A novel tumor immunotherapy-related signature for risk stratification, prognosis prediction, and immune status in hepatocellular carcinoma.

Immunotherapy as a strategy to deal with cancer is increasingly being used clinically, especially in hepatocellular carcinoma (HCC). We aim to create an immunotherapy-related signature that can play a role in predicting HCC patients' survival and therapeutic outcomes. Immunotherapy-related genes were discovered first. Clinical information and gene expression data were extracted from GSE140901. By a series of bioinformatics methods to analyze, overlapping genes were used to build an immunotherapy-related signature that could contribute to predict both the prognosis of people with hepatocellular carcinoma and responder to immune checkpoint blockade therapy of them in TCGA database. Differences of the two groups in immune cell subpopulations were then compared. Furthermore, A nomogram was constructed, based on the immunotherapy-related signature and clinicopathological features, and proved to be highly predictive. Finally, immunohistochemistry assays were performed in HCC tissue and normal tissue adjacent tumors to verify the differences of the four genes expression. As a result of this study, a prognostic protein profile associated with immunotherapy had been created, which could be applied to predict patients' response to immunotherapy and may provide a new perspective as clinicians focus on non-apoptotic treatment for patients with HCC.

Analytical modeling and numerical analysis of thermoelastic damping in ultrathin elastic films due to surface effects.

Analytical techniques used for estimating thermoelastic damping by incorporating both mechanical and thermal interactions between surfaces and the rest of the bulk are intricate and challenging due to the limited understanding of the damping mechanisms in extra-thin films subjected to forced vibrations. This paper proposes a modified model to analytically calculate the thermoelastic damping of ultrathin elastic films due to surface effects and analyzes the thermoelastic damping variation with different factors through numerical experiments on two materials. The model considers surface stresses derived from the elastic surface theory using Kirchhoff's kinetic hypothesis and determines thermoelastic damping by considering thermal dissipation and elastic potential energy. The results show that surface effects significantly influence the thermoelastic damping of the film, and the specific behavior of a thin film's thermoelastic damping with respect to film thickness is impacted by various factors, including material property, the variation range of film thickness, and the forced vibration frequency. This study provides insights into the thermoelastic damping behavior of thin films and has important implications for the development of nanoscale oscillators in MEMS or NEMS systems.

Facile Construction of Iron/Nickel Phosphide Nanocrystals Anchored on N-B-Doped Carbon-Based Composites with Advanced Catalytic Capacity for 4-Nitrophenol and Methylene Blue.

The search for a simple and effective method to remove organic dyes and color intermediates that threaten human safety from the water environment is urgent. Herein, we report a simple method for constructing iron/nickel phosphide nanocrystals anchored on N-B-doped carbon-based composites, using steam-exploded poplar (SEP) and graphene oxide (GO) as a carrier. The stability and catalytic activity of N-B-NixFeyP/SEP and GO were achieved by thermal conversion in a N2 atmosphere and modifying the Fe/Ni ratio in gel precursors. N-B-Ni7Fe3P/SEP was employed for the catalytic hydrogenation of 4-nitrophenol (4-NP) and methylene blue (MB), using sodium borohydride in aqueous media at room temperature. This showed much better catalytic performances in terms of reaction rate constant (0.016 S-1 and 0.041 S-1, respectively) and the activity factor, K (1.6 S-1·g-1 and 8.2 S-1·g-1, respectively) compared to the GO carrier (0.0053 S-1 and 0.035 S-1 for 4-NP and MB, respectively). The strong interaction between the carrier's morphology and structure, and the vertically grown bimetallic phosphide nanoclusters on its surface, enhances charge transfer, electron transfer kinetics at the interface and Ni-Fe phosphide dispersion on the nanoclusters, and prevents dissolution of the nanoparticles during catalysis, thereby improving stability and achieving catalysis durability. These findings provide a green and simple route to efficient catalyst preparation and provide guidance for the rational selection of catalyst carriers.

Kub3 Deficiency Causes Aberrant Late Embryonic Lung Development in Mice by the FGF Signaling Pathway.

