Glyoxalase 1 inhibitor BBGC suppresses the progression of chronic lymphocytic leukemia and promotes the efficacy of Palbociclib.

Chronic lymphocytic leukemia (CLL) is a highly heterogeneous disease. Despite recent tremen-dous progress in managing CLL, the disease remains incurable with clinical therapies, and relapse is inevitable. To overcome this, new diagnostic and prognostic markers need to be investigated. We thus screened through the public database for genes with diagnostic, prognostic, and therapeutic implications in CLL. We further performed RT-qPCR and Western blot analysis to measure the candidate gene and protein expression levels, respectively, in peripheral blood mononuclear cells. Our results indicated that Glyoxalase 1 (GLO1) expression was significantly higher in patients with CLL than in healthy controls. Furthermore, cell proliferation, apoptosis, and cell cycle assay results together indicated that S-p-bromobenzylglutathione cyclopentyl diester (BBGC), an effective inhibitor of GLO1, suppresses the progression of CLL. Bioinformatics analysis revealed that GLO1 expression is closely associated with CDK4 expression in a wide variety of cancer types, and inhibition of CDK4 through silencing of genes or inhibitors can downregulate GLO1 expression. Subsequent validation experiments demonstrated that GLO1 protein levels were downregulated in MEC-1 and Jurkat cell lines after palbociclib exposure, and combination treatment of palbociclib with GLO1 inhibitor BBGC effectively delayed the growth of tumor cell lines.

Molecular Basis and Hematologic Phenotype of Hemoglobin H Disease Combined with Two Rare ß-Globin Mutations.

In area where α-thalassemia and ß-thalassemia are prevalent, the coinheritance of hemoglobin H disease (Hb H disease) and ß-thalassemia are not uncommon and could result in complex thalassemia intermedia syndromes. In this study, we investigate the hematological and molecular characteristics of two previously undescribed cases that co-inherited Hb H disease and rare ß-globin gene (HBB) mutations found in Chinese populations. Proband I was a boy with Hb H disease in association with IVS-II-5(G > C) (HBB:c0.315 + 5G > C) mutation. Proband II was a boy with a combination of Hb H and Hb Zengcheng [ß114(G16) Leu > Met; HBB:c.343C > A]. Both of them had mild hypochromic microcytic anemia, and neither had ever received a blood transfusion. In both cases, the level of Hb A2 was within normal range, and no Hb H was detected, but a small amount of Hb Bart's was observed in proband I. Routine DNA analysis detected the deletional Hb H disease in both cases. IVS-II-5(G > C) (HBB:c0.315 + 5G > C) and Hb Zengcheng (HBB:c.343C > A) mutations were found by DNA sequencing of ß-globin gene. The co-inheritance of Hb H disease with rare ß-thalassemia may result in an atypical pattern of Hb H disease, and further investigation of rare genotypes should be conducted to avoid missed diagnosis.

Clinical significance of serum bilirubin in primary Sjögren syndrome patients.

OBJECTIVE: The purpose of our research was to demonstrate the clinical significance of serum bilirubin in primary Sjögren syndrome patients (pSS). PATIENTS AND METHODS: A total of 116 patients with primary Sjögren syndrome and 138 matched individuals were included in our study. The laboratory parameters of patients with pSS and healthy controls were retrospectively analyzed. RESULTS: Serum total bilirubin, direct bilirubin, and indirect bilirubin were significantly reduced (P < .001, P = .001, P < .001) while ESR was significantly increased (P < .001) in patients with pSS when compared with healthy checkup individuals. Statistically, the AUC in patients with pSS is as follows: TBIL = 0.77, P < .001, cutoff value = 7.96; DBIL = 0.617, P = .001 cutoff value = 2.2; and IBIL = 0.786, P < .001 cutoff value = 4.5. Furthermore, our study revealed that TBIL, DBIL, and IBIL were significantly negativity related to ESR (r = -.406, P < .001; r = -.206, P = .026; r = -.429, P < .001). Interestingly, multiple linear regression analysis showed that when adjusted for sex, age, ALT, and AST, the levels of TBIL, DBIL, and IBIL in patients with pSS were independently correlated with ESR. CONCLUSIONS: This study found that the levels of serum bilirubin were reduced and the inflammatory marker was elevated in patients with pSS. Additionally, serum bilirubin was negatively related with ESR and TBIL, DBIL, and IBIL can be used in the clinical diagnosis and follow-up visits of the patients with pSS.

