RATIONALE: The presence of a mediastinal neurilemmoma accompanied by intrapulmonary sequestration is a rare occurrence. The clinical symptoms of a neurilemmoma depend on the site of the tumor. Diagnosis of pulmonary sequestration mainly depends on the presence of aberrant feeding arteries.
PATIENT CONCERNS: A 78-year-old woman was admitted to our hospital with a mediastinal space-occupying lesion of 50 years. Computed tomography and magnetic resonance imaging showed 2 roundish low-density shadows in the left posterior mediastinum.
DIAGNOSIS: The pathological findings of the upper cystic mass support the diagnosis of neurilemmoma. A branch of aorta was found supplying blood to the lower mass; it was considered a pulmonary sequestration.
INTERVENTIONS: Left-sided thoracotomy was planned to remove the chest space-occupying lesions. Two masses were completely removed. Severe adhesion between the left lower lobe and the diaphragm was successfully separated, the aberrant feeding vessel was properly managed, and the lower lobe was resected completely.
OUTCOMES: The patient experienced remission of symptoms, had no significant postoperative complications, and was discharged from the hospital.
LESSONS: Special attention should be paid to neurological involvement of the neurilemmoma and the fragile feeding arteries of the intrapulmonary sequestration. Early diagnosis and treatment are important in such cases.

Background: Exploration of the genes with abnormal expression during the development of breast cancer is essential to provide a deeper understanding of the mechanisms involved. Transcriptome sequencing and bioinformatics analysis of invasive ductal carcinoma and paracancerous tissues from the same patient were performed to identify the key genes and signaling pathways related to breast cancer development.
Methods: Samples of breast tumor tissue and paracancerous breast tissue were obtained from 6 patients. Sequencing used the Illumina HiSeq platform. All. Only perfectly matched clean reads were mapped to the reference genome database, further analyzed and annotated based on the reference genome information. Differentially expressed genes (DEGs) were identified using the DESeq R package (1.10.1) and DEGSeq R package (1.12.0). Using KOBAS software to execute the KEGG bioinformatics analyses, enriched signaling pathways of DEGs involved in the occurrence of breast cancer were determined. Subsequently, quantitative real time PCR was used to verify the accuracy of the expression profile of key DEGs from the RNA-seq result and to explore the expression patterns of novel cancer-related genes on 8 different clinical individuals.
Results: The transcriptomic sequencing results showed 937 DEGs, including 487 upregulated and 450 downregulated genes in the breast cancer specimens. Further quantitative gene expression analysis was performed and captured 252 DEGs (201 downregulated and 51 upregulated) that showed the same differential expression pattern in all libraries. Finally, 6 upregulated DEGs (CST2, DRP2, CLEC5A, SCD, KIAA1211, DTL) and 6 downregulated DEGs (STAC2, BTNL9, CA4, CD300LG, GPIHBP1 and PIGR), were confirmed in a quantitative real time PCR comparison of breast cancer and paracancerous breast tissues from 8 clinical specimens. KEGG analysis revealed various pathway changes, including 20 upregulated and 21 downregulated gene enrichment pathways. The extracellular matrix-receptor (ECM-receptor) interaction pathway was the most enriched pathway: all genes in this pathway were DEGs, including the THBS family, collagen and fibronectin. These DEGs and the ECM-receptor interaction pathway may perform important roles in breast cancer.
Conclusion: Several potential breast cancer-related genes and pathways were captured, including 7 novel upregulated genes and 76 novel downregulated genes that were not found in other studies. These genes are related to cell proliferation, movement and adhesion. They may be important for research into breast cancer mechanisms, particularly CST2 and CA4. A key signaling pathway, the ECM-receptor interaction signal pathway, was also identified as possibly involved in the development of breast cancer.

OBJECTIVE: The objective of this study was to evaluate the role and limit of iodine maps by dual-energy computed tomography (CT) single scan for pancreatic cancer.
METHODS: Thirty patients with suspected solitary pancreatic cancer were enrolled in this study and underwent CT perfusion and iodine maps. The parameters of pancreatic cancer and normal pancreatic tissue were calculated. Pearson correlation and paired t test were used for evaluating 2 techniques.
RESULTS: Iodine concentration had a moderate positive correlation with blood flow or blood volume (P < 0.05 for both). All values of iodine concentration and blood flow, iodine concentration, and blood volume had significant positive correlations (P < 0.001 for both). The mean effective dose for CT perfusion and iodine maps had significant difference (8.61 ± 0.00 mSv vs 1.13 ± 0.14 mSv, P < 0.001).
CONCLUSIONS: Iodine maps had the potential to replace routine CT perfusion for pancreatic cancer with low radiation dose.