As a Ku70-binding protein of the KUB family, Kub3 has previously been reported to play a role in DNA double-strand break repair in human glioblastoma cells in glioblastoma patients. However, the physiological roles of Kub3 in normal mammalian cells remain unknown. In the present study, we generated Kub3 gene knockout mice and revealed that knockout (KO) mice died as embryos after E18.5 or as newborns immediately after birth. Compared with the lungs of wild-type (WT) mice, Kub3 KO lungs displayed abnormal lung morphogenesis and pulmonary atelectasis at E18.5. No difference in cell proliferation or cell apoptosis was detected between KO lungs and WT lungs. However, the differentiation of alveolar epithelial cells and the maturation of type II epithelial cells were impaired in KO lungs at E18.5. Further characterization displayed that Kub3 deficiency caused an abnormal FGF signaling pathway at E18.5. Taking all the data together, we revealed that Kub3 deletion leads to abnormal late lung development in mice, resulting from the aberrant differentiation of alveolar epithelial cells and the immaturation of type II epithelial cells due to the disturbed FGF signaling pathway. Therefore, this study has uncovered an essential role of Kub3 in the prenatal lung development of mice which advances our knowledge of regulatory factors in embryonic lung development and provides new concepts for exploring the mechanisms of disease related to perinatal lung development.

Regulation and management of the biosecurity for synthetic biology.

Synthetic biology (SynBio) is a high-profile interdiscipline combining engineering with science. As a dual-purpose discipline, SynBio is bringing large changes to many fields and providing great benefits to humans. However, due to its characteristic of complexity and uncertainty, SynBio also presents potential biosafety and biosecurity risks. Biosecurity risks refer to unauthorized access, loss, theft, misuse, diversion or intentional release. If a biosecurity accident happens, it would pose a huge threat to humans and nature. Therefore, it is crucial to establish a set of regulations and management practices for the biosecurity risks of SynBio. In this paper, we summarized the sources of the biosecurity risks of SynBio, from its research materials, products, technologies, information to Do-it-yourself synthetic biology. We reviewed and analyzed the current situation of regulation and management of biosecurity for SynBio in the international community and in China. We found that in most countries and regions, SynBio risks commonly follow the regulation and management of Genetically Modified Organisms which has loopholes if applied to the regulation for SynBio without any amendments. Here, we proposed suggestions for the Chinese-featured regulation and management of biosecurity for SynBio, including a top-to-bottom governing framework, a think-tank implementation mechanism, a Synthetic Biology Laboratory Biosecurity Manual safeguarding system, and strengthening biosecurity education on synthetic biology and self-regulation awareness among relevant personnel. Through this work, we aim to improve the standardized process of biosecurity regulation and management for SynBio in China and thereby map out a peaceful, profitable, and practical development path for synthetic biology.

T1121G Point Mutation in the Mitochondrial Gene COX1 Suppresses a Null Mutation in ATP23 Required for the Assembly of Yeast Mitochondrial ATP Synthase.

Nuclear-encoded Atp23 was previously shown to have dual functions, including processing the yeast Atp6 precursor and assisting the assembly of yeast mitochondrial ATP synthase. However, it remains unknown whether there are genes functionally complementary to ATP23 to rescue atp23 null mutant. In the present paper, we screen and characterize three revertants of atp23 null mutant and reveal a T1121G point mutation in the mitochondrial gene COX1 coding sequence, which leads to Val374Gly mutation in Cox1, the suppressor in the revertants. This was verified further by the partial restoration of mitochondrial ATP synthase assembly in atp23 null mutant transformed with exogenous hybrid COX1 T1121G mutant plasmid. The predicted tertiary structure of the Cox1 p.Val374Gly mutation showed no obvious difference from wild-type Cox1. By further chase labeling with isotope [35S]-methionine, we found that the stability of Atp6 of ATP synthase increased in the revertants compared with the atp23 null mutant. Taking all the data together, we revealed that the T1121G point mutation of mitochondrial gene COX1 could partially restore the unassembly of mitochondrial ATP synthase in atp23 null mutant by increasing the stability of Atp6. Therefore, this study uncovers a gene that is partially functionally complementary to ATP23 to rescue ATP23 deficiency, broadening our understanding of the relationship between yeast the cytochrome c oxidase complex and mitochondrial ATP synthase complex.

Atp23p and Atp10p coordinate to regulate the assembly of yeast mitochondrial ATP synthase.

