{
  "abstract": "Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide.1 While genetic mutations have long been recognised as key drivers of CRC development, the substantial role of environmental factors, particularly the gut microbiome, in shaping cancer phenotypes has emerged as a critical area of investigation. In recent years, mounting evidence has linked gut microbial dysbiosis to CRC by modulating the mucosa through the reprogramming of host gene expression, promoting inflammatory pathways and contributing to barrier dysfunction.2 The interplay between microbiome, host immunity and epigenetic regulation is now recognised as a central axis in host gene reprogramming and predisposition to CRC.3 However, the molecular mechanisms underlying these interactions remain incompletely understood.",
  "authors": [
    {
      "affiliations": [
        "Gastroenterology Research Center (GRC), Department of Internal Medicine, The University of Texas Health Science Center at Houston, Houston, Texas, USA"
      ],
      "name": "Xiangsheng Huang"
    },
    {
      "affiliations": [
        "Gastroenterology Research Center (GRC), Department of Internal Medicine, The University of Texas Health Science Center at Houston, Houston, Texas, USA",
        "MD Anderson Cancer Center-UTHealth Houston Graduate School of Biomedical Sciences, Houston, Texas, USA"
      ],
      "name": "Faraz Bishehsari"
    }
  ],
  "title": "Microbial imprints on colorectal cancer: the epigenetic silencing of PHLPP1 as a prognostic nexus",
  "uid": "507b318b-8f4e-5ac0-a3f1-8e369824fbe1"
}