RATIONALE: Hürthle cell adenoma (HCA) of the thyroid is a rare thyroid tumor, and there are limited studies on the contrast-enhanced computed tomography (CT).
PATIENT CONCERNS: We report the case of a 63-year-old woman with gradual enlargement of the thyroid over 10 years.
DIAGNOSES: Preoperative contrast-enhanced CT revealed typical lesion characteristics of HCA, confirmed by postoperative pathology.
INTERVENTIONS: Left thyroidectomy and partial right thyroidectomy were performed on the patient after general anesthesia.
OUTCOMES: At follow-up of 12 months after surgery, the patient was in good health without recurrence.
LESSONS: The typical imaging features of HCA on contrast-enhanced CT are helpful for the early diagnosis of thyroid eosinophilic adenoma. This will provide an important basis for the preoperative diagnosis and treatment strategy of HCA of the thyroid in future.

PURPOSE: Aspirin, one of the most commonly used nonsteroidal anti-inflammatory drugs (NAIDS), not only shows cancer chemoprevention effects but also improves cancer therapeutic effects when combined with other therapies. Studies that focus on aspirin regulation of the hallmarks of cancer and the associated molecular mechanisms facilitate a more thorough understanding of aspirin in mediating chemoprevention and may supply additional information for the development of novel cancer therapeutic agents.
METHODS: The relevant literatures from PubMed have been reviewed in this article.
RESULTS: Current studies have revealed that aspirin regulates almost all the hallmarks of cancer. Within tumor tissue, aspirin suppresses the bioactivities of cancer cells themselves and deteriorates the tumor microenvironment that supports cancer progression. In addition to tumor tissues, blocking of platelet activation also contributes to the ability of aspirin to inhibit cancer progression. In terms of the molecular mechanism, aspirin targets oncogenes and cancer-related signaling pathways and activates certain tumor suppressors.
CONCLUSION: Beyond a chemopreventive agent, aspirin is a master regulator of the hallmarks of cancer.

BACKGROUND Studies have shown inconsistent associations of nitrite and nitrate intake with the risk of gastric cancer or its associated mortality. We performed a meta-analysis of observational studies to evaluate the correlation of nitrite and nitrate intake with the risk of gastric cancer. MATERIAL AND METHODS We searched for studies reporting effect estimates and 95% confidence intervals (CIs) of gastric cancer in PubMed, EMBASE, and the Cochrane Library through November 2018. The summary results of the included studies were pooled using a random-effects model. RESULTS Eighteen case-control and 6 prospective cohort studies recruiting 800 321 participants were included in this study. The summary results indicated that the highest (odds ratio [OR], 1.27; 95%CI, 1.03-1.55; P=0.022) or moderate (OR: 1.12; 95%CI, 1.01-1.26; P=0.037) nitrite intake were associated with a higher risk of gastric cancer. However, we noted that high (OR, 0.81; 95%CI, 0.68-0.97; P=0.021) or moderate (OR, 0.86; 95%CI, 0.75-0.99; P=0.036) nitrate intakes were associated with a reduced risk of gastric cancer. These associations differed when stratified by publication year, study design, country, the percentage of male participants, assessment of exposure, adjusted model, and study quality. CONCLUSIONS High or moderate nitrite intake was associated with higher risk of gastric cancer, whereas high or moderate nitrate intake was correlated with lower risk of gastric cancer.

Glioblastoma multiforme (GBM) is a brain tumor that deeply infiltrates adjacent tissues and causes significant mortality. Thus, understanding the mechanisms that derive the invasion of brain tissue by GBM might help the treatment of this cancer. To this end, we examined the impact of BMP4 on invasion of GBM. In this study, Human GBM samples, GBM cells and human orthotopic GBM-xenografted animal model, quantitative PCR, immunostaining, immunoblotting, Scratch wound and transwell assays were used to detect the effect and the mechanism of BMP4 in GBM cells. BMP4 expression was found to positively correlate with E-cadherin and claudin expression in human GBM samples. Elevation or suppression of BMP4 expression resulted in a respective increase or decrease in E-cadherin and claudin levels, both

An association between genetic polymorphisms in encoding X-ray repair cross complementing group 1 (XRCC1) and encoding xeroderma pigmentosum group D (XPD) and risks of non-small-cell lung cancer (NSCLC) in East Chinese Han population has been observed. Herein we hypothesized that genetic polymorphisms in these two DNA repair genes are likely to be important in the NSCLC in Chinese nonsmoking female patients. We recruited 327 nonsmoking female patients with NSCLC and 342 individuals with benign lung diseases or healthy controls. Genotype frequencies of XRCC1 T-77C, Arg194Trp, Arg280His and Arg399Gln, Pro206Pro, and XPD Asp312Asn and Lys751Gln were calculated after Polymerase Chain Reaction amplification and sequencing. Generalized multifactor dimensionality reduction (GMDR) was used to detect the interactive effect of XRCC1 and XPD gene polymorphisms. The ratio of cooking oil mist exposure history and soot exposure history, and the gene frequencies of XRCC1 T-77C TC + CC, XRCC1 AG + GG, XRCC1 399Gln/Gln, and XPD 751Gln/Gln were higher in female patients with NSCLC than those with benign lung diseases or healthy controls. The haplotypes of XRCC1 T-Arg-Arg-Gln and XRCC1 C-Arg-Arg-Arg were positively associated with the NSCLC occurrence in nonsmoking female patients. GMDR discovered that there was an interactive model of XRCC1 and XPD genes in multiple gene loci. Logistic regression analysis showed that XRCC1 T-77C, XRCC1 Pro206Pro polymorphism, cooking oil mist and soot exposure history and tumor-node-metastasis (TNM) stage were related to NSCLC occurrence for nonsmoking female patients. Taken together, XRCC1 and XPD polymorphisms, cooking oil mist, and soot exposure history may be interactively correlated with NSCLC incidence for nonsmoking female patients.

