infrared spectra and single-crystal X-ray diffraction analyses. Subsequently, the complexes were used for in vitro cell level experiments to determine potential antitumor effects. The results demonstrated that the complexes exhibited a similar structure; however, they were crystallized with distinct space groups. In comparison with the uncomplexed penh ligand, all four complexes were able to markedly decrease the proliferation rate of various types of tumor cell, including the human lung cancer cell line A549, human gastric cancer cell line BGC823 and human esophageal cancer cell line Eca109, in a concentration-dependent manner. Furthermore, the complexes promoted tumor cell apoptosis, as demonstrated in the apoptosis assay, and this was confirmed using electrophoresis.

Synthesis, characterization and antitumor activity of Ln(III) complexes with hydrazone Schiff base derived from 2-acetylpyridine and isonicotinohydrazone.

In the present study, two isostructural lanthanide (Ln)(III) complexes, namely Ln(HL)2(NO3)(CH3OH)2)·CH3OH, where Ln = La in complex 1 and Ce in complex 2, and hydrogen ligand (HL) = (E)-N'-[1-(2-pyridinyl)ethylidene]isonicotinohydrazone, have been isolated and characterized by elemental analysis, infrared spectra and single-crystal X-ray diffraction analysis. The results revealed that the acylhydrazone ligand HL in each complex was deprotonated as an anionic ligand and coordinated to the central La(III) ion via enolization of oxygen and nitrogen atoms. Furthermore, the antitumor effects and potential mechanisms of the two complexes were explored in the human lung cancer cell line A549 and in the human gastric cancer cell lines BGC823 and SGC7901. In the present study, the roles the two complexes on the proliferation and apoptosis of the above tumor cell lines were determined by MTT assay and Annexin V/propidium iodide flow cytometry, respectively. Furthermore, various apoptosis-associated key genes, including caspase 3, B cell lymphoma (Bcl)-2-associated X protein (Bax) and Bcl-2, were detected by western blotting to explore the possible antitumor mechanisms of the two complexes. The results revealed that the two complexes had comparable antitumor activities in terms of inhibiting proliferation and inducing apoptosis in tumor cell lines. The changes in the protein expression levels of caspase 3, Bax and Bcl-2 further verified the apoptosis-promoting mechanisms of the two complexes in tumor cell lines. These findings have a great potential in biomedical applications of novel Ln(III) complexes.

Design and synthesis of novel N()-substituted thiosemicarbazones bearing a pyrrole unit as potential anticancer agents.

A series of N(4)-substituted thiosemicarbazones (TSCs) bearing pyrrole unit (1a-1e) were synthesized and fully characterized by elemental analyses, infrared spectra, 1H nuclear magnetic resonance and single crystal X-ray diffraction. The compounds were assessed as potential chemotherapeutic agents. All newly synthesized compounds were screened for their anticancer activity against lung cancer PC-9, esophageal cancer Eca-109 and gastric cancer SGC-7901 cell lines. The results of MTT, Terminal deoxynucleotidyl transferase dUTP nick end labeling and fluorescence-activated cell sorting assays indicated that all the prepared compounds exhibited cytotoxicity against PC-9, Eca-109 and SGC-7901 cells in vitro. All the compounds significantly induced cancer cell apoptosis accompanied by increasing the Bax/Bcl-2 ratio and activation of caspase-3. The structure-activity association was discussed and the potential pre-clinical trials may be conducted. The present findings have a great potential in biomedical applications of novel N(4)-substituted TSCs.

Using fluorescently-labeled magnetic nanocomposites as a dual contrast agent for optical and magnetic resonance imaging.

Dual-modality imaging probes synergistically combine magnetic resonance (MR) and fluorescence into a single nanocomposite. This promising technique affords a new level of flexibility for molecular imaging uses in biomedical research. In this study, we report a new strategy for the synthesis of a novel attapulgite nanorod-based atta@Fe3O4@[Ru(bpy)2(fmp)]Cl2 nanocomposite (atta@Fe3O4@Ru NC). Our synthesized NC has both photoluminescent and magnetic properties, bright fluorescence, as well as significant magnetic resonance. Transmission electron microscopy, energy dispersive spectroscopy, fluorescence spectrometry, and magnetization measurements were all used to validate its properties. In vitro studies showed that our functionalized NC had high cellular biocompatibility and was successfully used to label living cells through endocytosis of cells. Moreover, a CCK8 assay showed that even high concentrations of the atta@Fe3O4@Ru NC had low toxicity. Finally, the intravenous administration of the atta@Fe3O4@Ru NC to a rabbit model of hepatic carcinoma resulted in a marked and negatively enhanced T2-weighted MRI in both normal liver and tumor, which can further enhance the visibility of the liver cancer tissue and normal liver tissue. Collectively, these results suggest that the atta@Fe3O4@Ru NC can be used for tumor discovery and diagnosis.

