Background And Aim: "Inflammatory bowel disease" (IBD) is a chronic, relapsing inflammatory disease of the intestinal tract that typically begins at a young age and might transit to colorectal cancer (CRC). In this manuscript, we discussed the epigenetic and metabolic change to present a extensive view of IBDs transition to CRC. This study discusses the possible biomarkers for evaluating the condition of IBDs patients, especially before the transition to CRC.
Research Approach: We searched "PubMed" and "Google Scholar" using the keywords from 2000 to 2022.
Discussion: In this manuscript, interesting titles associated with IBD and CRC are discussed to present a broad view regarding the epigenetic and metabolic reprogramming and the biomarkers.
Conclusion: Epigenetics can be the main reason in IBD transition to CRC, and Hypermethylation of several genes, such as VIM, OSM4, SEPT9, GATA4 and GATA5, NDRG4, BMP3, ITGA4 and plus hypomethylation of LINE1 can be used in IBD and CRC management. Epigenetic, metabolisms and microbiome-derived biomarkers, such as Linoleic acid and 12 hydroxy 8,10-octadecadienoic acid, Serum M2-pyruvate kinase and Six metabolic genes (NAT2, XDH, GPX3, AKR1C4, SPHK and ADCY5) expression are valuable biomarkers for early detection and transition to CRC condition. Some miRs, such as miR-31, miR-139-5p, miR -155, miR-17, miR-223, miR-370-3p, miR-31, miR -106a, miR -135b and miR-320 can be used as biomarkers to estimate IBD transition to CRC condition.
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http://dx.doi.org/10.1186/s12935-023-03117-z | DOI Listing |
Background: Healthcare is a major contributor to global greenhouse gas emissions. Colorectal cancer (CRC) screening is one of the most widely used healthcare services in the US, indicated for approximately 134 million adults. Recommended screening options include fecal immunochemical tests (FITs) every year, CT colonographies (CTCs) every 5 years, or colonoscopies every 10 years.
View Article and Find Full Text PDFAntibiotics (Basel)
January 2025
Department of Laboratory Medicine and Biotechnology, Tzu Chi University, Hualien 970374, Taiwan.
Background: Increasing evidence shows that () largely affects colorectal cancer (CRC) growth and progression; therefore, the inhibition of intratumoral may be one realistic approach to combat CRC. Although antibiotics are helpful in eliminating bacteria, the major problem remains the rise of potential antibiotic-resistant strains and antibiotic-associated adverse effects. Currently, bacteriophage therapy has gained interest because of its high selectivity to bacterial hosts and may become a realistic approach in treating bacteria-associated cancers.
View Article and Find Full Text PDFCancers (Basel)
January 2025
Innovative Oncology Research and Regenerative Medicine, Osaka International Cancer Institute, Osaka 541-8567, Japan.
Liquid biopsy methods have gained prominence as minimally invasive tools to improve cancer treatment outcomes. Circulating tumor cells (CTCs) offer valuable insights into both primary and metastatic lesions. However, validating the CTC test results requires confirmation that the detected cells originate from cancer tissue.
View Article and Find Full Text PDFCancers (Basel)
January 2025
Department of Human Genetics, National Institute of Health Dr. Ricardo Jorge, 1649-016 Lisbon, Portugal.
The risk of developing colorectal cancer (CRC) is increased in ulcerative colitis patients compared to the general population. This increased risk results from the state of chronic inflammation, a well-known tumour-promoting condition. This review explores the pathologic and molecular characteristics of colitis-associated colon cancer (CAC), emphasizing the distinct features from sporadic CRC.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Cell Res
January 2025
Department of Pathology, Affiliated Hospital of Qingdao University, Qingdao, China. Electronic address:
Among patients with colorectal cancer (CRC), metastasis accounts for the majority of deaths, and epithelial-mesenchymal transition (EMT) is important in the metastatic process. However, the mechanism underlying the correlation between the two in CRC is unknown. Here, we verified that a receptor-independent protein, G-protein signaling modulator 1 (GPSM1), was increased in CRC and had a significant positive correlation with matrix metalloproteinase 19 (MMP19).
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