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1.
Clin Cancer Res ; 2020 Apr 24.
Artigo em Inglês | MEDLINE | ID: mdl-32332018

RESUMO

PURPOSE: To identify a predictive biomarker of sorafenib for HCC personalized therapy. EXPERIMENTAL DESIGN: The patients treated with or without sorafenib after HCC recurrence from multi-centers were matched with propensity score matching analysis. The expression levels of FLT3 in HCC specimens of the matched patients (n=276) were analyzed by immunohistochemistry. The optimal cutoff point of FLT3 levels for overall survival (OS) was defined via Cutoff Finder. Subgroup analysis of OS was employed to investigate the association between FLT3 levels and sorafenib benefit. The predictive value was assessed via Cox regression models with an interaction term. HCC and para-tumoral normal tissues were used to investigate the expression and CNV of FLT3. PDX models were used to confirm the association between FLT3 levels and sorafenib response. RESULTS: HCC patients with high FLT3 levels exhibited a superior OS upon sorafenib treatment. High FLT3 levels were predictive of sorafenib benefit in term of OS (p of interaction=0.00006). Copy number losses and decreased expression of FLT3 in HCC were detected in about 64% of patients. Moreover, the PDXs derived from tumors with high FLT3 levels also displayed a better response to sorafenib. CONCLUSIONS: Sorafenib may be able to delay tumor progression in FLT3-High HCC patients. This potential biomarker needs to be further validated in independent cohorts prior to helping stratify patients for precision therapy in advanced HCC.

2.
Thorac Cancer ; 11(5): 1211-1215, 2020 May.
Artigo em Inglês | MEDLINE | ID: mdl-32162769

RESUMO

BACKGROUND: To develop a model of malignant risk prediction of solitary pulmonary nodules (SPNs) using metabolic characteristics of lesions. METHODS: A total of 362 patients who underwent PET/CT imaging from January 2013 to July 2017 were analyzed. Differences in the clinical and imaging characteristics were analyzed between patients with benign SPNs and those with malignant SPNs. Risk factors were screened by multivariate nonconditional logistic regression analysis. The self-verification of the model was performed by receiver operating characteristic (ROC) curve analysis, and out-of-group verification was performed by k-fold cross-validation. RESULTS: There were statistically significant differences in age, maximum standardized uptake value (SUVmax ), size, lobulation, spiculation, pleural traction, vessel connection, calcification, presence of vacuoles, and emphysema between patients with benign nodules and those with malignant nodules (all P < 0.05). The risk factors for malignant nodules included age, SUVmax , size, lobulation, calcification and vacuoles. The logistic regression model was as follows: P = l/(1 + e-x ), x = - 5.583 + 0.039 × age + 0.477 × SUVmax + 0.139 × size + 1.537 × lobulation - 1.532 × calcification + 1.113 × vacuole. The estimated area under the curve (AUC) for the model was 0.915 (95% CI: 0.883-0.947), the sensitivity was 89.7%, and the specificity was 78.9%. K-fold cross-validation showed that the training accuracy was 0.899 ± 0.011, and the predictive accuracy was 0.873 ± 0.053. CONCLUSIONS: The risk factors for malignant nodules included age, SUVmax , size, lobulation, calcification and vacuoles. After verification, the model has satisfactory accuracy, and it may assist clinics make appropriate treatment decisions.

3.
Breast Cancer Res Treat ; 180(2): 379-384, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32034579

RESUMO

PURPOSE: Protease-activated receptor 1 (PAR1) is a signaling protein ubiquitously present on the surface of tumor cells, and its homologous protein fragment, PAR1-activating peptide (P1AP), can inhibit protein signal transduction of PAR1/G in tumor cells. pH (Low) insertion peptide (pHLIP) can target the acidic tumor microenvironment (TME) and can be used as an excellent carrier to deliver P1AP to tumor cells for therapeutic purposes. METHODS: PAR1 expression on the surface of MDA-MB-231 cells and human MCF10A mammary epithelial cells was observed. The binding between fluorescent-labeled pHLIP(Var7)-P1AP and MDA-MB-231 cells under different pH values was analyzed. The effect of pHLIP(Var7)-P1AP on the proliferation of MDA-MB-231 cells was analyzed under the conditions of pH 7.4 and 6.0. RESULTS: PAR1 was highly expressed on the surface of MDA-MB-231 cells. In an acidic environment (pH 6.0 and 5.0), fluorescent-labeled pHLIP(Var7)-P1AP and MDA-MB-231 cells had a high binding ability, and the binding ability increased with the decrease in pH. In an acidic environment (pH 6.0), pHLIP(Var7)-P1AP significantly inhibited MDA-MB-231 cell proliferation. With 0.5 µg, 1 µg, 2 µg, 4 µg, and 8 µg of pHLIP(Var7)-P1AP, the cell proliferation inhibition rates were 3.39%, 5.27%, 14.29%, 22.14%, and 35.69%, respectively. CONCLUSION: PAR1 was highly expressed on the surface of MDA-MB-231 cells. pHLIP(Var7)-P1AP can effectively target MDA-MB-231 cells in an acidic environment and inhibit the growth of MDA-MB-231 cells by inhibiting the signal transduction of PAR1/G protein.