AIMS: Kinesin family member 11 (Kif11) is a member of the kinesin family motor proteins, which is associated with spindle formation and tumour genesis. In this study, we investigated the relationship between Kif11 expression and clear cell renal cell carcinoma (CCRCC) development.
METHODS: The relationship between Kif11 expression and CCRCC development was analysed by quantitative real-time (qRT)-PCR analyses, and tissue immunohistochemistry. The prognostic significance of Kif11 expression was explored by univariable and multivariable survival analyses of 143 included patients. Furthermore, SB743921 was used as a specific Kif11 inhibitor to treat 786-O cells with the epithelial to mesenchymal transition (EMT) process analysed by qRT-PCR, and cell survival rates analysed with Annexin V-FITC/PI staining followed by flow cytometric analyses. Disease-free survival curves of Kif11 with different cancers and the relationships between Kif11 and the von Hippel-Lindau disease tumour suppressor gene (
RESULTS: The levels of
CONCLUSIONS: These results combined with bioinformation analyses suggest that high Kif11 expression was associated with unfavourable prognosis in CCRCC and could be used as a potential prognostic marker in the clinical diagnosis of CCRCC.

This study aimed to deeply analyze the application of DWI and DCE-MRI imaging in breast cancer, the correlation between the imaging characteristics of DWI and DCE-MRI and the molecular subtypes and prognostic factors of breast cancer was studied. Firstly, DWI and DCE-MRI scans of all patients before interventional therapy were performed, and relevant information of the subjects was introduced in turn. Secondly, molecular subtypes were determined according to immunohistochemical results and gene amplification. Siemens 3.0 T post-processing workstation was used for image post-processing. The time signal curve (TIC), early enhancement rate (EER) and ADC values were measured, morphological characteristics were recorded, and the correlation between each image feature and molecular subtypes, prognostic factors (tumor size, pathological grade, lymph node metastasis, ER, PR, HER2, Ki67) was analyzed. The results showed that parameters such as ADC value, EER, lobulation sign, burr sign, enhancement way and TIC type were correlated with prognostic factors and molecular subtypes. And Bayesian model discriminant analysis showed that the above imaging parameters couldn't well predict the expression of immunohistochemical factors and molecular subtypes. However, the above characteristics had a good effect on the prediction of pathological grade, with a false diagnosis rate of 9.69%.

A 40-year-old man with biopsy-proven papillary thyroid cancer received I radiotherapy. Posttherapy scan showed not only multiple foci of intense activity in the neck but also a small focal activity in the region of right upper mediastinum, confirmed by SPECT/CT images. This activity was suspected as mediastinal lymph node metastasis. However, pathology examination after the resection showed thymic cyst.

OBJECTIVE: This study aims to investigate the accuracy of the preoperative localization of small nodules by computerized tomography (CT)-guided placing wire and intrapleural fibrin glue near the nodules at 3 days before the operation.
METHODS: From October 2015 to December 2017, a total of 79 patients, who received preoperative localization of small pulmonary nodules and surgical treatment in the Department of Thoracic Surgery of Hohhot First Hospital, were enrolled into this study. These patients were randomly divided into 2 groups: methylene blue localization group (n = 47), and modified localization group (n = 32), where the patients received preoperative localization of the small nodules by CT-guided placing wire and intrapleural fibrin glue near the nodule at 3 days before the operation. Localization accuracy, operation time and difficulty in postoperative seeking for pathological specimens were compared between these 2 groups.
RESULTS: In the methylene blue localization group, 3 patients had localization failure due to the intrathoracic diffusion of methylene blue, and the success rate was 93.61%. In the modified localization group, all 32 patients succeeded in the localization, and the success rate was 100%. Operation time and difficulty of finding the specimen was significantly lower in the modified localization group than in the methylene blue localization group (P < .05).
CONCLUSION: The application of preoperative localization of small nodules by placing wire and intrapleural fibrin glue improves the success rate of resection, reduces operation time and the risk of the operation, and lowers the difficulty of finding pathological specimens after the operation. Hence this operative procedure is worthy of popularization.

