Screening for colorectal cancer

Choi, Youngjee; Sateia, Heather F.; Peairs, Kimberly S.; Stewart, Rosalyn W.

doi:10.1053/j.seminoncol.2017.02.002

Cited by 38 publications

(35 citation statements)

References 88 publications

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“…1 Risk factors for colorectal cancer can be divided into two aspects: Non-modifiable risk factors and Modifiable risk factors. 2 Main non-modifiable risk factors are age, sex, ethnicity, family history, hereditary syndrome, prior adenomatous or sessile serrated polyp, inflammatory bowel disease, diabetes mellitus and BRCA mutations. 2,3 Unhealthy lifestyles, including consuming red and processed meat, obesity, smoking and alcohol consumption, are main modifiable risk factors.…”

Section: Introductionmentioning

confidence: 99%

“…2 Main non-modifiable risk factors are age, sex, ethnicity, family history, hereditary syndrome, prior adenomatous or sessile serrated polyp, inflammatory bowel disease, diabetes mellitus and BRCA mutations. 2,3 Unhealthy lifestyles, including consuming red and processed meat, obesity, smoking and alcohol consumption, are main modifiable risk factors. 2,4 The stage of the patient at the time of diagnosis is one of the most important factors affecting the prognosis of patients with colorectal cancer.…”

Section: Introductionmentioning

confidence: 99%

“…2,3 Unhealthy lifestyles, including consuming red and processed meat, obesity, smoking and alcohol consumption, are main modifiable risk factors. 2,4 The stage of the patient at the time of diagnosis is one of the most important factors affecting the prognosis of patients with colorectal cancer. In the United States, localized stage CRC is diagnosed in 39% of patients, for which the 5-year survival rate is 90%.…”

Section: Introductionmentioning

confidence: 99%

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<p>Potential Prognostic and Diagnostic Values of CDC6, CDC45, ORC6 and SNHG7 in Colorectal Cancer</p>

Hu¹,

Wang²,

Li³

et al. 2019

OTT

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Background: Colorectal cancer (CRC) is a common human malignancy. The aims of this study are to investigate the gene expression profile of CRC and to explore potential strategy for CRC diagnosis, therapy and prognosis. Methods: We use affy and Limma package of Bioconductor R to do differential expression genes (DEGs) and differential expression lncRNAs (DELs) analysis from the gene datasets (GSE8671, GSE21510, GSE32323, GSE39582 and TCGA) respectively. Then, DEGs were analyzed by GO and KEGG pathway and Kaplan-Meier survival curve and Cox regression analyses were used to find aberrantly expressed genes associated with survival outcome of CRC patients. Real-time PCR assay was used to verify the aberrantly expressed genes expression in CRC samples. Results: 306 up-regulation and 213 down-regulation common DEGs were found. A total of 485 DELs were identified, of which 241 up-regulated and 244 down-regulated. Then, GO and KEGG pathway analyses showed that DEGs were involved in cell cycle, mineral absorption, DNA replication, and Nitrogen metabolism. Among them, Kaplan-Meier survival curve and Cox regression analyses revealed that CDC6, CDC45, ORC6 and SNHG7 levels were significantly associated with survival outcome of CRC patients. Finally, real-time PCR assay was used to verify that the CDC6, CDC45, ORC6 and SNHG7 expression were upregulated in 198 CRC samples compared with the expression levels in individual-matched adjacent mucosa samples. Conclusion: CDC6, CDC45, ORC6 and SNHG7 are implicated in CRC initiation and progression and could be explored as potential diagnosis, therapy and prognosis targets for CRC.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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<p>Potential Prognostic and Diagnostic Values of CDC6, CDC45, ORC6 and SNHG7 in Colorectal Cancer</p>

Hu¹,

Wang²,

Li³

et al. 2019

OTT

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“…Colon cancer affects human health. Due to the late stage of diagnosis and poor efficacy of treatment, the incidence and mortality rates are 8-9% (2). The 5-year survival rate of early-stage colon cancer exceeds 70-90%, although the survival rate of advanced colon cancer is unsatisfactory.…”

Section: Introductionmentioning

confidence: 99%

Genistein inhibits invasion and migration of colon cancer cells by recovering WIF1 expression