4.
Expert Opin Ther Targets ; 24(4): 389-402, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-32106726

RESUMO

Objectives: Cepharanthine exhibits a wide range of therapeutic effects against numerous cancers by virtue of its pleiotropic mechanisms. However, cepharanthine monotherapy has insufficient drug efficacy for cancers in animal models and clinical trials. The mechanism of its limited efficacy is unknown.Methods: We investigated the possible mechanism for the limited drug efficacy of cepharanthine in cancer therapy using both hepatocellular carcinoma (HCC) primary cells and cell lines, in vitro and in mouse xenograft models.Results: We found that cepharanthine hydrochloride (CH), a semi-synthetic derivative of cepharanthine, induced mitophagy independent of mTOR signaling, and played an AMPK-dependent protective role in the cell fate of HCC in vitro and in vivo. Mechanistically, we demonstrated that CH may bind to GPR30 receptor to activate the subsequent signal cascade involving mitochondrial fission, thus facilitating mitophagy. Therefore, we proposed a new therapeutic regimen for HCC involving CH combined with an autophagy inhibitor. This regimen exhibited remarkable anti-cancer effects in HCC xenograft mouse model.Conclusion: These results identify CH as a new mitophagy inducer targeting GPR30 receptor. The combination therapy of CH and an autophagy inhibitor may become a novel strategy for enhancing the anti-tumor potential of cepharanthine in HCC.

5.
BMC Genomics ; 20(1): 825, 2019 Nov 08.
Artigo em Inglês | MEDLINE | ID: mdl-31703618

RESUMO

BACKGROUND: 5-Azacytidine (5-azaC) promotes the development of 'Kyoho' grape berry but the associated changes in gene expression have not been reported. In this study, we performed transcriptome analysis of grape berry at five developmental stages after 5-azaC treatment to elucidate the gene expression networks controlling berry ripening. RESULTS: The expression patterns of most genes across the time series were similar between the 5-azaC treatment and control groups. The number of differentially expressed genes (DEGs) at a given developmental stage ranged from 9 (A3_C3) to 690 (A5_C5). The results indicated that 5-azaC treatment had not very great influences on the expressions of most genes. Functional annotation of the DEGs revealed that they were mainly related to fruit softening, photosynthesis, protein phosphorylation, and heat stress. Eight modules showed high correlation with specific developmental stages and hub genes such as PEROXIDASE 4, CAFFEIC ACID 3-O-METHYLTRANSFERASE 1, and HISTONE-LYSINE N-METHYLTRANSFERASE EZA1 were identified by weighted gene correlation network analysis. CONCLUSIONS: 5-AzaC treatment alters the transcriptional profile of grape berry at different stages of development, which may involve changes in DNA methylation.

6.
Mol Carcinog ; 58(10): 1897-1907, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-31313392

RESUMO

The mechanism of hepatocellular carcinoma (HCC) metastasis remains poorly understood. Tropomodulin 3 (TMOD3) is a member of the pointed end capping protein family that contributes to invasion and metastasis in several types of malignancies. It has been found to be crucial for the membranous skeleton and embryonic development, although, its role in HCC progression remains largely unclear. We observed increased levels of Tmod3 in HCCs, especially in extrahepatic metastasis. High Tmod3 expression correlated with aggressive carcinoma and poor patient with HCC survival. Loss-of-function studies conducted by us determined Tmod3 as an oncogene that promoted HCC growth and metastasis. Mechanistically, Tmod3 increases transcription of matrix metalloproteinase-2, -7, and -9 which required PI3K-AKT. Interaction between Tmod3 and epidermal growth factor receptor (EGFR) that supports the activation of EGFR phosphorylation, is essential for signaling activation of PI3K-AKT viral oncogene homolog. These findings reveal that Tmod3 enhances aggressive behavior of HCC both in vitro and in vivo by interacting with EFGR and by activating the PI3K-AKT signaling pathway.


