The Crosstalk of PTGS2 and EGF Signaling Pathways in Colorectal Cancer

Wang, Dingzhi; Xia, Dianren; DuBois, Raymond N.

doi:10.3390/cancers3043894

Cited by 45 publications

(41 citation statements)

References 85 publications

(83 reference statements)

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“…47,48 The development and progression of colorectal neoplasia is attributable to the accumulation of genetic and epigenetic changes and the complex interaction of aberrations in various signaling pathways. 49–52 Each tumor has its own unique characteristics in terms of molecular phenotype, tumor microenvironment, and interactomes within and between neoplastic and host cells. 1,53 Therefore, tumor biomarker testing contributes to personalized medicine research and, ultimately, to clinical practice.…”

Section: Discussionmentioning

confidence: 99%

SMO Expression in Colorectal Cancer: Associations with Clinical, Pathological, and Molecular Features

Liao

Lochhead

et al. 2014

Ann Surg Oncol

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Section: Discussionmentioning

confidence: 99%

SMO Expression in Colorectal Cancer: Associations with Clinical, Pathological, and Molecular Features

Liao

Lochhead

et al. 2014

Ann Surg Oncol

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“…Inflammation appears to play a crucial role in carcinogenesis, 327–329 and has been linked to energetics, 330,331 and epigenetics. 332 Cellular epigenetic changes may be induced by inflammation and associated oxidative damage, 333–335 while cellular epigenetic aberrations may cause inflammatory diseases.…”

Section: Microbiota Inflammation Immunity and Epigeneticsmentioning

confidence: 99%

“…336 A study has demonstrated that the inflammatory mediator, prostaglandin E2, upregulates DNMT3B, resulting in promoter CpG island hypermethylation and promotion of intestinal tumorigenesis in mice. 335 Regular use of anti-inflammatory drugs such as aspirin, an inhibitor of PTGS2 (cyclooxygenase 2), has been associated with a decrease in cancer incidence and mortality, 57,329 Cancer-preventive effect of aspirin is apparent against PTGS2-positive colorectal cancer. 71,337,338 Moreover, aspirin appears to be very effective to treat PIK3CA -mutated colorectal cancer, suggesting PIK3CA mutation as a predictive tumor biomarker for clinical use.…”

Section: Microbiota Inflammation Immunity and Epigeneticsmentioning

confidence: 99%

Molecular pathological epidemiology of epigenetics: emerging integrative science to analyze environment, host, and disease

et al. 2013

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Epigenetics acts as an interface between environmental / exogenous factors, cellular responses and pathological processes. Aberrant epigenetic signatures are a hallmark of complex multifactorial diseases, including non-neoplastic disorders (e.g., cardiovascular diseases, hypertension, diabetes mellitus, autoimmune diseases, and some infectious diseases) and neoplasms (e.g., leukemias, lymphomas, sarcomas, and breast, lung, prostate, liver and colorectal cancers). Epigenetic signatures (DNA methylation, mRNA and microRNA expression, etc.) may serve as biomarkers for risk stratification, early detection, and disease classification, as well as targets for therapy and chemoprevention. DNA methylation assays are widely applied to formalin-fixed paraffin-embedded archival tissue specimens as clinical pathology tests. To better understand the interplay between etiologic factors, cellular molecular characteristics, and disease evolution, the field of “Molecular Pathological Epidemiology (MPE)” has emerged as an interdisciplinary integration of “molecular pathology” and “epidemiology”, with a similar conceptual framework to systems biology and network medicine. In contrast to traditional epidemiologic research including genome-wide association studies (GWAS), MPE is founded on the unique disease principle; that is, each disease process results from unique profiles of exposomes, epigenomes, transcriptomes, proteomes, metabolomes, microbiomes, and interactomes in relation to the macro-environment and tissue microenvironment. The widespread application of epigenomics (e.g., methylome) analyses will enhance our understanding of disease heterogeneity, epigenotypes (CpG island methylator phenotype, LINE-1 hypomethylation, etc.), and host-disease interactions. MPE may represent a logical evolution of GWAS, termed “GWAS-MPE approach”. Though epigenome-wide association study attracts increasing attention, currently, it has a fundamental problem in that each cell within one individual has a unique, time-varying epigenome. This article will illustrate increasing contribution of modern pathology to broader public health sciences, which attests pivotal roles of pathologists in the new integrated MPE science towards our ultimate goal of personalized medicine and prevention.

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“…3 Aspirin is an inhibitor of prostaglandin-endoperoxide synthase 2 (PTGS2; cyclooxygenase-2), a key mediator of inflammatory responses. 4 We have previously shown that aspirin use is associated with a lower risk of colorectal cancer with PTGS2 overexpression. 5 However, since colorectal cancer represents a complex disease that cannot be explained by a single biomarker, 6 the association of aspirin with various tumorigenic processes requires further investigation, which may help us develop effective preventive strategies.…”

Section: Introductionmentioning

confidence: 95%