Alterations of tumor-related genes do not exactly match the histopathological grade in gastric adenocarcinomas

AIM:To investigate the diverse characteristics of different pathological gradings of gastric adenocarcinoma (GA) using tumor-related genes.METHODS:GA tissues in different pathological gradings and normal tissues were subjected to tissue arrays.Expressions of 15 major tumor-related genes were detected by RNA in situ hybridization along with 3' terminal digoxin-labeled anti-sense single strandedoligonucleotide and locked nucleic acid modifying probe within the tissue array.The data obtained were processed by support vector machines by four different feature selection methods to discover the respective critical gene/gene subsets contributing to the GA activities of different pathological gradings.RESULTS:In comparison of poorly differentiated GA with normal tissues,tumor-related gene TP53 plays a key role,although other six tumor-related genes could also achieve the Area Under Curve (AUC) of the receiver operating characteristic independently by more than 80%.Comparing the well differentiated GA with normal tissues,we found that 11 tumor-related genes could independently obtain the AUC by more than 80%,but only the gene subsets,TP53,RB and PTEN,play a key role.Only the gene subsets,Bcl10,UVRAG,APC,Beclin1,NM23,PTEN and RB could distinguish between the poorly differentiated and well differentiated GA.None of a single gene could obtain a valid distinction.CONCLUSION:Different from the traditional point of view,the well differentiated cancer tissues have more alterations of important tumor-related genes than the poorly differentiated cancer tissues.

Tumor-related factor complement Clq/TNF-related protein 6 affects the development of digestive system tumors through the phosphatidylinositol 3-kinase pathway

In this editorial,we review the work of Razali et al published in World J Gas-troenterology,with a particular focus on the effect of rs10889677 variation in the phosphatidylinositol 3-kinase(PI3K)pathway and buparlisib on colitis-associated cancer.The role of PI3K in promoting cancer progression has been widely recognized,as it is involved in regulating the survival,differentiation,and prolif-eration of cancer cells.The complement Clq/TNF-related protein 6(CTRP6)is a newer tumor-associated factor.Recent studies have revealed the pro-tumor effect of CTRP6 in gastric cancer,hepatocellular carcinoma,colorectal cancer,and other gastrointestinal tumors through the PI3K pathway.This article attempts to reveal the mechanism through which the CTRP6 affects the development of digestive system tumors through the PI3K pathway by summarizing recent research.

Analysis of genotype polymorphism of tumor-related genes harbored in chromosome arm 1p and 8p in hepatocellular carcinoma patients by cSNP chip

The majority of single nucleotide polymorphisms(SNPs)found in the coding region(cSNPs)are single base substitutions that may or may not lead to amino acid substitutions,most of which are related to diseases.Some cSNPs may prove useful for their potential links to functional cSNPs via linkage disequilibrium mapping.We have selected 48 cSNPs located in the coding regions of 25 genes to construct the cSNP chip.These genes are harbored in the high frequency loss regions of the chromosome 1p and 8p and related with apoptosis,cell cycles,signal transduction,oncogene,tumor suppressor genes and so on.All of the cSNPs can lead to amino acid substitutions except TP73(rs1801174).The PCR products amplified from 31 hepatocellular carcinoma(HCC)specimens were labeled with Dig-dUTP and then hybridized with the cSNP chips.The results showed that there was no hybridization signal when there was more than one site of mutation in the amplification sequence,indicating that the cSNP chip had a high sensitivity.The statistic data of the SNP(MT,homozygous and HT,heterozygous)in the HCC patients with different phenotypes(HBV+/-,differentiation stage,family history positive or negative,tumor size)indicated that the number of MT was distinctly different between patients with positive HBV and negative HBV.The MT and HT numbers of all the 48 cSNPs were significantly different between low differentiation and high differentiation HCC patients.The numbers of MT and HT were not different between positived and negative family history groups and between tumor size>3 cm and≤3 cm groups.The study results provided useful information for understanding the molecular mechanisms of HCC development.