Assuntos
Carcinoma Hepatocelular/genética , Proliferação de Células/genética , Neoplasias Hepáticas/genética , Tropomodulina/genética , Animais , Carcinoma Hepatocelular/patologia , Progressão da Doença , Intervalo Livre de Doença , Transição Epitelial-Mesenquimal/genética , Receptores ErbB/genética , Feminino , Regulação Neoplásica da Expressão Gênica/genética , Xenoenxertos , Humanos , Neoplasias Hepáticas/patologia , Masculino , Camundongos , Pessoa de Meia-Idade , Metástase Neoplásica , Proteína Oncogênica v-akt/genética , Fosfatidilinositol 3-Quinases/genética , Transdução de Sinais/genética
7.
Genes (Basel) ; 10(7)2019 07 06.
Artigo em Inglês | MEDLINE | ID: mdl-31284601

RESUMO

Previous study has demonstrated that the riboflavin treatment promoted the early ripening of the 'Kyoho' grape berry. However, the molecular mechanism causing this was unclear. In order to reveal the regulation mechanism of riboflavin treatment on grape berry development and ripening, the different berry developmental stages of the 'Kyoho' berry treated with 0.5 mmol/L of riboflavin was sampled for transcriptome profiling. RNA-seq revealed that 1526 and 430 genes were up-regulated and down-regulated, respectively, for the comparisons of the treatment to the control. TCseq analysis showed that the expression patterns of most of the genes were similar between the treatment and the control, except for some genes that were related to the chlorophyll metabolism, photosynthesis-antenna proteins, and photosynthesis, which were revealed by the enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). The differentially expressed genes and weighted gene co-expression network analysis (WGCNA) analysis identified some significantly differentially expressed genes and some hub genes, including up-regulation of the photosynthesis-related ELIP1 and growth and development-related GDSL; and down-regulation of the oxidative stress-related ATHSP22 and berry softening-related XTH32 and GH9B15. The results suggested that the riboflavin treatment resulted in the variations of the expression levels of these genes, and then led to the early ripening of the 'Kyoho' berry.


Assuntos
Frutas/efeitos dos fármacos , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Riboflavina/farmacologia , Vitis/efeitos dos fármacos , Frutas/genética , Vitis/genética
8.
Sci Rep ; 9(1): 9820, 2019 Jul 08.
Artigo em Inglês | MEDLINE | ID: mdl-31285444

RESUMO

MicroRNA-212-3p inhibits several human cancers but its effects on hepatocellular carcinoma (HCC) remain unclear. In this study, we show that miR-212-3p is down-regulated in HCC cell lines and tissues, and correlates with vascular invasion (p = 0.001), and the absence of capsule formation (p = 0.009). We found that miR-212-3p influenced the epithelial to mesenchymal transition (EMT) of HCCLM3 and Huh7 cells. Mechanistically, miR-212-3p repressed cell invasion through the suppression of connective tissue growth factor (CTGF). We therefore validate the anti-HCC effects of miR-212-3p through its ability to suppress CTGF and subsequent EMT.

9.
Oncol Lett ; 17(2): 2317-2327, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30675297

RESUMO

MicroRNAs (miRNAs) serve an important regulatory role in carcinogenesis and cancer progression. Aberrant expression of miR-197-3p has been reported in various human malignancies. However, the role of miR-197-3p in the progression and prognosis of hepatocellular carcinoma (HCC) remains unknown. The present study demonstrated that miR-197-3p was downregulated in HCC tissues and that the low level of miR-197-3p expression in HCC tumours correlated with aggressive clinicopathological characteristics; thus, miR-197-3p may serve as a predictor for poor prognosis in patients with HCC. Additionally, miR-197-3p markedly inhibited the metastasis of HCC cells in vitro and in vivo. Bioinformatics analysis further identified zinc finger protein interacted with K protein 1 (ZIK1) as a novel target of miR-197-3p in HCC cells. These findings suggest that miR-197-3p may regulate the survival of HCC cells, partially through the downregulation of ZIK1. Therefore, the miR-197-3p/ZIK1 axis may serve as a novel therapeutic target in patients with HCC.