BACKGROUND: Patients with cancer are vulnerable to depression or other depressive conditions. The aim of this paper was to evaluate the efficacy and safety of Chinese herbal medicine (CHM) for the treatment of depression or depressive symptoms in cancer patients.
METHODS: CENTRAL, MEDLINE, EMBASE, PsycINFO, CNKI, VIP, SinoMed, and online clinical trial registry websites were searched for relevant RCTs until May 2017. The methodological quality of each included study was assessed with the "risk of bias" tool. Review Manager 5.3.5 was used to analyze the data.
RESULTS: We identified 18 RCTs that included data from 1441 participants. Twelve different types of Chinese herbal preparations were investigated by these studies, and they showed a better therapeutic effect in most comparisons when measured in terms of depression rating scale scores, with SMDs (95% CI) of - 2.30 (- 3.54, - 1.05) (CHM versus no treatment), - 0.61 (- 1.03, - 0.18) (CHM versus antidepressants), and - 0.55 (- 1.07, - 0.02) (CHM plus psychological treatments versus psychological treatments), or when measured in terms of treatment response rate, with RRs (95% CI) of 1.65 (1.19, 2.29) (CHM versus no treatment), 1.15 (1.03, 1.28) (CHM versus psychological treatments), 1.32 (1.07, 1.63) (CHM plus antidepressants versus antidepressants), and 1.70 (1.02, 2.85) (CHM plus psychological treatments versus psychological treatments). Compared with antidepressants, these CHMs showed borderline superiority for improving the response rate, with an RR (95% CI) of 1.08 (0.93, 1.26). Subgroup analysis based on psychiatric diagnosis (depression versus depressive symptoms) did not modify the direction of these estimates and neither could it explain the high level of heterogeneity. Patients in the CHM group experienced fewer adverse events of cardiac toxicity (P = 0.02), functional gastrointestinal disorders (P = 0.008), sleep disturbances (P = 0.02), blurred vision (P = 0.02) and fatigue (P = 0.03) than the patients in the no treatment group or the antidepressants group.
CONCLUSIONS: According to the investigation of the twelve herbal preparations, the CHM intervention appears to alleviate depressive symptoms in cancer patients, either alone or combined with antidepressants or psychological treatments. However, a high risk of bias and high heterogeneity made the mean estimates uncertain. Well-designed trials with comprehensive and transparent reporting are warranted in the future.

Backgroud: Induction chemotherapy, as a larynx preservation treatment, has been available for over 20 years. We conducted a retrospective study to evaluate the efficacy of this protocol with taxene, cisplatin and 5-fluorouracil in Chinese patients with hypopharyngeal cancer that chose preservation strategy.
MATERIAL AND METHODS: 170 patients with locally advanced hypopharyngeal cancer were assigned to receive induction chemotherapy. 107 patients (63%) with complete response or partial response received larynx preservation treatment and 63 non-responders (37%) received radical surgery.
RESULTS: Median survival time was 30 months (range: 3-59 months). 63 patients (37%) had local-regional failure and 15 (9%) had distant metastasis. Three-year LFS was 27.8% (95% CI: 23.6-32.0%). The estimated three-year overall survival rate was 44.5% (95% CI: 39.5-49.5%). There was no significant difference in the three-year survival rate between responders (44.8%) and non-responders (43.9%) (p = .237), however patients with a partial response had a significant decrease in survival (32.2%) (p < .001).
CONCLUSIONS: In patients with hypopharyngeal cancer, ICT with TPF regimen followed by RT, as a larynx preservation treatment, may be suitable for complete responders, but not partial responders.

Numerous microRNAs (miRNAs) are dysregulated in tongue squamous cell carcinoma (TSCC), and their dysregulation has been demonstrated to have a strong correlation with TSCC progression via regulation of their targets. Therefore, miRNAs have potential use in the diagnosis and treatment of patients with TSCC. In the present study, miRNA‑758 (miR‑758) expression in TSCC tissues and cell lines was detected through reverse transcription‑quantitative polymerase chain reaction, and the effects of miR‑758 on TSCC cell proliferation and invasion were investigated by using Cell Counting kit‑8 and Transwell invasion assays. A luciferase reporter assay was performed to determine the target interaction between miR‑758 and metadherin (MTDH) in TSCC cells. The results revealed that miR‑758 was downregulated in TSCC tissues and cell lines. miR‑758 overexpression restricted the proliferation and invasion of TSCC cells. Additionally, MTDH was verified as a direct target gene of miR‑758 in TSCC cells. Furthermore, MTDH was observed to be upregulated in TSCC tissues, and the upregulation of MTDH was inversely correlated with miR‑758 expression. Moreover, restored MTDH expression significantly counteracted the suppressive effects of miR‑758 overexpression on TSCC cells. These results suggested that miR‑758 may prevent TSCC progression and development by directly targeting MTDH, thereby providing evidence that miR‑758 is a novel therapeutic target for the treatment of patients with TSCC.

