• CD44-targeting
• Combinatory therapy
• Hyaluronic acid
• PLGA nanoparticles
• Targeted delivery

• Humans
• Triple Negative Breast Neoplasms/pathology
• Triple Negative Breast Neoplasms/drug therapy
• Triple Negative Breast Neoplasms/metabolism
• Nanoparticles/chemistry
• Doxorubicin/pharmacology
• Doxorubicin/chemistry
• Indocyanine Green/chemistry
• Indocyanine Green/pharmacology
• Cell Proliferation/drug effects
• Polylactic Acid-Polyglycolic Acid Copolymer/chemistry
• Cell Line, Tumor
• Female
• Cell Survival/drug effects
• Hyaluronic Acid/chemistry
• Drug Screening Assays, Antitumor
• Particle Size
• Hyaluronan Receptors

• Cancer
• Cardiotoxic drugs
• Heart failure
• Mechanisms

Cancer is a catastrophic disease that seriously affects human health. HIF1α plays an important role in cancer initiation, progression, and prognosis. However, little is known about the specific role of HIF1α in pan-cancer. Therefore, we systematically and comprehensively analyzed HIF1α using GEPIA, HPA, GeneMANIA, STRING, SMPDB, cBioPortal, UALCAN, and TISDB databases and also 33 cancer and normal tissues in TCGA downloaded from the Genome Data Commons (GDC) data portal. Data and statistical analysis were performed using R software v4.0.3. Our results found that there were differences in the mRNA expression levels of HIF1α in human pan-cancer and its corresponding normal tissues. The expression level of HIF1α correlated with tumor stage in LIHC and also significantly correlated with prognosis in LIHC, LUSC, STAD, OV, PAAD, PRAD, THCA, LUAD, MESO, and READ. The small molecule pathways involved in HIF1α include succinate signaling, fumarate, and succinate carcinogenesis-related pathways. The highest mutation frequency of the HIF1α gene in pan-cancer was head and neck cancer, and the HIF1α methylation level in most tumors is significantly reduced. HIF1α was not only associated with immune cell infiltration but also with immune checkpoint genes and immune regulators TMB and MSI. There were currently 5 small molecule drugs targeting HIF1α.

Patients with lower-risk myelodysplastic syndromes (LR-MDS) have a generally favorable prognosis; however, a small proportion of cases progress rapidly. This study aimed to define molecular biomarkers predictive of LR-MDS progression and to uncover cellular pathways contributing to malignant transformation. The mutational landscape was analyzed in 214 LR-MDS patients, and at least one mutation was detected in 137 patients (64%). Mutated RUNX1 was identified as the main molecular predictor of rapid progression by statistics and machine learning. To study the effect of mutated RUNX1 on pathway regulation, the expression profiles of CD34 + cells from LR-MDS patients with RUNX1 mutations were compared to those from patients without RUNX1 mutations. The data suggest that RUNX1-unmutated LR-MDS cells are protected by DNA damage response (DDR) mechanisms and cellular senescence as an antitumor cellular barrier, while RUNX1 mutations may be one of the triggers of malignant transformation. Dysregulated DDR and cellular senescence were also observed at the functional level by detecting γH2AX expression and β-galactosidase activity. Notably, the expression profiles of RUNX1-mutated LR-MDS resembled those of higher-risk MDS at diagnosis. This study demonstrates that incorporating molecular data improves LR-MDS risk stratification and that mutated RUNX1 is associated with a suppressed defense against LR-MDS progression.

The hypoxic tumor microenvironment was reported to be involved in different tumorigenesis mechanisms of triple-negative breast cancer (TNBC), such as invasion, immune evasion, chemoresistance, and metastasis. However, a systematic analysis of the prognostic prediction models based on multiple hypoxia-related genes (HRGs) has not been established in TNBC before in the literature. We aimed to develop and verify a hypoxia gene signature for prognostic prediction in TNBC patients.

The RNA sequencing profiles and clinical data of TNBC patients were generated from the TCGA, GSE103091, and METABRIC databases. The TNBC-specific differential HRGs (dHRGs) were obtained from differential expression analysis of hypoxia cultured TNBC cell lines compared with normoxic cell lines from the GEO database. Non-negative matrix factorization (NMF) method was then performed on the TNBC patients using the dHRGs to explore a novel molecular classification on the basis of the dHRG expression patterns. Prognosis-associated dHRGs were identified by univariate and multivariate Cox regression analysis to establish the prognostic risk score model.