10.
J Hepatol ; 70(5): 904-917, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30654066

RESUMO

BACKGROUND & AIMS: Genetic variability in the hepatitis B virus X gene (HBx) is frequently observed and is associated with hepatocellular carcinoma (HCC) progression. However, a genotype classification based on the full-length HBx sequence and the impact of genotypes on hepatitis B virus (HBV)-related HCC prognosis remain unclear. We therefore aimed to perform this genotype classification and assess its clinical impact. METHODS: We classified the genotypes of the full-length HBx gene through sequencing and a cluster analysis of HBx DNA from a cohort of patients with HBV-related HCC, which served as the primary cohort (n = 284). Two independent HBV-related HCC cohorts, a validation cohort (n = 171) and a serum cohort (n = 168), were used to verify the results. Protein microarray assay analysis was performed to explore the underlying mechanism. RESULTS: In the primary cohort, the HBx DNA was classified into 3 genotypes: HBx-EHBH1, HBx-EHBH2, and HBx-EHBH3. HBx-EHBH2 (HBx-E2) indicated better recurrence-free survival and overall survival for patients with HCC. HBx-E2 was significantly correlated with the absence of liver cirrhosis, a small tumor size, a solitary tumor, complete encapsulation and Barcelona Clinic Liver Cancer (BCLC) stage A-0 tumors. Additionally, HBx-E2 served as a significant prognostic factor for patients with BCLC stage B HCC after hepatectomy. Mechanistically, HBx-E2 is unable to promote proliferation in HCC cells and normal hepatocytes. It also fails to activate the Janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3)/STAT5 pathway. CONCLUSION: Our study identifies a novel HBx genotype that is unable to promote the proliferation of HCC cells and suggests a potential marker to preoperatively predict the prognosis of patients with BCLC stage B, HBV-associated, HCC. LAY SUMMARY: We classified a novel genotype of the full-length hepatitis B virus X gene (HBx), HBx-E2. This genotype was identified in tumor and nontumor tissues from patients with hepatitis B virus-related hepatocellular carcinoma. HBx-E2 could preoperatively predict the prognosis of patients with intermediate stage hepatocellular carcinoma, after resection.

11.
Clin Nucl Med ; 44(4): 299-300, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30688747

RESUMO

Kimura's disease is a clinically rare, chronic, benign lymphoproliferative disorder of unknown etiology. A 36-year-old man presented with painless axillary swelling, which was suspected as lymphoma. PET/CT was performed for staging. The images showed multiple foci of increased activity in bilateral axillary and right inguinal lymph nodes. Laboratory tests revealed an increased eosinophil ratio and eosinophil count. Pathological examination from dissected axillary lymph nodes was consistent with Kimura's disease.


Assuntos
Hiperplasia Angiolinfoide com Eosinofilia/complicações , Fluordesoxiglucose F18 , Linfadenopatia/diagnóstico por imagem , Linfadenopatia/etiologia , Linfoma/diagnóstico por imagem , Tomografia Computadorizada com Tomografia por Emissão de Pósitrons , Adulto , Diagnóstico Diferencial , Humanos , Masculino
12.
Oncotarget ; 9(54): 30240-30252, 2018 Jul 13.
Artigo em Inglês | MEDLINE | ID: mdl-30100986

RESUMO

Lysosomal associated membrane protein 2 (Lamp2) influences a broad range of physiological and pathological processes. However, little is known about the role of Lamp2 in hepatocellular carcinoma (HCC) metastasis. This study found that Lamp2 expression was significantly lower in HCC tissues than in adjacent nontumor tissues (ANTs), and its expression level correlated with HCC metastasis. Low Lamp2 expression was significantly correlated with the AFP serum level (> 20 ng/Ml, P = 0.024), capsular formation (absent, P = 0.024), and microvascular invasion (present, P < 0.001), and low expression of Lamp2 indicated a poor prognosis in HCC. LowLamp2 expression was an independent and significant risk factor for recurrence-free survival (RFS; P < 0.001) and overall survival (OS; P < 0.001) in HCC. In this study, we demonstrated that Lamp2 overexpression inhibited cell motility and invasiveness in vitro and inhibited lung metastasis in vivo. In addition, Lamp2 could reverse the EMT program. Lamp2 silencing by siRNA in HCC cell lines enhanced the expression of mesenchymal markers and decreased the expression of epithelial markers. Consistent with these findings, Lamp2 overexpression had the opposite effects. Mechanistically, we found that Lamp2 could suppress Snail expression, upregulate E-cadherin, and inhibit HCC cell epithelial-mesenchymal transition (EMT).Together, these findings suggest that Lamp2 attenuates EMT by suppressing Snail expression in HCC.