The present study aims to construct a miRNA-based predictive signature of Uveal melanoma (UM) based on the database of the cancer genome atlas (TCGA). We obtained miRNA expression profiles and clinical information of 80 UM patients from TCGA, and randomly divided them into a training and a testing set. After data processing and forward screening, a total of 204 miRNAs with prognostic value were then examined by the Cox proportional hazard regression model in the training set. Receiver operating curve (ROC) analysis was applied to validate the accuracy of the signature. The biological relevance of putative miRNA target genes was also analyzed using the bioinformatics method. As a result, a linear prognostic model consisting of 9 miRNAs (miR-195, miR-224, miR-365a, miR-365b, miR-452, miR-4709, miR-7702, miR-513c, miR-873) was developed to divide UM patients into a high- and a low-risk group. Patients assigned to the high-risk group had significantly shorter overall survival than those in the low-risk group, which was further confirmed by the Area under curve (AUC) value of 0.858 at 5 year obtained from ROC. Gene Ontology (GO) analysis indicated that predicted target genes of these miRNAs are primarily associated with the modulation of protein expression and function, such as the activity of ubiquitin protein ligase and protein kinase. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that these genes were involved in multiple signaling pathways linked to carcinogenesis. The tumor specific 9-miRNA signature was also verified in the testing and entire set. In summary, based on UM data of TCGA, we identified and validated a 9-miRNA-based prognostic signature.

BACKGROUND Hepatocellular carcinoma (HCC) is the fifth most common malignancy in China, and China's annual number of new cases accounts for about 45% of the world total. This research was aimed to study the expression of TBX3 protein in HCC and exploring its clinical significance. MATERIAL AND METHODS We collected tumor tissues and adjacent non-tumoral tissues of 174 patients with HCC undergoing surgical resection. The expression of TBX3 protein in different tissues and cell lines in vitro (LO2, HHL-5, MHC97-L, MHC97-H) was detected by immunohistochemistry or Western blotting, and the relationship between TBX3 expression and clinical data of patients with HCC was analyzed. RESULTS The expression of TBX3 protein in HCC was significantly correlated with histological grade, tumor size, cancer cell metastasis, hepatitis B surface antigen, and the expression of Ki-67 in tumor tissues (P<0.05), and it was positively correlated with serum AFP level (r=0.766, P<0.05). The expression of TBX3 increased with increased histological grade in HCC (P<0.05). Cox regression analysis showed that the expression of TBX3 protein in HCC was an independent risk factor for prognosis (OR=0.524, 95% CI=0.283-0.964). The 5-year survival rate of patients with HCC that highly expressed TBX3 protein was 20.83%, which was significantly lower than the 40.20% rate in patients with low expression (P<0.05). CONCLUSIONS The expression of TBX3 in HCC patients undergoing surgical resection is high, and its expression increases with the degree of tumor differentiation. It is related to the metastasis of tumor cells and is positively correlated with the serum level of AFP and may affect the survival time of HCC patients undergoing surgical resection.

The present study was conducted to establish a risk assessment model for evaluating osteosarcoma prognosis based on prognosis-associated long non-coding RNA (lncRNA) expression. Human osteosarcoma expression profiles were obtained from the NCBI GEO and EBI ArrayExpress databases and differently expressed lncRNAs between good and poor prognosis groups were evaluated using Student's t-test and Wilcoxon rank test in R (v. 3.1.0). A multivariate Cox regression was used to establish a risk assessment system based on lncRNA expression levels, with the associated regression coefficients used as the weight. Survival analysis and receiver operating characteristic (ROC) curves were constructed to verify the accuracy of the risk assessment model. Associations between the prognosis, risk assessment model and clinical features were also investigated using univariate and multivariate Cox regression analyses. Furthermore, differentially expressed genes associated with the lncRNAs in the risk assessment model were identified, and functional enrichment analysis was performed. A total of 9 from the 211 differentially expressed lncRNAs were selected to establish the risk assessment model. The risk assessment model exhibited a good prognostic prediction ability, with high area under the curve values in the training and validation sets. Additionally, the calculated risk score based on the 9 selected lncRNAs was identified to be an independent prognostic factor for osteosarcoma. Furthermore, differentially expressed genes were primarily enriched in the cell cycle, oxidative phosphorylation and cell adhesion processes. The present study described a risk assessment model based on 9 significantly differentially expressed lncRNAs, which was identified to have a high accuracy in potentially predicting patient prognosis.