Advances in the study of the effect of tumor stromal cells on oral cancer

Oral squamous cell carcinoma (OSCC) is the most common malignant tumour in oral and maxillofacial region. The interaction between stromal cells and tumor cells is involved in the proliferation, differentiation, apoptosis, adhesion and migration of tumor cells, and is closely related to the malignant degree and prognosis of tumors. The development of OSCC is of great significance to the treatment of OSCC. This paper summarizes the sources of several important stromal cells and their effects on tumor cells, which provides a theoretical basis for the treatment of OSCC.

Integrative Identification by Hi‑C Revealed Distinct Advanced Structural Variations in Lung Adenocarcinoma Tissue

Advanced three-dimensional structure variations of chromatin in large genome fragments,such as conversion of A/B compartment,topologically associated domains(TADs)and chromatin loops are related closely to occurrence of malignant tumors.However,the structural characteristics of lung cancer still remain uncovered.In this study,we used high-throughput chromosome(Hi-C)conformation capture technology to detect the advanced structural variations in chromatin of two nonsmoking lung adenocarcinoma(LUAD)tumor and paired normal tissues.The results indicate that significant chromatin variations are detected in tumor tissues compared with normal tissues.At compartment scale,the main conversion type of compartment is A→B in tumor tissues,which are concentrated mainly on chromosome 3(Chr3)(33.6%).A total of 216 tumor-specific TADs are identified in tumor tissues,which are distributed mainly in Chr1(19),Chr2(15)and Chr3(17).Forty-one distinct enhancer-promoter loops are observed in tumor tissue,which are associated closely to tumor-related pathways including mitogen-activated protein kinase(MAPK),Phosphatidylinositol-3-kinase-Protein kinase B(PI3K-AKT),Ras,Wnt and Ras1.The most important observation in this study is that we identify five important genes(SYT16,NCEH1,NXPE3,MB21D2,and DZIP1L),which are detected in both A→B compartment,TADs and chromatin loops in tumor samples,and four of these genes(NCEH1,NXPE3,MB21D2,and DZIP1L)locate on q arm of Chr3.Further gene expression and invasion experiment analysis show that NCEH1,MB21D2 and SYT16 are involved in the tumor development.Thus,we provide a comprehensive overview of advanced structures in LUAD for the first time and provide a basis for further research on the genetic variation of this tumor.

Clinical characteristics of brain tumorrelated epilepsy and factors influencing the identification of epilepsy-associated tumors

Background:To analyze the clinical features of brain tumor-related epilepsy(BTRE)and explore the factors influencing the identification of epilepsy-associated tumor(EAT),in order to advance the clinical understanding of BTRE and EAT.Methods:Intracranial tumor origin and location as well as the type of epilepsy were retrospectively reviewed in 153 BTRE patients.The patients were further divided into the EAT and non-EAT groups,and comparisons were made for age,sex,tumor origin and location,and epilepsy type between the two groups.Results:The 153 BTRE patients were divided into 78 cases with primary intracranial tumor and 75 cases with tumor originating from extracranial metastasis,according to the origin of tumor.According to the location of tumor,116 cases had tumor lesions located in the brain parenchyma,and 37 cases had tumor lesions located in the meninges.Further,in the group with a brain parenchyma location,77 cases had single lobular involvement,and 39 cases had multiple-lobular involvement;84 cases had tumor lesions located in one hemisphere and 32 cases in both hemispheres.According to the type of epilepsy,92 cases had generalized seizures,and 61 cases had focal seizures.The type of epilepsy did not significantly correlate with the origin of intracranial tumor,the location of tumor lesions(in brain parenchyma or meninges)(P>0.05),or the hemispherical location(in one or two hemispheres)of lesions(P>0.05),but was significantly related with the lobular localization of lesions(P<0.05).The 153 cases of BTRE consisted of 87 EAT and 66 non-EAT,with significant differences in the origin,location and type(being glioma/non-glioma)of tumor.Logistic regression analysis showed that the type of tumor(i.e.whether being glioma)served as an independent factor for EAT identification;the lower the World Health Organization grade of glioma,the more likely the EAT is to be diagnosed(P<0.05).Conclusion:The majority of BTRE patients in this study had tumors located in the brain parenchyma.In addition,the patients with generalized seizures outnumbered those with focal seizures,and the type of epilepsy was correlated with the lobular location of tumor lesions.The EATs are mostly low-grade gliomas.