A 4-gene panel as a marker at chromosome 8q in Asian gastric cancer patients

Cheng, Lei; Zhang, Qing; Yang, Sheng; Yang, Yanqing; Zhang, Wen; Gao, Hengjun; Deng, Xiaxing; Zhang, Qinghua

doi:10.1016/j.ygeno.2013.05.004

Cited by 27 publications

(26 citation statements)

References 37 publications

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“…Limited studies indicate that INTS8 contains mutations in peripheral T cell lymphoma compared with non-malignant samples from 12 patients [36], and a combination of INTS8 with SULF1 , ATP6V1C1 , and GPR172A can be used to discriminate gastric carcinomas from adjacent noncancerous tissues [37]. In this study, we found that, potentially regulated by demethylation (Fig.…”

Section: Discussionmentioning

confidence: 57%

Microarray-based identification of genes associated with cancer progression and prognosis in hepatocellular carcinoma

Yin

Shu

Liu

et al. 2016

J Exp Clin Cancer Res

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BackgroundHepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths. The average survival and 5-year survival rates of HCC patients still remains poor. Thus, there is an urgent need to better understand the mechanisms of cancer progression in HCC and to identify useful biomarkers to predict prognosis.MethodsPublic data portals including Oncomine, The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) profiles were used to retrieve the HCC-related microarrays and to identify potential genes contributed to cancer progression. Bioinformatics analyses including pathway enrichment, protein/gene interaction and text mining were used to explain the potential roles of the identified genes in HCC. Quantitative real-time polymerase chain reaction analysis and Western blotting were used to measure the expression of the targets. The data were analysed by SPSS 20.0 software.ResultsWe identified 80 genes that were significantly dysregulated in HCC according to four independent microarrays covering 386 cases of HCC and 327 normal liver tissues. Twenty genes were consistently and stably dysregulated in the four microarrays by at least 2-fold and detection of gene expression by RT-qPCR and western blotting showed consistent expression profiles in 11 HCC tissues compared with corresponding paracancerous tissues. Eleven of these 20 genes were associated with disease-free survival (DFS) or overall survival (OS) in a cohort of 157 HCC patients, and eight genes were associated with tumour pathologic PT, tumour stage or vital status. Potential roles of those 20 genes in regulation of HCC progression were predicted, primarily in association with metastasis. INTS8 was specifically correlated with most clinical characteristics including DFS, OS, stage, metastasis, invasiveness, diagnosis, and age.ConclusionThe significantly dysregulated genes identified in this study were associated with cancer progression and prognosis in HCC, and might be potential therapeutic targets for HCC treatment or potential biomarkers for diagnosis and prognosis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-016-0403-2) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 57%

Microarray-based identification of genes associated with cancer progression and prognosis in hepatocellular carcinoma

Yin

Shu

Liu

et al. 2016

J Exp Clin Cancer Res

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“…Of note, we experimentally validated their transcriptional alteration in primary breast and colon tumor samples (Figure 6), confirming TCGA data re-analysis. Interestingly, microarray- and exome sequencing-based studies proposed a role of INTS8 in gastric cancer and peripheral T-cell lymphoma [26,27]. Unfortunately, freely available data from TCGA (tier 1) did not include RNA-Seq data from paired stomach adenocarcinoma (STAD) samples and datasets of peripheral T-cell lymphoma (see Table 1).…”

Section: Discussionmentioning

confidence: 99%

“…Similarly, INTS3 was found to be significantly overexpressed in cell lines and tumor tissues from hepatocellular carcinoma (HCC) patients compared with their non-cancerous counterparts [25]. In the last few years, both microarray and exome sequencing analyses have suggested a possible role of INTS8 in gastric cancer and peripheral T-cell lymphoma, respectively [26,27]. Furthermore, INTS14/VWA9 was found to be upregulated in immortalized cells, cancer cells, and non-small-cell lung cancer tissues [28].…”

