Decoding colorectal cancer epigenomics

Bairi, Khalid El; Tariq, Kanwal; Himri, Imane; Jaafari, Abdeslam; ., Wiam. Smaili; Kandhro, Abdul Hafeez; Gouri, Adel; Ghazi, Bouchra

doi:10.1016/j.cancergen.2017.11.001

Cited by 43 publications

(39 citation statements)

References 266 publications

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“…Increased methylation in classical tumor suppressor Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00384-020-03757-x) contains supplementary material, which is available to authorized users. genes, genes regulating mitosis, and DNA repair is considered an early event in CRC tumorigenesis [1,11]. Many individual markers have been investigated to date [11][12][13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

DNA methylation markers detected in blood, stool, urine, and tissue in colorectal cancer: a systematic review of paired samples

Laugsand

Brenne

Skorpen

2020

Int J Colorectal Dis

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Purpose Methylated cell-free DNA in liquid biopsies are promising non-invasive biomarkers for colorectal cancer (CRC). Optimal markers would have high sensitivity and specificity for early detection of CRC and could be detected in more than one type of material from the patient. We systematically reviewed the literature on DNA methylation markers of colorectal cancer, detected in more than one type of material, regarding their potential as contributors to a panel for screening and follow-up of CRC. Methods The databases MEDLINE, Web of Science, and Embase were systematically searched. Data extraction and review was performed by two authors independently. Agreement between methylation status in tissue and other materials (blood/stool/urine) was analyzed using the McNemar test and Cohen’s kappa. Results From the 51 included studies, we identified seven single markers with sensitivity ≥ 75% and specificity ≥ 90% for CRC. We also identified one promising plasma panel and two stool panels. The correspondence of methylation status was evaluated as very good for four markers, but only marginal for most of the other markers investigated (12 of 21). Conclusion The included studies reported only some of the variables and markers of interest and included few patients. Hence, a meta-analysis was not possible at this point. Larger, prospective studies must be designed to study the discordant detection of markers in tissue and liquid biopsies. When reporting their findings, such studies should use a standardized format.

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Section: Introductionmentioning

confidence: 99%

DNA methylation markers detected in blood, stool, urine, and tissue in colorectal cancer: a systematic review of paired samples

Laugsand

Brenne

Skorpen

2020

Int J Colorectal Dis

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“…[2][3][4][5][6][7] Large-scale genome sequencing has indicated that the human genome encodes approximately 20 000 protein-coding transcripts, which account for only around 2% of the genome, while more than 90% of the total genome is actively transcribed, but lack of protein-coding potential, referred to as ncRNAs. [2][3][4][5][6][7] Large-scale genome sequencing has indicated that the human genome encodes approximately 20 000 protein-coding transcripts, which account for only around 2% of the genome, while more than 90% of the total genome is actively transcribed, but lack of protein-coding potential, referred to as ncRNAs.…”

Section: Introductionmentioning

confidence: 99%

“…Increasing evidence has demonstrated that CRC is a heterogeneous disease, and its pathogenesis is involved with the activation of oncogenes and inactivation of tumour-suppressive genes, which are mostly resulting from genetic mutations and epigenetic alterations, the latter including DNA methylation, histone modification and noncoding RNAs (ncRNAs). [2][3][4][5][6][7] Large-scale genome sequencing has indicated that the human genome encodes approximately 20 000 protein-coding transcripts, which account for only around 2% of the genome, while more than 90% of the total genome is actively transcribed, but lack of protein-coding potential, referred to as ncRNAs. 8,9 For several decades, ncRNAs were considered as 'evolutionary junk'.…”

Section: Introductionmentioning

confidence: 99%

Small non‐coding RNA and colorectal cancer

Chen

Liu

2019

J Cellular Molecular Medi

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Colorectal cancer (CRC) is the third most common malignance. Although great efforts have been made to understand the pathogenesis of CRC, the underlying mechanisms are still unclear. It is now clear that more than 90% of the total genome is actively transcribed, but lack of protein‐coding potential. The massive amount of RNA can be classified as housekeeping RNAs (such as ribosomal RNAs, transfer RNAs) and regulatory RNAs (such as microRNAs [miRNAs], PIWI‐interacting RNA [piRNAs], tRNA‐derived stress‐induced RNA, tRNA‐derived small RNA [tRFs] and long non‐coding RNAs [lncRNAs]). Small non‐coding RNAs are a group of ncRNAs with the length no more than 200 nt and they have been found to exert important regulatory functions under many pathological conditions. In this review, we summarize the biogenesis and functions of regulatory sncRNAs, such as miRNAs, piRNA and tRFs, and highlight their involvements in cancers, particularly in CRC.

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“…The initial, and probably most important, among such modifications determines a constitutive activation of the βcatenin signaling pathway, resulting in an increased proliferation of CRC cells. Although mutations inactivating the APC oncosuppressor gene represent the main factor responsible for β-catenin activation, a growing body of evidence suggests that loss of cadherin expression, believed to occur as a consequence of epigenetic events, significantly contributes to the same effect, playing also an important role in the acquisition of an invasive phenotype [4,5]. In this regard, the assessment of E-cadherin involvement has led to controversial results in the past, indicating that, at best, the expression of this cadherin is lost in a limited number of CRCs.…”

Section: Introductionmentioning

confidence: 99%

Loss of expression of μ-protocadherin and protocadherin-24 in sporadic and hereditary nonpolyposis colorectal cancers

et al. 2019

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Colorectal cancer (CRC) is a neoplastic disease in which normal mucosa undergoes a process of malignant transformation due to the progressive accumulation of molecular alterations affecting protooncogenes and oncosuppressor genes. Some of these modifications exert their carcinogenic potential by promoting a constitutive activation of the β-catenin signaling proliferation pathway, and when present, loss of cadherin expression also significantly contributes to the same effect. Using a combined approach of molecular and immunohistochemical analysis, we have previously demonstrated that most sporadic CRCs exhibit a down-regulated expression of a cadherin, named μ-protocadherin, that is generally observed in association with a higher proliferation rate and a worse prognosis. The aim of this report was to perform a comparative immunohistochemical assessment of μ-protocadherin and a similar cadherin, named protocadherin-24, in sporadic CRC and hereditary nonpolyposis colorectal cancer. The data obtained put in evidence that double-negative CRCs, lacking both the analyzed protocadherins, are more represented among sporadic tumors, whereas double-positive CRCs, maintaining their expression, exhibit an opposite trend. As expected, loss of protocadherin expression was accompanied by nuclear localization of β-catenin and increased positivity of the Ki-67 proliferation marker. This finding is consistent with the different clinical evolution of the 2 considered CRC sets according to which patients with hereditary nonpolyposis colorectal cancer experience a better prognosis as compared with those affected by a sporadic CRC.

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Decoding colorectal cancer epigenomics

Cited by 43 publications

References 266 publications

DNA methylation markers detected in blood, stool, urine, and tissue in colorectal cancer: a systematic review of paired samples

DNA methylation markers detected in blood, stool, urine, and tissue in colorectal cancer: a systematic review of paired samples

Small non‐coding RNA and colorectal cancer

Loss of expression of μ-protocadherin and protocadherin-24 in sporadic and hereditary nonpolyposis colorectal cancers

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