2018

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Colon cancer is characterized by invasion and migration. DNA methylation of CpG islands in tumor suppressor genes is considered to be an epigenetic mechanism underlying cancer development. Epigenetic silencing of a gene may be reversed by drugs, including genistein. The present study aimed to determine the effect of genistein on Wnt inhibitory factor 1 (WIF1) and invasion, and migration of colon cancer cells. The viability of HT29 colon cancer cells was suppressed by genistein in a dose dependent manner. Following 72 h of treatment with 10, 20 and 60 µmol/l genistein, increased demethylation of WIF1 was induced in a dose‑dependent manner. Additionally, the invasive/migratory abilities of cells treated with genistein decreased in a dose‑dependent manner. Reverse transcription‑quantitative polymerase chain reaction and western blot analyses were performed to identify the mRNA and protein expression levels of invasion/migration‑associated factors. Following treatment with genistein, matrix metalloproteinase (MMP) 2 and MMP9 expression levels decreased, whereas the expression of metalloproteinase inhibitor 1 and E‑cadherin increased significantly. In addition, the expression levels of proto‑oncogene Wnt‑1 (Wnt‑1)/β‑catenin pathway‑associated factors, β‑catenin, c‑Myc proto‑oncogene protein and cyclin D1 decreased in a dose‑dependent manner following treatment with genistein. The invasive/migratory abilities of cells transfected with WIF1‑small interfering (si) RNA, and those transfected with WIF1‑siRNA and treated with genistein, increased notably compared with the control group. The present study demonstrated that genistein was able to inhibit the cell invasion and migration of colon cancer cells by inducing demethylation, and recovering the activity of WIF1 by altering the expression of invasion‑associated factors, and components of the Wnt signaling pathway.

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“…Colorectal cancer (CRC), the world's fourth leading cause of cancer-associated mortality, is the third most common type of malignancy in females and the third most common type in males (1)(2)(3). At present, >1 million patients suffer from CRC, and >600,000/year succumb to it worldwide.…”

Section: Introductionmentioning

confidence: 99%

Delineating the underlying molecular mechanisms and key genes involved in metastasis of colorectal cancer via bioinformatics analysis

Chen

Zhou

et al. 2018

Oncol Rep

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Colorectal cancer (CRC) is considered the world's fourth most deadly cancer. Its metastasis is associated with poor prognosis and weakens the effects of treatment. However, the potential molecular mechanisms and key genes involved in CRC metastasis have remained to be comprehensively elucidated. The objective of the present study was to identify the key genes and molecular pathways underlying CRC metastasis. Differentially expressed genes (DEGs) between primary CRC tissues and metastatic CRC were identified by analyzing the GSE2509 dataset from the Gene Expression Omnibus database. Subsequently, the DEGs were subjected to Gene Ontology (GO) term and Kyoto Encyclopedia of Genes and Genome (KEGG) pathway enrichment analyses via the Database for Annotation, Visualization and Integrated Discovery (DAVID). Next, the top ten hub genes were identified in a protein-protein interaction (PPI) network. Sub-network and pathway enrichment analysis were respectively performed with the plugin MCODE and DAVID. Finally, reverse transcription-quantitative polymerase chain reaction assays were performed to corroborate the expression levels of the top five potential metastasis-associated genes in the clinical samples of CRC patients. A total of 7,384 DEGs were obtained, among which 3,949 were upregulated and 3,435 were downregulated. GO and KEGG enrichment analyses identified numerous possible biological processes and pathways that may have a role in the metastasis of CRC. The leading ten hub genes, recognized from the PPI, were epidermal growth factor receptor (EGFR), Has proto-oncogene GTPase (HRas), Wnt family member 5A (Wnt5a), serine/threonine kinase 1 (Akt1), cyclin-dependent kinase inhibitor 1A (CDKN1a), early growth response 1, Ras homolog family member A, cyclin D1 and Ras-related C3 botulinum toxin substrate 1. Sub-network analysis disclosed the most prominent three modules. Ultimately, EGFR, HRas and Akt1 were verified to be upregulated DEGs, while Wnt5a and CDKN1a were downregulated DEGs when compared with the primary controls. In conclusion, the present study revealed several key genes and relevant molecular mechanisms that may enhance the current understanding of CRC metastasis, making them significant potential foci for the discovery of further CRC treatments.

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Screening for colorectal cancer

Cited by 38 publications

References 88 publications

<p>Potential Prognostic and Diagnostic Values of CDC6, CDC45, ORC6 and SNHG7 in Colorectal Cancer</p>

<p>Potential Prognostic and Diagnostic Values of CDC6, CDC45, ORC6 and SNHG7 in Colorectal Cancer</p>

Genistein inhibits invasion and migration of colon cancer cells by recovering WIF1 expression

Delineating the underlying molecular mechanisms and key genes involved in metastasis of colorectal cancer via bioinformatics analysis

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