RATIONALE: Ciliopathies is a group of clinically and genetically overlapping disorders due to cilia abnormalities and multiple organ systems are involved in.
PATIENT CONCERNS: We present a young female patient who showed renal function impairment, Caroli syndrome (CS), liver cirrhosis, polycystic ovarian syndrome, and multiple subcutaneous cysts.
DIAGNOSES: The patient was diagnosed with ciliopathy according to the clinical manifestations and whole-genome sequencing.
INTERVENTIONS: She received treatment of intravenous albumin, polyene phosphatidyl choline, furosemide, and antisterone.
OUTCOMES: The patient showed clinical improvement in her edema and liver tests, and ultrasonography revealed that the ascites had disappeared. Unfortunately, the edema relapsed a year later. The patient received the same treatment as before, and there was clinical improvement of the edema. Since the family cannot afford liver and kidney transplantation, the patient only accepted symptomatic treatment.
LESSONS: Polycystic ovarian syndrome and multiple subcutaneous cysts have never before been reported to be associated with ciliopathy. This finding could remind doctors to consider the possibility of ciliopathy disease for patients suffering from similar conditions. In addition, the phenotype of the patient differs from those of patients reported with the same mutations, which also reminds doctors that the clinical manifestation of a given mutation may show patient-specific differences. This case report extends the phenotypic spectrum of ciliopathy, and these findings might represent a new ciliopathy syndrome, which could facilitate the diagnosis of ciliopathies.

Extrahepatic metastasis of hepatocellular carcinoma (HCC) may cause a diagnostic problem. All 195 cases of histologic and immunostained sections were reviewed retrospectively in one center. The expression of arginase-1 (Arg-1), hepatocyte paraffin-1 (HepPar-1), glypican-3 (GPC-3), and α-Fetoprotein (AFP) was evaluated. Eighty cases of metastatic tumors of the liver were also collected to verify their effectiveness. Totally 151 cases had previous history of HCC, in whom 49 had history of liver transplantation. Forty-four cases were diagnosed as metastatic HCC at initial presentation. The most common extrahepatic metastatic sites were bone (57%), followed by lung, lymph node, etc. Around 19 cases were positive for 1 marker, 22 were positive for 2 markers, 95 were positive for 3 markers, and 59 were positive for 4 markers. With the number of antibody increased in the panel, the negative cases decreased. The sensitivity of ARG, GPC-3, HepPar-1, and AFP was 82.6%, 89.2%, 83.6% and 53.8%, and the specificity was 98.3%, 94.8%, 96.2% and 100%, respectively. These data suggest that the panel of ARG-1, GPC-3, HepPar-1 and AFP has a high sensitivity and specificity to differentiate HCC from non-HCC. This study indicated that HCC should be considered when diagnosing metastasis of unclear origin. It is recommended to use the panel of ARG-1, GPC-3, HepPar-1 and AFP to differentiate HCC from non-HCC in extrahepatic metastasis, because of their sensitivity and specificity, especially in poorly differentiated lesions.

Ubiquitin-conjugating enzyme E2S (UBE2S), a family of E2 protein in the ubiquitination process, is involved in development of various cancers. However, its role in lung adenocarcinoma, has not been well elucidated. In this report, we attempted to investigate expression and function of UBE2S in lung adenocarcinoma. Up-regulation of UBE2S at mRNA, and protein level, was observed in human cancer tissues and lung adenocarcinoma cells. Higher UBE2S expression correlated with poorer prognosis of lung adenocarcinoma patients. UBE2S expression was efficiently suppressed by lentivirus-mediated shRNA strategy in A549 cells, and UBE2S silencing led to reduced cell proliferation, colony formation, and enhanced apoptosis. Inverse results were observed, in UBE2S over-expressed H1299 cells. Microarray analysis indicated that a large number of genes were regulated by UBE2S, and p53 signaling pathway may be critical, to the role of UBE2S in cancer development. Together, UBE2S could be a potential target for lung adenocarcinoma. [BMB Reports 2018; 51(12): 642-647].

Aberrant expression of miR‑154 is usually found in cancer studies; however, the role of miR‑154 has seldom been reported in bladder cancer (BCa). In this study, we observed that miR‑154 expression was significantly downregulated in BCa tissues and cell lines, and was associated with several clinicopathological characteristics, including advanced T stage, lymphatic invasion, and distant metastasis. Low expression level of miR‑154 was associated with poor survival outcomes in BCa patients. Overexpression of miR‑154 led to significant decrease in the proliferation, migration, and invasion of BCa cells, while knockdown of miR‑154 yielded the opposite effect. ATG7 was identified as a direct target of miR‑154. ATG7 expression was negatively correlated with miR‑154 expression in BCa tissues. Silencing of ATG7 achieved a similar effect to miR‑154 overexpression; overexpression of ATG7 reversed the inhibitory effect of miR‑154 on BCa cell proliferation, migration and invasion. A xenograft study revealed that miR‑154 inhibited BCa cell growth in vivo, and suppressed ATG7 expression. Altogether, this study demonstrated that miR‑154 may function as a tumor suppressor in BCa and indicated that miR‑154 may be a potential therapeutic target for BCa patients.