Based on the expressions of 205 dHRGs, all the patients in the TCGA training cohort were categorized into two subgroups, and the patients in Cluster 1 demonstrated worse OS than those in Cluster 2, which was validated in two independent cohorts. Additionally, the effects of somatic copy number variation (SCNV), somatic single nucleotide variation (SSNV), and methylation level on the expressions of dHRGs were also analyzed. Then, we performed Cox regression analyses to construct an HRG-based risk score model (3-gene dHRG signature), which could reliably discriminate the overall survival (OS) of high-risk and low-risk patients in TCGA, GSE103091, METABRIC, and BMCHH (qRT-PCR) cohorts.

In this study, a robust predictive signature was developed for patients with TNBC, indicating that the 3-gene dHRG model might serve as a potential prognostic biomarker for TNBC.

• hypoxic tumor microenvironment
• molecular classification
• prognostic model
• qRT-PCR
• triple-negative breast cancer

Traditional Chinese medicine has widely used Bolbostemma paniculatum to treat diseases, including cancer, but its underlying mechanisms remain unclear. The present study aimed to elucidate the potential pharmacological mechanisms of “Tu Bei Mu” (TBM), the Chinese name for Bolbostemmatis Rhizoma, the dry tuber of B. paniculatum, for the treatment of hepatocellular carcinoma (HCC).

The active components and putative therapeutic targets of TBM were explored using SwissTargetPrediction, Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), and Search Tool for Interactions of Chemicals (STITCH). The HCC-related target database was built using DrugBank, DisGeNet, Online Mendelian Inheritance in Man (OMIM), and Therapeutic Target Database (TTD). A protein–protein interaction network of the common targets was constructed, based on the matches between TBM potential targets and HCC-related targets, using Cytoscape software. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of the cluster networks were used to elucidate the biological functions of TBM.

Pharmacological network diagrams of the TBM compound-target network and HCC-related target network were successfully constructed. A total of 22 active components, 191 predicted biological targets of TBM, and 3775 HCC-related targets were identified. Through construction of an HCC-related target database and a protein–protein interaction network of the common targets, TBM was predicted to be effective in treating HCC mainly through the PI3K-Akt, HIF-1, p53, and PPAR signaling pathways.

The PI3K/Akt, HIF1, p53, and PPAR pathways may play vital roles in TBM treatment of HCC. Also, the potential anti-cancer effect of TBM on HCC appears to stem from the synergetic effect of multiple targets and mechanisms.

• hypoxia
• immune
• immunotherapy
• triple-negative breast cancer

• Biomarkers, Tumor/analysis
• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/immunology
• Female
• Gene Expression Profiling
• Gene Expression Regulation, Neoplastic
• Humans
• Hypoxia/diagnosis
• Hypoxia/genetics
• Hypoxia/immunology
• Prognosis
• Triple Negative Breast Neoplasms/diagnosis
• Triple Negative Breast Neoplasms/genetics
• Triple Negative Breast Neoplasms/immunology
• Tumor Hypoxia

The Warburg effect, also known as aerobic glycolysis, plays a dominant role in the development of gastrointestinal (GI) cancers. In this study, we analyzed the expression of key genes involved in the Warburg effect in GI cancers and investigated the effect of suppressing the Warburg effect in vitro in liver cancer cell lines.

The Cancer Genome Atlas (TCGA) RNA-Seq data were used to determine gene expression levels, which were analyzed with GraphPad Prism 7.00. Genetic alterations were queried with cBioPortal. The influence of the Warburg effect on liver cancer cell viability, migration and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) activity was determined by means of MTT, transwell and GAPDH activity assays.

The levels of expression of genes associated with the Warburg effect were increased in tumors. To our knowledge, this is the first report of upregulated expression of CUEDC2, HMGB2, PFKFB4, PFKP and SIX1 in liver cancer. Clinically, overexpression of these genes was associated with significantly worse overall survival of liver cancer patients. In vitro, selective inhibition of GADPH suppressed the growth and metastasis of Huh-7, Bel7404 and Hep3B hepatocellular carcinoma cell lines.

The Warburg effect may play an important role in GI cancers, especially in liver cancer.