Compound Heterozygosity for a Novel Mutation Codon 104 (-A) (HBB: c.313delA) and Codons 41/42 (-CTTT) (HBB: c.126_129delCTTT) Leading to ß-Thalassemia Major in a Chinese Family.

ß-Thalassemia (ß-thal) is a hereditary blood disorder characterized by the reduced or absent synthesis of ß-globin chains. Here, we report a case of severe thalassemia with compound heterozygosity for a novel deletion mutation at codon 104 (-A) (HBB: c.313delA) and codons 41/42 (-CTTT) (HBB: c.126_129delCTTT) on the ß-globin gene (HBB), and a coinheritance of the -α4.2 (leftward) deletion on the α-globin gene cluster. The proband was a 12-year-old boy, and four other family members were involved in this study. This novel frameshift mutation caused classical ß-thal trait in the heterozygote and a transfusion-dependent form of ß-thal major (ß-TM) in compound heterozygosity with other ß0 mutations.

[Molecular diagnosis of a family with May-Hegglin anomaly].

OBJECTIVE: To explore the molecular basis for a pedigree affected with May-Hegglin anomaly (MHA). METHODS: Peripheral blood samples were collected and subjected to DNA extraction. Exons 1, 10, 16, 24, 25, 26, 30, 31, 33, 38 and 40 and flanking sequences of the MYH9 gene were subjected to PCR amplification and Sanger sequencing. Changes in protein expression were determined by an indirect immunofluorescence assay. Platelet aggregation function of the proband was assessed by thromboelastogram. RESULTS: The proband and his second son both carried a heterozygous 5521G>A (GAG to AAG) missense variant in exon 38 of the MYH9 gene, leading to p.Glu1841Lys substitution at position 1841 of amino acid sequence. Immunofluorescence showed inclusions containing NMMHC-II A. Thromboelastogram suggested enhanced platelet aggregation function of the proband. CONCLUSION: The c.5521G>A variant of MYH9 gene has co-segregated with the phenotype of MHA in this pedigree. To assess the aggregation function of platelet by thromboelastogram can predict the risk of bleeding in MHA patients.

Is serum bilirubin associated with the severity of Guillain-Barré syndrome?

OBJECTIVE: Our aim was to assess the correlation between serum bilirubin levels and Guillain-Barré syndrome (GBS). PATIENTS AND METHODS: One hundred and one newly diagnosed patients with Guillain-Barré syndrome and 111 healthy age- and sex-matched individuals in the First Affiliated Hospital of Guangxi Medical University (Guangxi, China) from June 2012 to May 2017 were included in this study. Clinical characteristics and laboratory parameters of Guillain-Barré syndrome patients and healthy controls were retrospectively analysed. RESULTS: Serum bilirubin levels in Guillain-Barré syndrome patients were significantly lower as compared with those in healthy controls (p < 0.001); besides, log C-reactive protein and erythrocyte sedimentation rate were significantly higher. We found that there was a negative correlation between GBS disability scale scores and total bilirubin, direct bilirubin, indirect bilirubin (r = -0.541, P < 0.001; r = -0.403, P < 0.001; r = -0.526, P < 0.001), respectively. Among patients with GBS, serum total bilirubin, direct bilirubin, and indirect bilirubin levels were independently associated with Guillain-Barré syndrome disability scale scores in multiple linear regression analysis, respectively. CONCLUSIONS: We observed that serum bilirubin levels were lower in patients with Guillain-Barré syndrome, and suggested total bilirubin, direct bilirubin, and indirect bilirubin were independently and inversely associated with Guillain-Barré syndrome severity.

Retrospective analysis of 15 cases of Penicillium marneffei infection in HIV-positive and HIV-negative patients.

Penicillium marneffei (P. marneffei) causes systemic opportunistic infections in immunocompromised individuals, particularly in those infected with human immunodeficiency virus (HIV), and more rarely in HIV-negative patients. We retrospectively analyzed the cases of 15 patients infected with P. marneffei. The patients were divided into two groups: HIV-negative (n = 4) and HIV-positive (n = 11). Of the cases studied, three (75%) of the HIV-negative and six (55%) of the HIV-positive group had an accompanying lung infection. The ratio of CD4+/CD8+ was 1.2 (SD = 0.99) in the HIV-negative group and 0.10 (SD = 0.095) in the HIV-positive patients. A series of laboratory examinations were performed and bone marrow smears were observed after staining. P. marneffei is a disseminated fungal infection associated with severe disease symptoms and high mortality rates. Our findings indicate that timely diagnosis and treatment by clinicians is crucial for preventing the spread of localized infections into systemic infections, thereby improving the prognosis of patients.