Two chaperones, Atp23p and Atp10p, were previously shown to regulate the assembly of yeast mitochondrial ATP synthase, and extra expression of ATP23 was found to partially rescue an atp10 deletion mutant, by an unknown mechanism. Here, we identified that the residues 112-115 (LRDK) of Atp23p were required for its function in assisting assembly of the synthase, and demonstrated both functions of Atp23p, processing subunit 6 precursor and assisting assembly of the synthase, were required for the partial rescue of atp10 deletion mutant. By chasing labeling with isotope 35 S-methionine, we found the stability of subunit 6 of the synthase increased in atp10 null strain upon overexpression of ATP23. Further co-immunoprecipitation (Co-IP) and blue native PAGE experiments showed that Atp23p and Atp10p were physically associated with each other in wild type. Moreover, we revealed the expression level of Atp23p increased in atp10 null mutant compared with the wild type. Furthermore, we found that, after 72 hours growth, atp10 null mutant showed leaky growth on respiratory substrates, presence of low level of subunit 6 and partial recovery of oligomycin sensitivity of mitochondrial ATPase activity. Further characterization revealed the expression of Atp23p increased after 24 hours growth in the mutant. These results indicated, in atp10 null mutant, ATP10 deficiency could be partially complemented with increased expression of Atp23p by stabilizing some subunit 6 of the synthase. Taken together, this study revealed the two chaperones Atp23p and Atp10p coordinated to regulate the assembly of mitochondrial ATP synthase, which advanced our understanding of mechanism of assembly of yeast mitochondrial ATP synthase.

Effects of initial stress on band gap of Love waves in a layered domain-inverted phononic crystal structure.

Love wave propagation in periodically domain-inverted lithium niobate substrate with a homogeneous zinc oxide waveguide layer is theoretically investigated. Much attention is devoted to the effect of initial stress on the band gap and dispersion behavior of Love wave in the layered structure. The results reveal a strong dependency of the band structure on the waveguide layer. In particular, as the waveguide layer gradually thickens, the band gap shifts into a lower frequency range remarkably. Additionally, the initial stress has a significant influence on the location of the band gap, but a small effect on the bandgap width. This separate effect provides the potential to actively tune the surface acoustic waves by the stress.

A rapid and accurate method for the detection of four aminoglycoside modifying enzyme drug resistance gene in clinical strains of Escherichia coli by a multiplex polymerase chain reaction.

BACKGROUND: Antibiotics are highly effective drugs used in the treatment of infectious diseases. Aminoglycoside antibiotics are one of the most common antibiotics in the treatment of bacterial infections. However, the development of drug resistance against those medicines is becoming a serious concern. AIM: This study aimed to develop an efficient, rapid, accurate, and sensitive detection method that is applicable for routine clinical use. METHODS: Escherichia coli was used as a model organism to develop a rapid, accurate, and reliable multiplex polymerase chain reaction (M-PCR) for the detection of four aminoglycoside modifying enzyme (AME) resistance genes Aac(6')-Ib, Aac(3)-II, Ant(3″)-Ia, and Aph(3')-Ia. M-PCR was used to detect the distribution of AME resistance genes in 237 clinical strains of E. coli. The results were verified by simplex polymerase chain reaction (S-PCR). RESULTS: Results of M-PCR and S-PCR showed that the detection rates of Aac(6')-Ib, Aac(3)-II, Ant(3″)-Ia, and Aph(3')-Ia were 32.7%, 59.2%, 23.5%, and 16.8%, respectively, in 237 clinical strains of E. coli. Compared with the traditional methods for detection and identification, the rapid and accurate M-PCR detection method was established to detect AME drug resistance genes. This technique can be used for the clinical detection as well as the surveillance and monitoring of the spread of those specific antibiotic resistance genes.

CelB is a suitable marker for rapid and specific identification of Klebsiella pneumoniae by the loop-mediated isothermal amplification (LAMP) assay.

Klebsiella pneumoniae belongs to Enterobacteriaceae, which is the commonest bacterium causing nosocomial respiratory tract infection. It ranks second in bacteremia and urinary tract infection in gram-negative bacteria. Therefore, the rapid and accurate identification of K. pneumoniae was of great significance for the guide of clinical medication, and timely treatment of patients. The purpose of this study was to establish a rapid and sensitive molecular detection method for K. pneumoniae based on loop-mediated isothermal amplification (LAMP) technology. Firstly, local BLAST and NCBI BLAST were used to analyze the genome of K. pneumoniae. According to the principle of interspecific and intraspecific specificity, CelB (GenBank ID 11847805) was selected as the specific gene. Then, the LAMP and PCR identification systems were established with this target gene. Thirty-six clinical isolates of K. pneumoniae and 50 non-K. pneumoniae were used for the specific evaluation, and both LAMP and PCR could specifically distinguish K. pneumoniae from non-K. pneumoniae. A 10-fold series diluted positive plasmids and simulated infected blood samples were used as the templates in the sensitivity assay, and the results showed that the sensitivity could reach 1 copy/reaction. In summary, a rapid, specific, and sensitive LAMP method was established to detect K. pneumoniae in clinics.

