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Unveiling the genetic and epigenetic landscape of colorectal cancer: new insights into pathogenic pathways | Medical Oncology
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Colorectal cancer (CRC) is a complex disease characterized by genetic and epigenetic alterations, playing a crucial role in its development and progression. This review aims to provide insights into the emerging landscape of these alterations in CRC pathogenesis to develop effective diagnostic tools and targeted therapies. Genetic alterations in signaling pathways such as Wnt/β-catenin, and PI3K/Akt/mTOR are pivotal in CRC development. Genetic profiling has identified distinct molecular subtypes, enabling personalized treatment strategies. Epigenetic modifications, including DNA methylation and histone modifications, also contribute to CRC pathogenesis by influencing critical cellular processes through gene silencing or activation. Non-coding RNAs have emerged as essential players in epigenetic regulation and CRC progression. Recent research highlights the interplay between genetic and epigenetic alterations in CRC. Genetic mutations can affect epigenetic modifications, leading to dysregulated gene expression and signaling cascades. Conversely, epigenetic changes can modulate genetic expression, amplifying or dampening the effects of genetic alterations. Advancements in understanding pathogenic pathways have potential clinical applications. Identifying genetic and epigenetic markers as diagnostic and prognostic biomarkers promises more accurate risk assessment and early detection. Challenges remain, including validating biomarkers and developing robust therapeutic strategies through extensive research and clinical trials. The dynamic nature of genetic and epigenetic alterations necessitates a comprehensive understanding of their temporal and spatial patterns during CRC progression. In conclusion, the genetic and epigenetic landscape of CRC is increasingly being unraveled, providing valuable insights into its pathogenesis. Integrating genetic and epigenetic knowledge holds great potential for improving diagnostics, prognostics, and personalized therapies in CRC. Continued research efforts are vital to translate these findings into clinical practice, ultimately improving patient outcomes.
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Keywords {🔍}
pubmed, cancer, article, google, scholar, cas, central, colorectal, epigenetic, wang, mol, zhang, genetic, cell, signaling, therapy, therapeutic, cancers, mechanisms, dna, tumor, yang, httpsdoiorgs, review, alterations, molecular, sci, pathway, chen, pathways, biomarkers, liu, oncol, res, rev, int, targeting, potential, clinical, role, clin, progression, noncoding, colon, med, ther, methylation, regulation, epigenetics, target,
Topics {✒️}
mapk–ras–raf signaling pathway wnt/β-catenin signaling pathway pi3k/akt/mtor signaling pathway targeting wnt1/β-catenin pathway wnt/β-catenin pathway raf-mek-erk pathway pi3k/akt/mtor pathway pi3k-akt-mtor pathway month download article/chapter wnt/β-catenin signaling ras/mapk signaling pathway pi3k/akt/mtor pathways nf-κb signaling pathway mek/erk network wnt/β-catenin swi/snf complex offer pi3k/akt/mtor dna methylation-based diagnostic targeting aurka-cdc25c axis gastroenterol rev/przegląd gastroenterologiczny immune checkpoints pd-l1 noncoding rna-mediated mechanisms rna-binding proteins involved hippo–yap1 signaling pathways full article pdf immune‐related adverse events hippo signaling pathway braf-mutated colorectal cancer familial adenomatous polyposis npj precision oncology bmc med educ canonical wnt signaling dual proto-oncogene garcía-rodríguez jl receptor tyrosine kinases tgf-β signaling regulated cell death wnt pathway egfr-based targeted therapy privacy choices/manage cookies providing continuous support early-onset colorectal cancer related subjects tgf-β inhibitors check access instant access β-catenin noncoding cancer genome drug discovery today holds exclusive rights
Questions {❓}
- Crosstalk between PI3K/AKT/mTOR and WNT/β-Catenin signaling in GBM - Could combination therapy checkmate the collusion?
- Growth factors, PI3K/AKT/mTOR and MAPK Signaling pathways in colorectal cancer pathogenesis: where are we now?