13.
Ann Surg ; 268(6): 943-954, 2018 12.
Artigo em Inglês | MEDLINE | ID: mdl-29521740

RESUMO

BACKGROUND: Despite antiviral treatment has been shown to reduce hepatocellular carcinoma (HCC) recurrence after curative treatment for hepatitis B virus (HBV)-related HCC in patients with high preoperative HBV-DNA levels, it is still unclear whether antiviral therapy is useful in reducing recurrence in patients with low preoperative HBV-DNA levels. METHODS: In this randomized controlled trial, 200 patients who underwent curative resection for HCC with low baseline HBV-DNA levels were randomly assigned to receive preemptive antiviral therapy or not. The primary endpoints were recurrence-free survival. This study was censored on March 31, 2015 when all surviving patients had a minimum follow-up of 60 months. The analysis was done on an intention-to-treat basis. RESULTS: The baseline clinical, laboratory, and tumor characteristics of the 2 groups were comparable. The 1-, 3-, and 5-year recurrence-free survival rates for the antiviral group and the control group were 85.9%, 55.2%, and 52.0% and 80.6%, 40.9%, and 32.3%, respectively. The corresponding overall survival rates for the 2 groups were 94.0%, 75.7%, and 64.1% and 90.0%, 62.4%, and 43.7%, respectively. The recurrence-free survival and overall survival for the antiviral group were significantly better than the control group (P = 0.016, P = 0.004, respectively). After adjusting for confounding prognostic factors in a Cox model, the relative risks of recurrence and death for antiviral treatment were 0.601 [95% confidence interval (CI), 0.409-0.884; P = 0.010] and 0.509 (95% CI, 0.333-0.778; P = 0.002), respectively. Antiviral therapy was an independent protective factor of late tumor recurrence (hazard ratio [HR] = 0.316, 95% CI 0.157-0.637; P = 0.001) but not of early tumor recurrence (HR = 0.782, 95% CI, 0.493-1.240; P = 0.296). CONCLUSIONS: In patients with low preoperative HBV-DNA levels, antiviral therapy significantly reduced HCC recurrence after R0 hepatic resection.


Assuntos
Antivirais/uso terapêutico , Carcinoma Hepatocelular/tratamento farmacológico , Carcinoma Hepatocelular/virologia , DNA Viral/sangue , Neoplasias Hepáticas/tratamento farmacológico , Neoplasias Hepáticas/virologia , Recidiva Local de Neoplasia/prevenção & controle , Telbivudina/uso terapêutico , Carcinoma Hepatocelular/patologia , Carcinoma Hepatocelular/cirurgia , Feminino , Vírus da Hepatite B/genética , Humanos , Neoplasias Hepáticas/patologia , Neoplasias Hepáticas/cirurgia , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Taxa de Sobrevida
14.
J Hepatol ; 68(6): 1214-1227, 2018 06.
Artigo em Inglês | MEDLINE | ID: mdl-29378234