Cyfip1 is downregulated in acute lymphoblastic leukemia and may be a potential biomarker in acute lymphoblastic leukemia.

The aim of the present study was to analyze the expression of Cyfip1 in acute lymphoblastic leukemia (ALL) and its correlations with clinical pathologic features. A total of 86 ALL samples and 32 normal peripheral blood lymphocyte (PBL) samples were enrolled in our study. mRNA expression of the Cyfip1 was assessed by real-time fluorescent relatively quantitative PCR, and Cyfip1 protein expression was evaluated by Western blot analysis. As a result, both mRNA and protein expression levels of Cyfip1 were significantly lower in ALL patients than those in the control samples (P = 0.025 and 0.000, respectively). Moreover, both mRNA and protein expression of both had an inverse relation with lymph node metastasis (P = 0.015 and 0.007, respectively), In conclusion, detecting mRNA and protein expression of Cyfip1 could provide clinically significant information relevant to diagnosis, progression, and treatment modalities for ALL, and Cyfip1 may serve as a potential biomarker for diagnosis and prognosis in ALL.

Comprehensive assessment of the association between DNA repair gene XRCC3 Thr241Met polymorphism and leukemia risk.

The XRCC3 gene has been suggested to play an important role in the pathogenesis of leukemia risk. But the findings of publications are contradictory. To derive a more precise estimation of the association, we performed a meta-analysis. The PubMed, Embase, and China National Knowledge Infrastructure (CNKI) databases were searched for case-control studies published up to August 2013. The pooled odds ratio (OR) and its corresponding 95% confidence interval (CI) were calculated by using a fixed- or random-effect model. A total of 15 case-control studies met the inclusion criteria and were selected. The pooled OR showed that there was no statistically significant association between XRCC3 Thr241Met polymorphism and leukemia risk in overall including studies, while a risky association was observed for acute myeloid leukemia (AML) (dominant model TT/TC vs. CC: OR = 1.240, 95% CI = 1.018-1.511, P = 0.032). The XRCC3 Thr241Met polymorphism might be associated with risk of leukemia in AML. More studies with larger sample sizes are needed to validate this result.

A clinical update of compound heterozygosity for hemoglobin Hekinan II [a27(B8)Glu-Asp; HBA1: c.84G>T] variant in China.

BACKGROUND: Hemoglobin (Hb) Hekinan II (A27; Glu-Asp) is an α-chain variant, and its interaction with the common Southeast Asian (--SEA/) α-thalassemia (α-thal) deletion is rarely reported. This study provides a clinical update of Hb Hekinan II associated with (--SEA/) α-thal. METHODS: A total of 11 simple heterozygotes and 20 composite heterozygotes for Hb Hekinan II and (--SEA/) α-thal were included based on molecular diagnosis. RESULTS: Hb Hekinan II exhibited a significant increase in hemoglobin, mean corpuscular volume, and mean corpuscular hemoglobin content, but a decrease in red blood cell level compared with α+ thalassemia deletion. Compared with (--SEA/) α-thal, composite heterozygotes for Hb Hekinan II and (--SEA/) α-thal showed similar erythrocyte parameters. Both heterozygotes with and without (--SEA/) α-thal showed low Hb A2 level. Hb Hekinan II showed abnormal performance in high-performance liquid chromatography but not in capillary electrophoresis. CONCLUSION: Hb Hekinan II is a benign Hb variant. The heterozygotes exhibit clinically asymptomatic coinheritance with (--SEA/) α-thal having comparable hematological phenotype to simple (--SEA/) α-thal. The combination of hematological and molecular analysis helped to improve the detection rate of this rare variant.

Lack of association between Fas rs180082 polymorphism and risk of cervical cancer: an update by meta-analysis.