- PI3K/Akt/mTOR pathway and its role in cancer therapeutics: are we making headway?
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headline:Unveiling the genetic and epigenetic landscape of colorectal cancer: new insights into pathogenic pathways
description:Colorectal cancer (CRC) is a complex disease characterized by genetic and epigenetic alterations, playing a crucial role in its development and progression. This review aims to provide insights into the emerging landscape of these alterations in CRC pathogenesis to develop effective diagnostic tools and targeted therapies. Genetic alterations in signaling pathways such as Wnt/β-catenin, and PI3K/Akt/mTOR are pivotal in CRC development. Genetic profiling has identified distinct molecular subtypes, enabling personalized treatment strategies. Epigenetic modifications, including DNA methylation and histone modifications, also contribute to CRC pathogenesis by influencing critical cellular processes through gene silencing or activation. Non-coding RNAs have emerged as essential players in epigenetic regulation and CRC progression. Recent research highlights the interplay between genetic and epigenetic alterations in CRC. Genetic mutations can affect epigenetic modifications, leading to dysregulated gene expression and signaling cascades. Conversely, epigenetic changes can modulate genetic expression, amplifying or dampening the effects of genetic alterations. Advancements in understanding pathogenic pathways have potential clinical applications. Identifying genetic and epigenetic markers as diagnostic and prognostic biomarkers promises more accurate risk assessment and early detection. Challenges remain, including validating biomarkers and developing robust therapeutic strategies through extensive research and clinical trials. The dynamic nature of genetic and epigenetic alterations necessitates a comprehensive understanding of their temporal and spatial patterns during CRC progression. In conclusion, the genetic and epigenetic landscape of CRC is increasingly being unraveled, providing valuable insights into its pathogenesis. Integrating genetic and epigenetic knowledge holds great potential for improving diagnostics, prognostics, and personalized therapies in CRC. Continued research efforts are vital to translate these findings into clinical practice, ultimately improving patient outcomes.
datePublished:2023-10-19T00:00:00Z
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Genetic alterations
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β-catenin pathway
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Akt
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Hematology
Pathology
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description:Colorectal cancer (CRC) is a complex disease characterized by genetic and epigenetic alterations, playing a crucial role in its development and progression. This review aims to provide insights into the emerging landscape of these alterations in CRC pathogenesis to develop effective diagnostic tools and targeted therapies. Genetic alterations in signaling pathways such as Wnt/β-catenin, and PI3K/Akt/mTOR are pivotal in CRC development. Genetic profiling has identified distinct molecular subtypes, enabling personalized treatment strategies. Epigenetic modifications, including DNA methylation and histone modifications, also contribute to CRC pathogenesis by influencing critical cellular processes through gene silencing or activation. Non-coding RNAs have emerged as essential players in epigenetic regulation and CRC progression. Recent research highlights the interplay between genetic and epigenetic alterations in CRC. Genetic mutations can affect epigenetic modifications, leading to dysregulated gene expression and signaling cascades. Conversely, epigenetic changes can modulate genetic expression, amplifying or dampening the effects of genetic alterations. Advancements in understanding pathogenic pathways have potential clinical applications. Identifying genetic and epigenetic markers as diagnostic and prognostic biomarkers promises more accurate risk assessment and early detection. Challenges remain, including validating biomarkers and developing robust therapeutic strategies through extensive research and clinical trials. The dynamic nature of genetic and epigenetic alterations necessitates a comprehensive understanding of their temporal and spatial patterns during CRC progression. In conclusion, the genetic and epigenetic landscape of CRC is increasingly being unraveled, providing valuable insights into its pathogenesis. Integrating genetic and epigenetic knowledge holds great potential for improving diagnostics, prognostics, and personalized therapies in CRC. Continued research efforts are vital to translate these findings into clinical practice, ultimately improving patient outcomes.
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Genetic alterations
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β-catenin pathway
PI3K
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mTOR pathway
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Precision medicine
Oncology
Hematology
Pathology
Internal Medicine
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