• GAPDH
• Warburg effect
• bioinformatics
• gastrointestinal cancers
• liver cancer

HIF-1 (hypoxia-inducible factor 1) signaling played a vital role in HCC (hepatocellular carcinoma) prognosis. We aimed to establish an accurate risk scoring system for HCC prognosis prediction and treatment guidance. 424 samples from TCGA (The Cancer Genome Atlas) and 445 samples from GSE14520 dataset were included as the derivation and validation cohort, respectively. In the derivation cohort, prognostic relevant signatures were selected from sixteen HIF-1 related genes and LASSO regression was adopted for model construction. Tumor-infiltrating immune cells were calculated using CIBERSORT algorithm. HIF-1 signaling significantly increased in HCC samples compared with normal tissues. Scoring system based on SLC2A1, ENO1, LDHA and GAPDH exhibited a continuous predictive ability for OS (overall survival) in HCC patients. PCA and t-SNE analysis confirmed a reliable clustering ability of risk score in both cohorts. Patients were classified into high-risk and low-risk groups and the survival outcomes between the two groups showed significant differences. In the derivation cohort, Cox regression indicated the scoring system was an independent predictor for OS, which was validated in the validation cohort. Different infiltrating immune cells fraction and immune scores were also observed in different groups. Herein, a novel integrated scoring system was developed based on HIF-1 related genes, which would be conducive to the precise treatment of patients.

• Hypoxia-inducible factor 1
• gene expression omnibus
• hepatocellular carcinoma
• risk score
• the cancer genome atlas

The liver and its zonation contribute to whole body homeostasis. Acute and chronic, not always liver, diseases impair proper metabolic zonation. Various underlying pathways, such as β-catenin, hedgehog signaling, and the Hippo pathway, along with the physiologically occurring oxygen gradient, appear to be contributors. Interestingly, hypoxia and hypoxia-inducible transcription factors can orchestrate those pathways. In the current review, we connect novel findings of liver zonation in health and disease and provide a view about the dynamic interplay between these different pathways and cell-types to drive liver zonation and systemic homeostasis.

• HIF
• Hepatocytes
• ROS
• antioxidants
• antioxidative enzymes
• diet
• fibrosis
• homeostasis
• hypoxia
• liver
• matrix
• metabolic zonation
• metabolism
• morphogen signaling
• optimization
• pathology
• regulatory network
• sinusoid

Hypoxia-inducible factor-1α (HIF-1α) is upregulated in various tumors and associated with lymphangiogenesis and angiogenesis during tumor development and metastasis. However, the role of HIF-1α in cystic lymphatic malformations (cLM) remains unclear. In the present study, expression of HIF-1α and vascular endothelial growth factor receptor 3 (VEGFR-3) was evaluated in 20 pairs of cLM specimens from patients who accepted curative surgery at Children’s Hospital of Nanjing Medical University (Nanjing, China). Additionally, a stable HIF-1α-overexpressing human lymphatic endothelial cell (HLEC) line was established. Overexpression and silencing of HIF-1α were used to investigate the biological role in colony formation, migration and lymphatic tube formation. HIF-1α and VEGFR-3 were upregulated in cLM specimens compared with adjacent normal tissues. In addition, HIF-1α effectively induced HLEC colony formation and migration. Furthermore, lymphatic malformation of HLECs was promoted in vitro by overexpression of HIF-1α. HIF-1α overexpression upregulated VEGFR-3 during lymphangiogenesis. Additionally, expression of lymphatic endothelial markers prospero homeobox protein 1 and lymphatic vessel endothelial hyaluronan receptor 1 increased significantly during lymphatic tube malformation. The presented data demonstrated that HIF-1α overexpression in HLECs promoted colony formation, migration and tube malformation via upregulation of VEGFR-3. These findings may assist in the development of HIF-1α-targeted cLM therapeutics in the future.

• Alzheimer's disease
• angiogenesis
• beta amyloid
• erythropoiesis
• hypoxia
• hypoxia-inducible factors
• neurofibrillary tangles
• oxidative stress
• vascular endothelial growth factor

• Alzheimer Disease/immunology
• Alzheimer Disease/metabolism
• Alzheimer Disease/pathology
• Alzheimer Disease/prevention & control
• Amyloid beta-Peptides/metabolism
• Animals
• Drug Discovery
• Humans
• Hypoxia-Inducible Factor 1, alpha Subunit/biosynthesis
• Hypoxia-Inducible Factor 1, alpha Subunit/metabolism
• Neuroprotective Agents/pharmacology
• Neuroprotective Agents/therapeutic use
• Peptide Fragments/metabolism