RESUMO

BACKGROUND & AIMS: In recent years, circular RNAs (circRNAs) have been shown to have critical regulatory roles in cancer biology. However, the contributions of circRNAs to hepatocellular carcinoma (HCC) remain largely unknown. METHODS: cSMARCA5 (a circRNA derived from exons 15 and 16 of the SMARCA5 gene, hsa_circ_0001445) was identified by RNA-sequencing and validated by quantitative reverse transcription PCR. The role of cSMARCA5 in HCC progression was assessed both in vitro and in vivo. circRNAs in vivo precipitation, luciferase reporter assay, biotin-coupled microRNA capture and fluorescence in situ hybridization were conducted to evaluate the interaction between cSMARCA5 and miR-17-3p/miR-181b-5p. RESULTS: The expression of cSMARCA5 was lower in HCC tissues, because of the regulation of DExH-Box Helicase 9, an abundant nuclear RNA helicase. The downregulation of cSMARCA5 in HCC was significantly correlated with aggressive characteristics and served as an independent risk factor for overall survival and recurrence-free survival in patients with HCC after hepatectomy. Our in vivo and in vitro data indicated that cSMARCA5 inhibits the proliferation and migration of HCC cells. Mechanistically, we found that cSMARCA5 could promote the expression of TIMP3, a well-known tumor suppressor, by sponging miR-17-3p and miR-181b-5p. CONCLUSION: These results reveal an important role of cSMARCA5 in the growth and metastasis of HCC and provide a fresh perspective on circRNAs in HCC progression. LAY SUMMARY: Herein, we studied the role of cSMARCA5, a circular RNA, in hepatocellular carcinoma. Our in vitro and in vivo data showed that cSMARCA5 inhibits the growth and migration of hepatocellular carcinoma cells, making it a potential therapeutic target.


Assuntos
Adenosina Trifosfatases/genética , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/metabolismo , Proteínas Cromossômicas não Histona/genética , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/metabolismo , RNA/metabolismo , Animais , Carcinoma Hepatocelular/patologia , Linhagem Celular Tumoral , Movimento Celular , Proliferação de Células , RNA Helicases DEAD-box/antagonistas & inibidores , RNA Helicases DEAD-box/genética , RNA Helicases DEAD-box/metabolismo , Éxons , Feminino , Regulação Neoplásica da Expressão Gênica , Técnicas de Silenciamento de Genes , Humanos , Neoplasias Hepáticas/patologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , MicroRNAs/genética , MicroRNAs/metabolismo , Pessoa de Meia-Idade , Metástase Neoplásica/genética , Metástase Neoplásica/patologia , Proteínas de Neoplasias/antagonistas & inibidores , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/metabolismo , Prognóstico , Fatores de Risco , Análise de Sequência de RNA , Inibidor Tecidual de Metaloproteinase-3/genética , Inibidor Tecidual de Metaloproteinase-3/metabolismo
15.
J Med Case Rep ; 11(1): 202, 2017 Jul 27.
Artigo em Inglês | MEDLINE | ID: mdl-28747211

RESUMO

BACKGROUND: Colloid adenocarcinoma of the lung is a rare subtype of variants of invasive adenocarcinomas. We report the appearance of this unusual entity on 18F-fluorodeoxyglucose positron emission tomography/computed tomography. CASE PRESENTATION: A 60-year-old man of Chinese Han nationality coughed with a little white sputum for 1 month. Chest computed tomography showed multiple bilateral subpleural nodules and plaques accompanied by air bronchograms, which were most concentrated in the lower lobe of his right lung. Positron emission tomography indicated increased radioactivity uptake with a maximum standardized uptake value of 3.5. Positron emission tomography/computed tomography showed a soft tissue density lesion in his left adrenal gland with a maximum standardized uptake value of 4.1. The positron emission tomography/computed tomography appearance suggested a primary colloid adenocarcinoma in the lower lobe of his right lung accompanied by intrapulmonary and left adrenal gland metastases. The diagnostic rate of colloid adenocarcinoma can be increased by combining the anatomic and metabolic information of lesions. CONCLUSIONS: The advantage of positron emission tomography/computed tomography in the diagnosis of colloid adenocarcinoma, as with other cancers, is the ability to locate extrapulmonary disease, facilitating clinical staging.


Assuntos
Adenocarcinoma/diagnóstico por imagem , Neoplasias das Glândulas Suprarrenais/diagnóstico por imagem , Neoplasias Pulmonares/diagnóstico por imagem , Tomografia Computadorizada com Tomografia por Emissão de Pósitrons/métodos , Adenocarcinoma/patologia , Adenocarcinoma/secundário , Neoplasias das Glândulas Suprarrenais/secundário , Fluordesoxiglucose F18 , Humanos , Neoplasias Pulmonares/patologia , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Tomografia Computadorizada por Raios X
16.
Mol Clin Oncol ; 6(1): 111-114, 2017 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-28123741