Loop-Mediated Isothermal Amplification Assay for Rapid Detection of Hypothetical Protein Gene in Escherichia Coli Clinical Isolates.

BACKGROUND: Escherichia coli is the most common pathogenic bacteria that frequently causes life-threatening opportunistic human infections, diarrhea, and septicemia in immunocompromised hosts. METHODS: This study aimed to establish a loop-mediated isothermal amplification (LAMP) method for the rapid and sensitive detection of a hypothetical protein from an E. coli-specific gene (GenBank ID: 13702648). The gene was obtained through local and online BLAST, and specific primers were designed for this gene. Reaction conditions were optimized at 65ºC for 30 minutes and 80ºC for 2 minutes, whereas the reaction system contained 5.2 mM Mg2+, 8 U of Bst 2.0 DNA polymerase, 1.4 mM deoxyribonucleotide, and 0.2 and 1.6 µM of the outer and inner primers, respectively. The LAMP method was evaluated using 240 strains of E. coli and 150 strains of non-E. coli. RESULTS: Positive reactions were observed on all 240 strains of E. coli while all non-E. coli strains were negative. Plasmids with the specific gene and mice blood with E. coli were used for sensitivity analysis. The detection limit of LAMP was 100 bacterium/reaction. CONCLUSIONS: Results showed that the LAMP targeted to the hypothetical protein (GenBank ID: 13702648) is a fast, specific, sensitive, inexpensive, and suitable method for the detection of E. coli.

Rapid, specific, and sensitive detection of the ureR_1 gene in Klebsiella pneumoniae by loop-mediated isothermal amplification method.

Klebsiella pneumoniae is one of the main pathogenic bacteria that causes nosocomial infections, such as pneumonia, urinary tract infection, and sepsis. Therefore, the rapid and accurate detection of K. pneumoniae is important for the timely treatment of infectious patients. This study aimed to establish a loop-mediated isothermal amplification (LAMP) method for the rapid and sensitive detection of K. pneumoniae-specific gene ureR_1 (Gene ID: 11847803). The ureR_1 gene was obtained through local and online BLAST, and the specific primers were designed for its detection. Positive reactions were observed on all 140 K. pneumoniae clinical isolates while all the 82 non-K. pneumoniae clinical isolates were negative. Plasmids with the specific gene and the mouse blood with K. pneumoniae were used for sensitivity analysis. The detection limit of the LAMP was 1 bacterium/reaction. The results showed that the LAMP targeted to ureR_1 is a fast, specific, sensitive, inexpensive, and suitable method for the detection of K. pneumoniae.

Establishment of loop-mediated isothermal amplification for rapid detection of Pseudomonas aeruginosa.

Pseudomonas aeruginosa is one of the three most pathogenic bacteria that frequently cause life-threatening opportunistic human infections, pneumonia, and lower respiratory tract infections in immunocompromised hosts, particularly in the burns ward. The present study aimed to establish a loop-mediated isothermal amplification (LAMP) method for the rapid and sensitive detection of P. aeruginosa-specific gene hypothetical protein (GenBank ID: 882161). The gene was obtained through local and online BLAST, and specific primers were designed for this gene. Reaction conditions were optimized at 65°C for 30 min and 80°C for 2 min, whereas the reaction system contained 5.2 mM Mg2+, 8 U Bst 2.0 DNA polymerase, 1.4 mM deoxyribonucleotide and 0.2 and 1.6 µM of the outer and inner primers, respectively. The LAMP method was evaluated using 150 P. aeruginosa and 170 non-P. aeruginosa strains. Positive reactions were observed on 150 P. aeruginosa strains, whereas all non-P. aeruginosa strains exhibited negative results. Plasmids with the specific gene and mouse blood with P. aeruginosa were used for sensitivity assay. The detection limit of LAMP was 1 bacterium/reaction. Results indicated that the LAMP method targeted to hypothetical protein is a fast, specific, sensitive, inexpensive and suitable method for detection of P. aeruginosa.