Hypoxia-inducible factor (HIF)-1 is a transcription factor that allows cells to adapt to hypoxic situations. HIF-1 is known to control tissue proliferation, antiapoptosis, angiogenesis and glucose metabolism. Furthermore, HIF-1 is involved in the growth of numerous cancer types. The present study aimed to examine the expression of HIF-1α immunohistochemically in resected lung cancers. The present study included 216 consecutive patients with lung cancer who underwent resection between April 2013 and January 2015. The patients' clinicopathological data were summarized, including imaging findings, tumor pathological characteristics, and the patient's age, sex and smoking status. The intratumoral expression of HIF-1α, survivin, c-Myc and the Ki-67 proliferation index were evaluated immunohistochemically. The patients were divided into two groups, according to the expression of HIF-1α (low vs. high) and the clinicopathological characteristics of these groups were compared. It was revealed that HIF-1α expression was significantly associated with ground glass opacity ratio, maximum standardized uptake value index, histological type (squamous cell carcinoma), differentiation and lymphatic invasion. Regarding the immunohistochemical findings, HIF-1α expression was significantly correlated with the expression levels of c-Myc (P<0.01) and survivin (P<0.01). Furthermore, the Ki-67 proliferation index was significantly higher in high-HIF-1α tumors compared with in low-HIF-1α tumors (P=0.01). The multivariate analysis identified squamous cell carcinoma, high SUVmax and lymphatic invasion as significant and independent factors for high HIF-1α expression. In conclusion, HIF-1 was highly expressed in certain subgroups of lung cancer with specific histopathology and images. HIF-1α expression was associated with tumor proliferation and antiapoptosis in lung cancer.

• c-Myc
• hypoxia-inducible factor-1α
• immunohistochemistry
• lung cancer
• survivin

• Alcoholic liver disease
• Fatty liver
• HIF1α
• HIF2α
• Hepatocellular carcinoma
• Ischemia-reperfusion liver injury
• Viral hepatitis

• Animals
• Antineoplastic Agents/therapeutic use
• Basic Helix-Loop-Helix Transcription Factors/antagonists & inhibitors
• Basic Helix-Loop-Helix Transcription Factors/genetics
• Basic Helix-Loop-Helix Transcription Factors/metabolism
• Bevacizumab/therapeutic use
• Carcinoma, Hepatocellular/genetics
• Carcinoma, Hepatocellular/metabolism
• Carcinoma, Hepatocellular/pathology
• Carcinoma, Hepatocellular/therapy
• Clinical Trials as Topic
• Fatty Liver/genetics
• Fatty Liver/metabolism
• Fatty Liver/pathology
• Fatty Liver/therapy
• Gene Expression Regulation
• Hepatitis, Viral, Human/genetics
• Hepatitis, Viral, Human/metabolism
• Hepatitis, Viral, Human/pathology
• Hepatitis, Viral, Human/therapy
• Humans
• Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors
• Hypoxia-Inducible Factor 1, alpha Subunit/genetics
• Hypoxia-Inducible Factor 1, alpha Subunit/metabolism
• Liver Cirrhosis/genetics
• Liver Cirrhosis/metabolism
• Liver Cirrhosis/pathology
• Liver Cirrhosis/therapy
• Liver Diseases, Alcoholic/genetics
• Liver Diseases, Alcoholic/metabolism
• Liver Diseases, Alcoholic/pathology
• Liver Diseases, Alcoholic/therapy
• Liver Neoplasms/genetics
• Liver Neoplasms/metabolism
• Liver Neoplasms/pathology
• Liver Neoplasms/therapy
• Molecular Targeted Therapy
• Oligonucleotides/therapeutic use
• Signal Transduction

• R21 AA022387 NIAAA NIH HHS
• P01 HL114457 NHLBI NIH HHS
• R01 HL098294 NHLBI NIH HHS
• R01 DK050189 NIDDK NIH HHS
• U01 AA021723 NIAAA NIH HHS
• R01 DK103712 NIDDK NIH HHS
• I01 BX002182 BLRD VA
• R01 DK097075 NIDDK NIH HHS
• R37 DK050189 NIDDK NIH HHS
• R01 DK095491 NIDDK NIH HHS
• R01 HL092188 NHLBI NIH HHS
• R01 HL119837 NHLBI NIH HHS
• R01 DK104713 NIDDK NIH HHS
• National Institute on Alcohol Abuse and Alcoholism
• National Institute of Diabetes and Digestive and Kidney Diseases
• National Heart, Lung, and Blood Institute

• donor selection
• hepatocellular carcinoma
• liver transplantation
• microRNA
• single nucleotide polymorphism