Section: Introductionmentioning

confidence: 99%

Pan-Cancer Mutational and Transcriptional Analysis of the Integrator Complex

Federico

Rienzo

Abbondanza

et al. 2017

IJMS

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The integrator complex has been recently identified as a key regulator of RNA Polymerase II-mediated transcription, with many functions including the processing of small nuclear RNAs, the pause-release and elongation of polymerase during the transcription of protein coding genes, and the biogenesis of enhancer derived transcripts. Moreover, some of its components also play a role in genome maintenance. Thus, it is reasonable to hypothesize that their functional impairment or altered expression can contribute to malignancies. Indeed, several studies have described the mutations or transcriptional alteration of some Integrator genes in different cancers. Here, to draw a comprehensive pan-cancer picture of the genomic and transcriptomic alterations for the members of the complex, we reanalyzed public data from The Cancer Genome Atlas. Somatic mutations affecting Integrator subunit genes and their transcriptional profiles have been investigated in about 11,000 patients and 31 tumor types. A general heterogeneity in the mutation frequencies was observed, mostly depending on tumor type. Despite the fact that we could not establish them as cancer drivers, INTS7 and INTS8 genes were highly mutated in specific cancers. A transcriptome analysis of paired (normal and tumor) samples revealed that the transcription of INTS7, INTS8, and INTS13 is significantly altered in several cancers. Experimental validation performed on primary tumors confirmed these findings.

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“…Cytogenetic studies have been performed to evaluate genetic alterations associated with early GCs (1,2,4,5). Defining the genetic instability aids in the identification of the tumor-specific signatures involved in the initiation and progression of GCs, and thus aids in locating genomic biomarkers for the early detection of GC (5).…”

Section: Introductionmentioning

confidence: 99%

“…Defining the genetic instability aids in the identification of the tumor-specific signatures involved in the initiation and progression of GCs, and thus aids in locating genomic biomarkers for the early detection of GC (5). However, the molecular mechanism of GC development remains to be understood, and identification of the predictive markers in the early stage is crucial.…”

Section: Introductionmentioning

confidence: 99%

Chromosome 8q as the most frequent target for amplification in early gastric carcinoma

Kang¹

2014

Oncology Letters

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Early gastric carcinoma (GC) is considered to be a curable cancer, as it progresses to the advanced stage following varying durations. Understanding the early stage of GC may provide an insight into its pathogenesis and contribute to reducing the mortality rate of this disease. To investigate the genomic aberrations associated with 22 cases of early GC, high-density microarray comparative genomic hybridization was performed in the present study. The most notable finding was copy number gains (log2 ratio >0.25) on the long arm of chromosome 8, which occurred in 77.3% (17/22) of GC cases, and the delineated minimal common region was 8q22.1-q24.3. More specifically, two amplified (log2 ratio >1) loci in the 8q22.1-q24.3 region were detected in 18.2% (4/22) of GC cases. The first loci covered a region of 102.4–107.9 kb, mapping on 8q22.3-q23.1, and comprised the transcription factor CP2-like 3 gene. The second loci, spanning 128.7–145.7 kb on 8q24.21-q24.3, comprised the representative oncogene of myelocytomatosis. Furthermore, the following possible target genes that were not previously considered to play a pathogenic role in GC were identified: Plasmacytoma variant translocation 1, cysteine/histidine rich 1, kinesin family member C2, forkhead box H1, protein phosphatase 1 regulatory subunit 16A, glutamic-pyruvate transaminase, LOC113655 and RecQ protein-like 4. In the present study, previous findings showing that 8q mutations accumulate early during the multistage pathogenesis of GC were confirmed and expanded upon. The confirmation of previously reported 8q gains and the identification of novel target genes at 8q22.1-q24.3 amplified chromosomal sites should aid in improving our understanding of the molecular mechanisms underlying the tumorigenesis of early GC.

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A 4-gene panel as a marker at chromosome 8q in Asian gastric cancer patients

Cited by 27 publications

References 37 publications

Microarray-based identification of genes associated with cancer progression and prognosis in hepatocellular carcinoma

Microarray-based identification of genes associated with cancer progression and prognosis in hepatocellular carcinoma

Pan-Cancer Mutational and Transcriptional Analysis of the Integrator Complex

Chromosome 8q as the most frequent target for amplification in early gastric carcinoma

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