Rapid, specific, and sensitive detection of the ureR_1 gene in Klebsiella pneumoniae by loop-mediated isothermal amplification method

Klebsiella pneumoniae is one of the main pathogenic bacteria that causes nosocomial infections, such as pneumonia, urinary tract infection, and sepsis. Therefore, the rapid and accurate detection of K. pneumoniae is important for the timely treatment of infectious patients. This study aimed to establish a loop-mediated isothermal amplification (LAMP) method for the rapid and sensitive detection of K. pneumoniae-specific gene ureR_1 (Gene ID: 11847803). The ureR_1 gene was obtained through local and online BLAST, and the specific primers were designed for its detection. Positive reactions were observed on all 140 K. pneumoniae clinical isolates while all the 82 non-K. pneumoniae clinical isolates were negative. Plasmids with the specific gene and the mouse blood with K. pneumoniae were used for sensitivity analysis. The detection limit of the LAMP was 1 bacterium/reaction. The results showed that the LAMP targeted to ureR_1 is a fast, specific, sensitive, inexpensive, and suitable method for the detection of K. pneumoniae.

[Semi-quantitative detection of HPV L1 capsid protein in exfoliative cytological examination facilitates the differential diagnosis of cervical lesions].

OBJECTIVE: To evaluate the association of human papilloma virus (HPV) L1 capsid protein expression levels with cervical intraepithelial neoplasia (CIN) and its clinical significance. METHODS: Immunohistochemistry were performed to detect the expression of HPV L1 capsid protein in the cervical exfoliative cytological examination of 153 cases. The intensity (positive unit, PU) was assessed semi-quantitatively using ImagePro Plus image analysis software. The results were evaluated based on histopathologic diagnosis of cervical biopsy. RESULTS: PU of HPV L1 capsid protein in different cytopathological groups, including normal/inflammation, atypical squamous cells of unknown significance (ASCUS), low-grade squamous intraepithelial lesion (LSIL), high-grade squamous intraepithelial lesion (HSIL), was 46.87±24.46, 27.23±24.30, 24.10±22.45, 9.36±19.82, respectively, and the differences were statistically significant (P<0.01). PU of HPV L1 capsid protein in different histopathological groups, including normal cervixes or chronic cervicitis, LSIL and HSIL, was 41.30±26.66, 24.84±22.18, 8.69±19.20, respectively, and the differences were statistically significant (P<0.01). Patients with high-risk HPV16 and HPV18 had significantly lower PU of HPV L1 capsid protein than those with other high-risk HPV (P<0.01). PU of HPV L1 capsid protein were correlated negatively with both cytopathological groups and histopathological groups of cervical diseases (r=-0.458, P<0.01 and r=-0.441, P<0.01, respectively). PU of HPV L1 capsid protein was not associated with patients' age (P>0.05). CONCLUSION: Semi-quantitative analysis of HPV L1 capsid protein expression can directly reflect the precancerous progression of cervical cancer.

[Expression of Versican and its clinical significance in gastric carcinoma].

OBJECTIVE: To investigate the expression of Versican in gastric carcinoma and its relationship with tumor angiogenesis. METHODS: Protein expression of Versican, vascular endothelial growth factor and CD34 was evaluated by immunohistochemistry (EliVision method) in 80 cases of gastric carcinoma and 30 samples of normal gastric tissue. RESULTS: There were statistically significant differences in the expression of Versican, vascular endothelial growth factor and CD34 between gastric carcinoma and normal gastric tissue (P < 0.05). The expression of Versican was seen mainly in fibroblasts of the tumor and was correlated with tumor differentiation, clinical stage and lymph node metastasis (P < 0.05), whereas vascular endothelial growth factor was primarily seen in the cytoplasm of the tumor cells and correlated with tumor differentiation, clinical stage, Lauren classification and lymph node metastasis (P < 0.05). MVD was correlated with tumor differentiation, clinical stage, Lauren classification, depth of tumor invasion and lymph node metastasis (P < 0.05). In addition, positive correlation of Versican and VEGF protein expression was found in tumor cells (r = 0.467, P < 0.01). CONCLUSION: The expression of both Versican and vascular endothelial growth factor is closely associated with tumor angiogenesis in gastric carcinoma.

Analysis of clinical characteristics and differential diagnosis of the lung biopsy specimens in 99 adenocarcinoma cases and 111 squamous cell carcinoma cases: utility of an immunohistochemical panel containing CK5/6, CK34ßE12, p63, CK7 and TTF-1.