RESUMO

The aim of the present study was to report the case of a 55-year-old female patient with a sizeable (7.1×6.2 cm) hepatocellular carcinoma (HCC), who succumbed to massive pulmonary artery embolism. The main symptoms included sudden thoracodynia, dyspnea and transient coma. The initial diagnosis was HCC according to the typical abdominal ultrasound and triple-phase abdominal computed tomography (CT) findings, chronic hepatitis B infection and elevated α-fetoprotein levels (1,036 µg/l; normal, 0-20 µg/l). Two days following admission, the patient developed recurrent chest pain and shortness of breath. The electrocardiogram and myocardial enzyme levels were normal, but the D-dimer level was elevated to 7,210 µg/l (normal, 0-550 µg/l). Magnetic resonance angiography and a contrast-enhanced chest CT confirmed that the inferior vena cava and right atrium were invaded by tumor thrombi; the bilateral pulmonary embolism was also suspected to be formed by tumor thrombi. The final diagnosis was HCC with inferior vena caval and right atrial tumor thrombi, as well as massive pulmonary embolism. Anticoagulation therapy with low-molecular weight heparin calcium was administered; however, the patient succumbed to pulmonary embolism in <2 months.

17.
Oncotarget ; 8(12): 18872-18884, 2017 Mar 21.
Artigo em Inglês | MEDLINE | ID: mdl-28122351

RESUMO

Aberrant chromobox (CBX) family protein expression has been reported in a variety of human malignancies. However, the role of CBX6 in hepatocellular carcinoma (HCC) progression and patient prognosis remains unknown. In this study, we found that CBX6 was frequently up-regulated in HCC clinical samples and HCC cell lines and that CBX6 expression was significantly correlated with larger tumor sizes (≥ 5 cm, p = 0.011) and multiple tumors (n ≥ 2, p = 0.018). Survival analyses indicated that patients with higher CBX6 expression levels had significantly shorter recurrence-free survival (RFS) and overall survival (OS) than patients with lower CBX6 expression levels, and multivariate analyses confirmed that increased CBX6 expression was an independent unfavorable prognostic factor for HCC patients. Functional study demonstrated that CBX6 profoundly promoted HCC cell growth both in vitro and in vivo, and mechanistic investigation revealed that the S100A9/NF-κB/MAPK pathway was essential for mediating CBX6 function. In conclusion, our results represent the first evidence that CBX6 contributes to tumor progression and indicate that the protein may serve as a novel prognostic biomarker for HCC and as a therapeutic target in the treatment of the disease.


Assuntos
Biomarcadores Tumorais/análise , Carcinoma Hepatocelular/patologia , Neoplasias Hepáticas/patologia , Proteínas do Grupo Polycomb/biossíntese , Adulto , Idoso , Animais , Western Blotting , Carcinoma Hepatocelular/mortalidade , Progressão da Doença , Intervalo Livre de Doença , Feminino , Xenoenxertos , Humanos , Imuno-Histoquímica , Estimativa de Kaplan-Meier , Neoplasias Hepáticas/mortalidade , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Pessoa de Meia-Idade , Reação em Cadeia da Polimerase , Prognóstico , Análise Serial de Tecidos
18.
Nuklearmedizin ; 56(6): 239-242, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29533419

RESUMO

AIM: The liver is an important reference organ for positron emission tomography/ computed tomography (PET-CT) examination using 18F-fluorodeoxyglucose (18F-FDG). However, 18F-FDG uptake by the liver is affected by many factors. We therefore investigated the effect of hepatic function on 18F-FDG uptake in the liver. METHODS: A retrospective analysis of data on the hepatic function and the mean liver standardized up-take value (SUV) of 18F-FDG uptake in the liver during PET-CT examination of 500 (381 males, 119 females, aged 27-71) physical examinees. RESULTS: The mean liver SUV was 1.88 ± 0.20. The correlation coefficient and partial correlation coefficient for age, the levels of conjugated bilirubin, globulin, AST and the mean liver SUV were statistically significant (r' = 0.119, -0.197, -0.089 and 0.151, all p < 0.05). Multiple linear regression analysis showed that age and the levels of conjugated bilirubin, globulin and aspartate amino-transferase (AST) were independent factors that influenced changes in the mean liver SUV (ß = 0.008, -0.025, -0.151 and 0.005, all p < 0.05). The globulin level had the biggest predictive ability (ß' = -0.151, p < 0.05). CONCLUSIONS: The uptake of 18F-FDG in the liver was influenced by some liver function indexes. The levels of conjugated bilirubin, globulin and AST were independent factors for predicting changes in the uptake of 18F-FDG in the liver. Liver function test results should be combined with an evaluation of the metabolic activity of the liver.