BACKGROUND: The Fas rs180082 polymorphism has been reported to be associated with cervical cancer susceptibility, yet the results of these previous results have been inconsistent or controversial. The objective of this study was to explore whether the Fas rs180082 polymorphism confers susceptibility to cervical cancer. METHODS: The relevant studies were identified through a search of PubMed, Excerpta Medica Database (Embase), Elsevier Science Direct and Chinese Biomedical Literature Database (CBM) until July 2012. The association between the Fas rs180082 polymorphism and cervical cancer risk was assessed by odds ratios (ORs) together with their 95% confidence intervals (CIs). RESULTS: A total of 7 case-control studies were eventually identified. We found no association between Fas rs180082 polymorphism and cervical cancer susceptibility in overall population (G versus A: OR = 1.03, 95% CI = 0.99-1.07, P = 0.197; AG + GG versus AA: OR = 1.04, 95% CI = 0.98-1.09, P = 0.176; GG versus AA + AG: OR = 1.04, 95% CI = 0.84-1.31, P = 0.701). In subgroup analysis, similar results were found in Asian (G versus A: OR = 1.06, 95% CI = 0.97-1.15, P = 0.195; AG + GG versus AA: OR = 1.08, 95% CI = 0.98-1.19, P = 0.176; GG versus AA + AG: OR = 0.97, 95% CI = 0.51-1.84, P = 0.935) and African (G versus A: OR = 1.01, 95% CI = 0.97-1.15, P = 0.195; AG + GG versus AA: OR = 0.99, 95% CI = 0.91-1.07, P = 0.739; GG versus AA + AG: OR = 1.09, 95% CI = 0.94-1.25, P = 0.745). CONCLUSION: This meta-analysis has shown that there is a lack of association of the Fas rs180082 polymorphisms with cervical cancer susceptibility. However, larger scale primary studies with the consideration of gene-gene and gene-environment interactions are still required to further evaluate the interaction of Fas rs180082 polymorphism with cervical cancer susceptibility.

A prognostic model for bladder cancer based on cytoskeleton-related genes.

BACKGROUND: A typical cancerous growth in the urinary tract, bladder cancer (BLCA) has a dismal survival rate and a poor chance of being cured. The cytoskeleton has been shown to be tightly related to tumor invasion and metastasis. Nevertheless, the expression of genes associated with the cytoskeleton and their prognostic significance in BLCA remain unknown. METHODS: In our study, we performed differential expression analysis of cytoskeleton-related genes between BLCA versus normal bladder tissues. According to the outcomes of this analysis of differentially expressed genes, all BLCA cases doing nonnegative matrix decomposition clustering analysis be classified into different molecular subtypes and were subjected to Immune cell infiltration analysis. We then constructed a cytoskeleton-associated gene prediction model for BLCA, and performed risk score independent prognostic analysis and receiver operating characteristic curve analyses to evaluate and validate the prognostic value of the model. Furthermore, enrichment analysis, clinical correlation analysis of prognostic models, and immune cell correlation analysis were carried out. RESULTS: We identified 546 differentially expressed genes that are linked to the cytoskeleton, including 314 up-regulated genes and 232 down-regulated genes. All BLCA cases doing nonnegative matrix decomposition clustering analysis could be classified into 2 molecular subtypes, and we observed differences (P < .05) in C1 and C2 immune scores about 9 cell types. Next, we obtained 129 significantly expressed cytoskeleton-related genes. A final optimized model was constructed consisting of 11 cytoskeleton-related genes. Survival curves and risk assessment predicted the prognostic risk in both groups of patients with BLCA. Survival curves and receiver operating characteristic curves were used to evaluate and validate the prognostic value of the model. Significant enrichment pathways for cytoskeleton-associated genes in bladder cancer samples were explored by Gene set enrichment analysis enrichment analysis. After we obtained the risk scores, a clinical correlation analysis was performed to examine which clinical traits were related to the risk scores. Finally, we demonstrated a correlation between different immune cells. CONCLUSION: Cytoskeleton-related genes have an important predictive value for BLCA, and the prognostic model we constructed may enable personalized treatment of BLCA.

Patient with congenital factor VII deficiency undergoing brain tumor neurosurgery successfully treated with recombinant factor VIIa and fresh frozen plasma: A case report and literature review.