• Adult
• Aged
• Carcinoma, Hepatocellular/genetics
• Carcinoma, Hepatocellular/surgery
• Female
• Humans
• Liver Neoplasms/genetics
• Liver Neoplasms/surgery
• Liver Transplantation
• Male
• MicroRNAs/genetics
• Middle Aged
• Neoplasm Recurrence, Local/genetics
• Polymorphism, Single Nucleotide
• Tissue Donors

• AFP
• EpCAM
• IGFBP1
• SIRT
• circulating tumor cells
• epithelial cells
• hepatocellular carcinoma
• peripheral blood

Expression of E-cadherin has a central role in maintaining epithelial morphology. In solid tumors, reduction of E-cadherin results in disruption of intercellular contacts. Consequently, cells lose adhesive properties and gain more invasive mesenchymal properties. Nevertheless, the mechanism of E-cadherin regulation is not completely elucidated. Here we analyzed the distribution of E-cadherin expression at the cell level in human hepatocellular carcinoma, in which human liver paraffin blocks from 25 hepatocellular carcinoma patients were prepared from cancerous (CA) and noncancerous areas (NCA). In situ hybridization (ISH) was performed to detect E-cadherin and hypoxia-induced factor-1α (HIF1α) mRNAs and immunohistochemistry to stain E-cadherin protein. In parallel, RNA was extracted from CA and NCA, and E-cadherin and HIF1α were quantified by quantitative reverse transcription PCR. ISH revealed abundant E-cadherin mRNA in nuclei of hepatocellular carcinoma cells (HCCs), whereas immunohistochemistry showed depletion of E-cadherin protein from these areas. In sections of NCA, E-cadherin mRNA was also found in the cytosol, and E-cadherin protein was detected on the membrane of cells. Experiments in cell lines confirmed E-cadherin mRNA in nuclei of cells negative for E-cadherin protein. HIF1α expression is elevated in CAs, which is associated with a clear cytosolic staining for this mRNA. Our results demonstrate that E-caderhin mRNA is selectively retained in nuclei of HCCs, whereas other mRNAs are still exported, suggesting that translocation of E-cadherin mRNA from nuclei to cytoplasm has a role in regulating E-cadherin protein levels during epithelial mesenchymal transition.

The goal of this study is to explore the effects of A-W MGC (apatite-wollastonite magnetic bioactive glass-ceramic) loaded with BMP2 (bone morphogenetic protein 2)- and HIF1α^mu (hypoxia-inducible factor 1 mutation)-expressing BMSCs (bone marrow mesenchymal stem cells) on the bone defect repair.

(1) BMSCs were infected with viral solution containing BMP2 and HIF1α^mu with the best MOI (multiplicity of infection). The efficiency was observed via hrGFP (human renilla reniformis green fluorescent protein). (2) The cells were divided into five groups (A–E), and ALP (alkaline phosphatase) activity was measured. (3) BMP2 and HIF1α (hypoxia-inducible factor 1α) protein were measured. (4) A-W MGC was loaded with BMSCs that contain the genes and implanted into the bone defect model. The animals were sacrificed 8 and 12 weeks later. (5) The healing was measured with X-ray, histology, and biomechanics.

(1) BMSCs in A–D showed high transfection efficiency. (2) ALP in A and B was higher than the others (p = 0.041 or 0.038); A was higher than B (p = 0.038); (3) BMP2 in A and B was higher than the others (p = 0.014). HIF1α in A and C was higher than the others (p = 0.020). (4) 8 and 12 weeks after, an X-ray indicated that bone defect was nearly fully repaired in A and C. (5) 12 weeks after, the bone remodeling was complete in A and C. (6) The flexural strength in A and C was stronger than the others (p = 0.043).

Engineered A-W MGC with BMP2 and HIF1α^mu-expressing BMSCs exhibits comparable therapeutic effects of bone-defect repair as an autologous bone graft.

Hypoxia is a common feature of many solid tumors, including hepatocellular carcinoma (HCC). Hypoxia can promote tumor progression and induce radiation and chemotherapy resistance. As one of the major mediators of hypoxic response, hypoxia inducible factor-1 (HIF-1) has been shown to activate hypoxia-responsive genes, which are involved in multiple aspects of tumorigenesis and cancer progression, including proliferation, metabolism, angiogenesis, invasion, metastasis and therapy resistance. It has been demonstrated that a high level of HIF-1 in the HCC microenvironment leads to enhanced proliferation and survival of HCC cells. Accordingly, overexpression, of HIF-1 is associated with poor prognosis in HCC. In this review, we described the mechanism by which HIF-1 is regulated and how HIF-1 mediates the biological effects of hypoxia in tissues. We also summarized the latest findings concerning the role of HIF-1 in the development of HCC, which could shed light on new therapeutic approaches for the treatment of HCC.