Assuntos
Fluordesoxiglucose F18 , Fígado/diagnóstico por imagem , Fígado/metabolismo , Tomografia Computadorizada com Tomografia por Emissão de Pósitrons , Compostos Radiofarmacêuticos , Adulto , Idoso , Aspartato Aminotransferases/metabolismo , beta-Globulinas/metabolismo , Bilirrubina/metabolismo , Transtornos da Coagulação Sanguínea/congênito , Transtornos da Coagulação Sanguínea/metabolismo , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos
19.
Medicine (Baltimore) ; 95(48): e5462, 2016 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-27902598

RESUMO

The aim of the study was to investigate the correlation of glucose transporter-1 (Glut-1) and glucose transporter-3 (Glut-3) expression with F-18 FDG uptake in pulmonary inflammatory lesions.Twenty-two patients with pulmonary inflammatory lesions underwent positron emission tomography/computed tomography (PET/CT) examination preoperatively, and Glut-1 and Glut-3 expression were detected by immunohistochemistry in these lesions. Correlations of Glut-1 and Glut-3 with F-FDG uptake were assessed using Spearman's rank correlation test.The maximum standardized uptake value (SUVmax) of pulmonary inflammatory lesions in 22 patients was 0.50 to 7.50, with a mean value of 3.66 ±â€Š1.62. Immunohistochemical staining scores of Glut-1 and Glut-3 were 2.18 ±â€Š0.96 and 2.82 ±â€Š1.37, respectively. The expression of Glut-1 and Glut-3 was positively correlated with F-18 FDG uptake. Glut-3 expression was evidently higher than Glut-1 expression in 22 patients.Glut-1 and Glut-3 expressions are high in pulmonary inflammatory lesions, and Glut-3 plays a more important role in F-18 FDG uptake in pulmonary inflammatory lesions.


Assuntos
Fluordesoxiglucose F18/farmacocinética , Transportador de Glucose Tipo 1/metabolismo , Transportador de Glucose Tipo 3/metabolismo , Pneumopatias/diagnóstico por imagem , Compostos Radiofarmacêuticos/farmacocinética , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Imuno-Histoquímica , Inflamação/diagnóstico por imagem , Inflamação/metabolismo , Masculino , Pessoa de Meia-Idade , Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
20.
Oncotarget ; 7(38): 62327-62339, 2016 09 20.
Artigo em Inglês | MEDLINE | ID: mdl-27694689

RESUMO

Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related death worldwide. Despite the therapeutic advances that have been achieved during the past decade, the molecular pathogenesis underlying HCC remains poorly understood. In this study, we discovered that increased expression eukaryotic translation initiation factor 5B (eIF5B) was significantly correlated with aggressive characteristics and associated with shorter recurrence-free survival (RFS) and overall survival (OS) in a large cohort. We also found that eIF5B promoted HCC cell proliferation and migration in vitro and in vivo partly through increasing ASAP1 expression. Our findings strongly suggested that eIF5B could promote HCC progression and be considered a prognostic biomarker for HCC.


Assuntos
Proteínas Adaptadoras de Transdução de Sinal/genética , Carcinoma Hepatocelular/genética , Fatores de Iniciação em Eucariotos/metabolismo , Regulação Neoplásica da Expressão Gênica , Neoplasias Hepáticas/patologia , Proteínas Adaptadoras de Transdução de Sinal/metabolismo , Animais , Biomarcadores Tumorais/metabolismo , Carcinoma Hepatocelular/mortalidade , Carcinoma Hepatocelular/patologia , Linhagem Celular Tumoral , Proliferação de Células , Intervalo Livre de Doença , Seguimentos , Técnicas de Silenciamento de Genes , Humanos , Imuno-Histoquímica , Estimativa de Kaplan-Meier , Fígado/patologia , Masculino , Camundongos , Camundongos Nus , Pessoa de Meia-Idade , Invasividade Neoplásica/genética , Invasividade Neoplásica/patologia , Prognóstico , Interferência de RNA , RNA Interferente Pequeno/metabolismo , Análise Serial de Tecidos , Regulação para Cima , Ensaios Antitumorais Modelo de Xenoenxerto
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