RATIONALE: Congenital factor VII deficiency is the most common among rare bleeding disorders, characterized by spontaneous or traumatic bleeding. The clinical manifestation is heterogeneous, ranging from asymptomatic phenotype to life-threatening hemorrhages. Intracranial hemorrhage is a common complication of brain tumor neurosurgery, which significantly challenges the perioperative management of patients with hemostatic defects. PATIENT CONCERNS: This report presented a 55-year-old man with congenital factor VII deficiency, who had no history of hemorrhage or family history. He underwent a craniotomy for the treatment of papillary craniopharyngioma. DIAGNOSES: The patient was diagnosed as papillary craniopharyngioma, factor VII deficiency, and atrial fibrillation. INTERVENTIONS: To prevent bleeding, a total of 8 doses of recombinant activated factor VII and 1 dose of fresh frozen plasma were administered as the perioperative replacement therapy. This scheme was guided by a pharmacodynamic evaluation, laboratory tests, and imaging examinations. OUTCOMES: No excessive surgical bleeding was observed during the 22-day treatment. The patient was found to have compound heterozygous mutations, Ala304Thr (c.910G > A) and IVS5-2A > G (c.572-2A > G), in the F7 gene. LESSONS: This is the first reported case in which surgical hemorrhage secondary to brain tumor resection was successfully controlled in the presence of congenital factor VII deficiency. Perioperative coagulation state, hemostasis, and thrombosis events should be closely observed, and the interval and dosage of recombinant factor VIIa should be adjusted accordingly.

Identification of Phosphorylated Proteins Regulated by SDF2L1 in Nasopharyngeal Carcinoma Cells.

SDF2L1 is a new type of endoplasmic reticulum stress inducible protein, which is related to poor prognosis of various cancer, we initially studied the low expression level of SDF2L1 in NPC, but the molecular mechanism of SDF2L1 in NPC needs further elucidation. To identify phosphorylated proteins regulated by SDF2L1 in nasopharyngeal carcinoma (NPC), Label-free Quantitative (LFQ) Proteomics and 2D-LC-MS/MS analysis were performed on high metastatic NPC 5-8F cells with overexpression of SDF2L1 and empty segment. Western blotting was applied to validate the differentially expressed phosphorylated proteins (DEPPs). As a result, 331 DEPPs were identified by proteomics, and PARVA phosphorylation (ser8) was validated. The present results suggested that PARVA phosphorylation may be a new promising biomarker for predicting NPC and play a key role in the occurrence and development of NPC.

Corrigendum to "SDF2L1 Inhibits Cell Proliferation, Migration, and Invasion in Nasopharyngeal Carcinoma".

[This corrects the article DOI: 10.1155/2020/1970936.].

Identification of key genes and pathways associated with diabetes of the exocrine pancreas.

This study aimed to identify potential essential genes and pathways in diabetes of the exocrine pancreas (DEP) and explore possible molecular mechanisms. The array dataset GSE76895 was downloaded from the Gene Expression Omnibus database. Pancreatic tissue samples from 20 Diabetes of the exocrine pancreas and 32 nondiabetic individuals were selected for analysis. GEO2R analyzed differentially expressed genes (DEGs) in the 2 groups. Gene ontology annotation, Kyoto Encyclopedia of Genes Genomes and Reactome pathway enrichment analyses and Gene Set Enrichment Analysis were performed in this study. Protein-protein interaction (PPI) networks were constructed using Cytoscape software, and core networks were identified using MCODE plugins. A total of 62 genes, including 59 up-regulated and 3 down-regulated genes, were differentially expressed in DEP samples compared with nondiabetic patients. PPI network with 53 nodes and 138 edges was established. HLA-DRA is identified as the central gene of the PPI network and maybe a marker gene for DEP. Furthermore, up-regulated DEGs are mainly enriched in pathways related to the immune system and infection. The results of this study suggest that HLA-DRA and immune system pathways may play essential roles in DEP.

Tubulin polymerization promoting protein family member 3 (TPPP3) overexpression inhibits cell proliferation and invasion in nasopharyngeal carcinoma.