• Angiogenic factors
• Biochemical markers
• Epigenetic variations
• Hepatocellular carcinoma
• Micro-interfering RNA
• Tumor stroma

• Animals
• Biomarkers, Tumor/genetics
• Biomarkers, Tumor/metabolism
• Carcinoma, Hepatocellular/genetics
• Carcinoma, Hepatocellular/metabolism
• Carcinoma, Hepatocellular/pathology
• Carcinoma, Hepatocellular/therapy
• Epigenesis, Genetic
• Gene Expression Regulation, Neoplastic
• Humans
• Liver Neoplasms/genetics
• Liver Neoplasms/metabolism
• Liver Neoplasms/pathology
• Liver Neoplasms/therapy
• MicroRNAs/metabolism
• Predictive Value of Tests
• Prognosis
• Stromal Cells/metabolism
• Stromal Cells/pathology
• Tumor Microenvironment

• HIF-1α
• HIF-2α
• disease-free survival
• hepatocellular carcinoma
• overall survival

Chronic hepatitis C virus (HCV) induced hepatocellular carcinoma (HCC) is a primary indication for liver transplantation (LT). In western countries, the estimated rate of HCC recurrence following LT is between 15% and 20% and is a major cause of mortality. Currently, there is no standard method to treat patients who are at high risk for HCC recurrence. The aim of this study was to investigate the molecular signatures underlying HCC recurrence that may lead to future studies on gene regulation contributing to new therapeutic options. Two groups of patients were selected, one including patients with HCV who developed HCC recurrence (HCC-R) ≤3 years from LT and the second group including patients with HCV who did not have recurrent HCC (HCC-NR). Microarray analysis containing more than 29,000 known genes was performed on formalin-fixed-paraffin-embedded (FFPE) liver tissue from explanted livers. Gene expression profiling revealed 194 differentially regulated genes between the two groups. These genes belonged to cellular networks including cell cycle G1/S checkpoint regulators, RAN signaling, chronic myeloid leukemia signaling, molecular mechanisms of cancer, FXR/RXR activation and hepatic cholestasis. A subset of molecular signatures associated with HCC recurrence was found. The expression levels of these genes were validated by quantitative PCR analysis.

• hypoxia-inducible factor
• steatosis
• liver injury
• fibrosis
• inflammation

• Acetaminophen/poisoning
• Animals
• Humans
• Hypoxia/complications
• Hypoxia/metabolism
• Hypoxia-Inducible Factor 1/metabolism
• Immunity, Innate
• Lipid Metabolism
• Liver/drug effects
• Liver/metabolism
• Liver Diseases/etiology
• Liver Diseases/metabolism
• Liver Regeneration
• Metals/metabolism
• Oxygen/metabolism
• Reperfusion Injury/metabolism
• Sleep Apnea, Obstructive/metabolism

• R21 AA017544 NIAAA NIH HHS
• R21 AA017544-02 NIAAA NIH HHS

• Adult
• Aged
• Angiopoietin-Like Protein 4
• Angiopoietins/physiology
• Carcinoma, Hepatocellular/metabolism
• Carcinoma, Hepatocellular/pathology
• Cell Line, Tumor
• Cell Movement
• Endothelial Cells/metabolism
• Female
• Humans
• Hypoxia-Inducible Factor 1, alpha Subunit/physiology
• Integrin beta1/physiology
• Liver Neoplasms/metabolism
• Liver Neoplasms/pathology
• Male
• Middle Aged
• Signal Transduction
• Vascular Cell Adhesion Molecule-1/physiology

• Adult
• Aged
• Aged, 80 and over
• Carcinoma, Hepatocellular/diagnosis
• Carcinoma, Hepatocellular/mortality
• Carcinoma, Hepatocellular/surgery
• Female
• Gene Expression Profiling
• Humans
• Liver Neoplasms/diagnosis
• Liver Neoplasms/mortality
• Liver Neoplasms/surgery
• Male
• MicroRNAs/analysis
• Middle Aged
• Postoperative Period
• Predictive Value of Tests
• Prognosis
• ROC Curve
• Recurrence
• Survival Analysis
• Time Factors