The upregulation of long non‑coding RNA (lncRNA) human ovarian cancer‑specific transcript 2 (HOST2) has been identified in breast cancer. The present study aimed to investigate whether lncRNA HOST2 regulated the proliferation of triple negative breast cancer (TNBC) cells, and the underlying molecular mechanism. In total, 30 patients with primary TNBC, who were treated at Wuhai People's Hospital (Wuhai, China), were recruited for the present study. Reverse transcription‑quantitative polymerase chain reaction analysis was used for the examination of gene expression levels. A Cell Counting kit‑8 (CCK‑8) assay was used for the detection of cell proliferation. Phases of the cell cycle were evaluated by flow cytometry. Western blot analysis was performed to detect protein expression levels. A dual luciferase activity assay was performed to examine the interaction between microRNA (miRNA) and the 3' untranslated region (UTR) of target mRNA. The results revealed increased expression levels of HOST2 in tumor tissues from patients with TNBC. A positive correlation was identified between the expression of HOST2 and cyclin‑dependent kinase 6 (CDK6) in tumor tissues. The silencing of HOST2 induced cell proliferation inhibition and cell cycle redistribution in MDA‑MB‑231 and MDA‑MB‑468 TNBC cells. In these two cell lines, HOST2 silencing caused a decrease in the phosphorylation of RB1 and CDK6, which was observed at the mRNA and protein levels. However, the silencing of CDK6 did not alter the expression of HOST2. It was hypothesized and confirmed that let‑7b, a previously reported target miRNA of HOST2, was able to directly bind to the 3'UTR of CDK6 and repress its expression. The expression of let‑7b was negatively correlated with the expression of HOST2 and CDK6 in tumor tissues. Overall, the data suggested that lncRNA HOST2 acts as an oncogene in TNBC via the upregulation of CDK6.

Heat shock protein 90 (HSP90) has been reported to promote the growth and inhibit apoptosis of hepatocellular carcinoma (HCC) cells. However, the underlying mechanisms are not fully understood. Immunostaining of the tissue array demonstrated that HSP90 was upregulated in HCC clinical samples and was associated with clinical features. HSP90 interacted with 3‑hydroxy‑3‑methylglutaryl‑CoA reductase (HMGCR), the rate‑limiting enzyme of mevalonate pathway, in the immunoprecipitation assay and regulated its protein expression level by inhibiting protein degradation. In addition, lovastatin, an inhibitor of HMGCR, impaired the oncogenic functions of HSP90 in the cell growth, migration and colony formation assays. Taken together, this study demonstrated that HSP90 promoted the progression of HCC by positively regulating the mevalonate pathway and indicated that HSP90 may be a promising therapeutic target.

Unresectable advanced pancreatic cancer (APC) is a highly lethal malignancy. Although numerous chemotherapeutic regimens are available, evidence regarding the survival extension, the life quality improvement, the associated risks and occurrence rates of adverse effects, is required. The effects of 19 chemotherapy regimens on survival and treatment‑associated toxicities in the context of APC treatment were comparatively assessed. A total of 23 randomized controlled trials were included in this network meta‑analysis. For overall survival, five regimens, Gemcitabine (Gem)+radiotherapy (Radio), Gem+cisplatin (Cis), Gem+erlotinib (Erl)+bevacizumab (Bev), Gem+capecitabine (Cap)+Erl, and Gem+exatecan, were the most effective treatments, according to their respective high surface under the cumulative ranking (SUCRA) probabilities. Regarding the progression‑free survival, five regimens, including Gem+Radio, Gem+Erl+Bev, Gem+Cis, Gem+Cap+Erl and Gem+pemetrexed, were the most effective treatments based on their SUCRA probabilities. Each regimen exhibited advantages and disadvantages, and 14 common treatment‑associated toxicities were present in different proportions. The three principal toxic effects included haematological, gastrointestinal and constitutional symptoms. To improve survival, chemotherapy regimens with high SUCRA probabilities require prioritizing. Although treatment‑associated toxicities are unavoidable, the regimens presented toxicities in distinct proportions. Therefore, clinicians should assess the disease status of the patients, and balance the benefits and risks of the selected treatment.