Overexpression of MAC30 is Resistant to Platinum-Based Chemotherapy in Patients With Non-Small Cell Lung Cancer.

Adjuvant platinum-based chemotherapy has developed its stability as the first-line treatment in advanced non-small cell lung cancer (NSCLC). The objective of this study was to investigate the prognostic value of meningioma-associated protein (MAC30) on adjuvant platinum-based chemotherapeutic response and survival in patients with NSCLC. A total of 174 retrospective stage III B to IV Chinese patients with NSCLC were enrolled in the study. Among all cases, 85 patients were given platinum-based chemotherapy and another 89 patients received molecularly targeted therapy. The expression of MAC30 in tumor samples was confirmed via immunohistochemical staining to correlate with the therapeutic response and survival of patients. Patients having NSCLC with MAC30 overexpression showed a poorer response to platinum-based chemotherapy, while there was no prognostic value of MAC30 expression on molecularly targeted therapy. Further, patients receiving platinum-based chemotherapy with enhanced MAC30 expression exhibited shorter survival. A multivariate analysis exhibited that increased MAC30 expression was an independent prognostic factor for overall survival in patients having NSCLC with platinum-based chemotherapy. In conclusion, patients having NSCLC with higher MAC30 expression resisted to platinum-based chemotherapy and exhibited worse survival.

Prognostic Value of MAC30 Expression in Human Pure Squamous Cell Carcinomas of the Lung.

Recent evidence haas indicated that meningioma-associate protein (MAC30) exhibits different expression patterns in various tumors. However, little is known about the value of MAC30 in human squamous cell carcinoma of lung (SQCLC). The purpose of our study was to investigate the expression of MAC30 and to explore its clinical significance in SQCLC patients. A total of 156 Chinese patients diagnosed with SQCLC were selected for this study. The expression of MAC30 in all tissues was confirmed by immunohistochemical staining. Quantitative real-time PCR was performed to analyze MAC30 mRNA expression in 32 cases of SQCLC patients with corresponding non-tumor lung tissues. We observed enhanced mRNA expression of MAC30 in SQCLC as compared to control samples. Further, elevated MAC30 protein expression was strongly associated with poor tumor differentiation, TNM stage, and lymph node metastasis. In addition, we observed that patients with increased MAC30 expression demonstrated poor overall survival. Multivariate analysis explicated that increased MAC30 expression was a valuable independent predictable factor for poor tumor differentiation and short survival in SQCLC patients. Our present study suggests that MAC30 may serve as a biomarker for poor tumor differentiation and outcomes of patients with SQCLC.

Multifunctional nanocomposite based on halloysite nanotubes for efficient luminescent bioimaging and magnetic resonance imaging.

A novel multifunctional halloysite nanotube (HNT)-based Fe3O4@HNT-polyethyleneimine-Tip-Eu(dibenzoylmethane)3 nanocomposite (Fe-HNT-Eu NC) with both photoluminescent and magnetic properties was fabricated by a simple one-step hydrothermal process combined with the coupling grafting method, which exhibited high suspension stability and excellent photophysical behavior. The as-prepared multifunctional Fe-HNT-Eu NC was characterized using various techniques. The results of cell viability assay, cell morphological observation, and in vivo toxicity assay indicated that the NC exhibited excellent biocompatibility over the studied concentration range, suggesting that the obtained Fe-HNT-Eu NC was a suitable material for bioimaging and biological applications in human hepatic adenocarcinoma cells. Furthermore, the biocompatible Fe-HNT-Eu NC displayed superparamagnetic behavior with high saturation magnetization and also functioned as a magnetic resonance imaging (MRI) contrast agent in vitro and in vivo. The results of the MRI tests indicated that the Fe-HNT-Eu NC can significantly decrease the T2 signal intensity values of the normal liver tissue and thus make the boundary between the normal liver and transplanted cancer more distinct, thus effectively improving the diagnosis effect of cancers.