The function of tubulin polymerization promoting protein family member 3 (TPPP3) in tumor cells is complicated, and the role of TPPP3 in nasopharyngeal carcinoma (NPC) remains unclear. This study aims to explore the expression of TPPP3 in NPC and its effect on NPC cells. The expression of TPPP3 in NPC tissues and other cancers were analyzed by using the Oncomine and Gene Expression Omnibus (GEO) databases. The mRNA and protein of TPPP3 were detected in NPC tissues by quantitative real-time PCR and immunohistochemistry. Furthermore, TPPP3 was overexpressed in 5-8 F and HONE1 cell lines by lentivirus transfection, and functional analysis of TPPP3 in NPC was evaluated through in vitro experiments. The expression of TPPP3 was significantly down-regulated in NPC tissues and cells. Overexpression of TPPP3 significantly inhibited proliferation of 5-8 F and HONE1 cells in vitro. In addition, overexpression of TPPP3 significantly attenuated the invasion ability of 5-8 F, HONE1 cells in vitro, but have no significant effect on migration ability. Furthermore, TPPP3 overexpression diminished the expression of MMP-2 and MMP-9 mRNA. By analyzing dataset GSE12452, it was interesting that TPPP3 high expression group mainly functioned in B cell receptor signaling pathway, cell cycle and DNA replication. In conclusion, our results suggest that TPPP3 may be considered as an antioncogene, which plays an important role in the occurrence and progression of NPC.Abbreviations: TPPP3: tubulin polymerization promoting protein family member 3; NPC: nasopharyngeal carcinoma; GEO: Gene Expression Omnibus; qRT-PCR: quantitative real-time PCR; GFP: green fluorescence protein; MOI, transfected multiplicity of infection; CCK-8: cell counting kit-8; OD: optical density; GSEA: gene set enrichment analysis; GO: Gene Ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes; MMP-2: matrix metalloproteinase-2; MMP-9: matrix metalloproteinase-9.

Human/eukaryotic ribosomal protein L14 (RPL14/eL14) overexpression represses proliferation, migration, invasion and EMT process in nasopharyngeal carcinoma.

Although human/eukaryotic ribosomal protein L14 (RPL14/eL14) is known to be associated with a variety of cancers, its role in nasopharyngeal carcinoma (NPC) remains unclear. The aim of this study was to explore the impact of RPL14(eL14) in NPC. The results of quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and immunohistochemical staining revealed that the expression of RPL14(eL14) significantly reduced in NPC tissues and cells. Furthermore, the protein expression of RPL14(eL14) was linked to NPC-related clinical pathological features, including the T and N classification of Tumor Node Metastasis (TNM) staging (all p < 0.05). Cell counting kit-8 (CCK-8) assay and colony formation assay revealed that RPL14(eL14) overexpression repressed NPC cell proliferation. In cell cycle assay, RPL14(eL14) overexpression significantly blocked NPC cells in S phase. Overexpression of RPL14(eL14) repressed cell migration and invasion in NPC as shown by transwell assay and cell scratch healing assay. In addition, RPL14(eL14) was closely correlated with the expression of epithelial-mesenchymal transition (EMT) biomarkers, including E-cadherin, N-cadherin, and vimentin as detected by western blot. In conclusion, our results revealed that RPL14(eL14) may be considered as an antioncogene in NPC, which greatly suppresses cancer progression.

The Autophagy Related Gene CHAF1B Is a Relevant Prognostic and Diagnostic Biomarker in Hepatocellular Carcinoma.

The role of autophagy in tumors is complex; based on known interactions between autophagy and hepatocellular carcinoma (HCC) pathogenesis, we hypothesized that autophagy-related genes (ARGs) may play an important role in HCC. The ARGs were obtained from the Human Autophagy Database and the Gene Set Enrichment Analysis. Based on the area under the curve (AUC) value >0.9 with p <0.0001 and Student's T-test analysis with p <0.0001, differently expressed autophagy-related genes (DEARGs) with high diagnostic efficiency were found. Besides that, we searched in the PubMed database to find novel DEARGs associated with HCC. Then the DEARGs were validated in the GSE25097, GSE54236, GSE76427, GSE64041, Oncomine, and Human Protein Atlas datasets. Finally, survival analysis of CHAF1B in HCC and correlations of clinico-pathological characteristics and CHAF1B were performed based on the TCGA database. The mRNA and protein expression of 531 ARGs were analyzed and validated in eight independent cohorts. First, 18 DEARGs with high diagnostic efficiency were selected from the TCGA database, and nine of them were identified that had not previously been associated with HCC. These nine DEARGs were validated in the GSE25097, GSE54236, GSE76427, GSE64041, Oncomine, and Human Protein Atlas datasets. Additionally, we found that CHAF1B was associated with overall survival and relapse free survival at one, three, and five years. Furthermore, the univariate and multivariate Cox analyses revealed that the high expression of CHAF1B was an independent risk factor in HCC patients. This research demonstrated that CHAF1B was a novel diagnostic and prognostic signature biomarker that could be potentially useful for predicting the development of HCC and may provide new insights for HCC tumorigenesis and treatments.