Breast cancer (BC) severely threatens women's life, and Triiodothyronine (T3) shows a positive role on BC cell proliferation, while the potential mechanism underlying it is still unclear. T3 was used to stimulate BC cell lines MCF-7 and T47-D. Real-time PCR was performed to determine the expression of miRNAs, while western blot was used to measure protein expression of Amphiregulin (AREG), AKT and p-AKT. The interaction between miR-204 and AREG was determined using luciferase reporter assay. MTT was performed to detect cell viability. The expression of miR-204 was decreased, while AREG and p-AKT was increased in T3 stimulated BC cell lines. T3 stimulation promoted cell viability. miR-204 targets AREG to regulate its expression. T3 promoted expression of AREG and p-AKT, while miR-204 overexpression reversed the effect of T3, however, pcDNA-AREG transfection abolished the effect of miR-204 mimic. T3 promoted cell viability of BC cells via modulating the AKT signaling pathway. The detailed mechanism was that the down-regulated miR-204 that induced by T3 stimulation promoted the expression of AREG, the up-regulated AREG activated AKT signaling pathway, while the activated AKT signaling promoted cell proliferation.

A 53-year-old man with tentative diagnosis of likely hepatocellular carcinoma underwent FDG PET/CT, which showed intense activity in both right lobe and caudate lobe of the liver. However, pathology examination from biopsy showed neuroendocrine tumor. He received transarterial chemoembolization and systemic chemotherapy. Posttherapy follow-up FDG PET/CT revealed no abnormal FDG activity in the liver.

AIM: Although the anti-neoplastic effects of physcion are well documented, its specific action in hepatocellular carcinoma (HCC) is not understood. Taken together, physcion is a promising drug candidate for the treatment and prevention of HCC.
MATERIAL AND METHODS: Cell Counting Kit-8 (CCK-8) assay utilized to examine the viability of Hep3B and SMMC7721 cells. Apoptotic cell population was measured by flow cytometry analysis assay. Cell migration and cell invasion were determined by wound healing and Transwell assay. Autophagy was determined by mRFP-GFP-LC3 adenovirus infection and monodansylcadaverine (MDC) staining. Western blot analysis was performed to examine the level of marker proteins in ovarian cancer cells. Moreover, xenograft model was established to evaluate the therapeutic effect of physcion in vivo.
KEY FINDINGS: We found that physcion inhibited proliferation, migration and invasion of HCC cells, and promoted apoptosis and autophagy in the HCC cells. Physcion-induced autophagy reduced the percentage of apoptotic cells, as well as the levels of pro-apoptotic proteins in the HCC cells. Pharmacological inhibition of autophagy with 3-MA, or Atg 5 knockdown, reversed this autophagy-mediated apoptosis inhibition, indicating a pro-survival role of the former in HCC. Furthermore, suppressing autophagy also abrogated the inhibitory effect of physcion on HCC cell migration and invasion, indicating that autophagy is essential for its anti-metastatic effects. Physcion induced protective autophagy by inactivating the JAK2-STAT3 pathway, and activating the latter by IL-6 reversed the pro-survival effects of autophagy.
SIGNIFICANCE: Physcion is a promising drug candidate for the treatment and prevention of HCC.

Radiotherapy resistance in patient with non‑small cell lung cancer (NSCLC) reduces patient survival and remains a significant challenge for the treatment of NSCLC. Radiation resistance has been demonstrated to be affected by secreted factors, yet it remains unclear how autocrine secretions affect the radioresistance of NSCLC cells. In the present study, the NSCLC cell line, NCI‑H460, was irradiated with γ‑rays (4 Gy) and then cultured in medium from H460 cells or normal medium to examine the potential influence of cell secretions on the radiation resistance of H460 cells. Cell viability, accumulation of reactive oxygen species and DNA repair capacity were all markedly improved in the irradiated H460 cells that were cultured in conditioned medium (CM), compared with those cells cultured in normal medium. In addition, G2/M cell cycle arrest and upregulation of homologous recombination repair proteins were observed in the CM‑treated cells, while exosomes secreted by H460 cells had no influence on the radiation resistance of H460 cells. Taken together, these results indicate that autocrine secretions enhance the radiation resistance of γ‑irradiated H460 cells and that these secretions mainly affect the DNA repair process.

The HGF/c-MET pathway is active in the development of digestive system cancers, indicating that inhibition of HGF/c-MET signaling may have therapeutic potential. Various HGF/c-MET signaling inhibitors, mainly c-MET inhibitors, have been tested in clinical trials. The observed efficacy and adverse events of some c-MET inhibitors were not very suitable for treating digestive system cancers. The development of new HGF/c-MET inhibitors in preclinical studies may bring promising treatments and synergistic combination (traditional anticancer drugs and c-MET inhibitors) strategies provided anacceptable safety and tolerability. Insights into miRNA biology and miRNA therapeutics have made miRNAs attractive tools to inhibit HGF/c-MET signaling. Recent reports show that several microRNAs participate in inhibiting HGF/c-MET signaling networks through antagonizing c-MET or HGF in digestive system cancers, and the miRNAs-HGF/c-MET axis plays crucial and novel roles for cancer treatment. In the current review, we will discuss recent findings about inhibitors of HGF/c-MET signaling in treating digestive system cancers, and how miRNAs regulate digestive system cancers via mediating HGF/c-MET pathway.