{
  "abstract": "Bidirectional interactions between gut microbiota and therapeutic drugs affecting efficacy or safety have garnered attention in oncology over the last decade.1–3 In particular, the intestinal toxicity of irinotecan has historically been attributed to the gut bacterial β-glucuronidases (BGUS), but this knowledge failed to be translated into efficient interceptive measures. In Gut, Hou et al4 unveiled a new mechanism of bacterial toxicity independent of the SN-38 active metabolite of irinotecan. By producing indole-3-acetate (I3A), Bacteroides intestinalis affects the PI3K/Akt-dependent proliferation of intestinal stem cells, exacerbating SN-38-mediated epithelial injury (figure 1).",
  "authors": [
    {
      "affiliations": [
        "INSERM U1015, Institut Gustave-Roussy, Villejuif, Île-de-France, France",
        "ClinicObiome, Institut Gustave-Roussy, Villejuif, Île-de-France, France"
      ],
      "name": "Marine Fidelle"
    },
    {
      "affiliations": [
        "INSERM U1015, Institut Gustave-Roussy, Villejuif, Île-de-France, France",
        "ClinicObiome, Institut Gustave-Roussy, Villejuif, Île-de-France, France",
        "Oncoimmunology, Université Paris-Saclay Faculté de Médecine, Le Kremlin-Bicêtre, Île-de-France, France"
      ],
      "name": "Laurence Zitvogel"
    }
  ],
  "title": "Tryptophan metabolite indole-3-acetate: a new culprit in irinotecan-induced gut epithelial injury",
  "uid": "fe4d009f-2f5b-5508-afc6-19404cf6a92a"
}