This study aimed at evaluating the utility of a panel of antibodies, consisting of cytokeratins (CK) 5/6, CK34ßE12, p63, thyroid transcription factor-1 (TTF-1), and CK7 for distinguishing between squamous cell carcinoma (SCC) and adenocarcinomas (Ad), as well as their expression with clinicopathological parameters and prognosis in SCC and Ad. 111 SCC of small biopsy specimens and 99 cases of Ad were stained by immunohistochemistry, among which 76 SCC and 64 Ad had complete follow-up data. Most of SCC displayed CK5/6 (91/99, 91.92%), CK34ßE12 (83/99, 83.84%), p63 (96/99, 96.97%), and most of Ad showed expression of CK7 (89/111, 80.18%) and TTF-1 (105/111, 94.59%). The combination of CK5/6/CK34ßE12/p63 seems to be useful for differentiating SCC from Ad with 100% sensitivity and 97.30% specificity, and TTF-1 was a useful biomarker for Ad with 94.59% sensitivity and 100% specificity. There were differences between CK5/6, p63, and TTF-1 expression with tumor differentiation (p<0.05) in SCC or Ad. Univariate analysis indicated that patients with high TTF-1 expression predicted better prognosis in Ad patients. Multivariate analysis showed that TTF-1 expression (HR=0.340, 95% CI 0.143-0.811, p=0.015) was a good independent predictor of Ad patient survival.

MicroRNA-137, an HMGA1 target, suppresses colorectal cancer cell invasion and metastasis in mice by directly targeting FMNL2.

BACKGROUND & AIMS: Formin-like (FMNL)2 is up-regulated in colorectal tumors and has been associated with tumor progression, but little is known about regulatory mechanisms. We investigated whether microRNAs regulate levels of FMNL2 in colorectal cancer (CRC) cells. METHODS: We used real-time polymerase chain reaction and immunoblot analyses to measure levels of miR-137, high-mobility group AT-hook (HMGA)1, and FMNL2 in CRC cells and tissue samples from patients (n = 50). We used luciferase reporter assays to determine the association between miR-137 and the FMNL2 3' untranslated region, and HMGA1 and the miR-137 promoter. Chromatin immunoprecipitation assays were used to assess direct binding of HMGA1 to the miR-137 promoter. RESULTS: miR-137 and miR-142-3p were predicted to bind FMNL2 based on bioinformatic data. Only the level of miR-137 had a significant inverse correlation with the level of FMNL2 protein in CRC cell lines and tissues. FMNL2 messenger RNA was targeted by miR-137; expression of miR-137 inhibited proliferation and invasion by CRC cells in vitro, and metastasis to liver and intestine by CRC xenografts in nude mice. HMGA1 bound to the promoter of miR-137 and activated its transcription, which reduced levels of FMNL2 in CRC cells. Ectopic expression of miR-137 in CRC cells inhibited phosphorylation of mitogen-activated protein kinase (MAPK) and Akt, which reduced levels of matrix metalloproteinase 2, matrix metalloproteinase 9, and vascular endothelial growth factor; it also reduced invasiveness of CRC cells, inhibiting signaling via phosphatidylinositol-4,5-bisphosphate 3-kinase, Akt, and MAPK. CONCLUSIONS: Levels of miR-137 and HMGA1 are reduced, and levels of FMNL2 are increased, in CRC samples compared with adjacent normal mucosa. In CRC cells, miR-137 targets FMNL2 messenger RNA and is regulated by the transcription factor HMGA1. Expression of miR-137 reduces CRC cell invasion in vitro and metastasis of tumor xenografts in mice. FMNL2 appears to activate phosphatidylinositol-4,5-bisphosphate 3-kinase, protein kinase B (Akt), and MAPK signaling pathways.

[Expression of MICA/B protein in esophageal cancer and its clinical significance].

OBJECTIVE: To explore the expression of MICA/B in human esophageal cancer, and to analyze its correlation with clinicopathological features. METHODS: The expression of MICA/B in 40 cases of esophagus carcinoma and corresponding normal esophageal mucosa tissues were examined by immunohistochemistry. RESULTS: The positive rate of expression of MICA/B protein in the esophageal carcinoma was 75.0% (30/40), and that in the corresponding normal esophageal mucosa was 0 (0/40). Up-regulation of MICA/B expression was found in the esophageal carcinomas. The expression of MICA/B was related with histological grade of the esophageal carcinoma (P = 0.012). CONCLUSION: MICA/B protein plays an important role in the esophageal carcinogenesis, and my become a useful molecular marker for the diagnosis of esophageal carcinoma.