@article{
 title = {Human microbiome signatures of differential colorectal cancer drug metabolism},
 type = {article},
 year = {2017},
 identifiers = {[object Object]},
 id = {2fc649c3-e16b-3630-adbb-83c921f13699},
 created = {2018-06-12T19:15:15.945Z},
 file_attached = {true},
 profile_id = {4dd55f2f-c613-3fe1-a600-5819fb65fcff},
 group_id = {e0d9c14f-8342-389b-84fc-a19963b606ff},
 last_modified = {2018-06-12T19:15:16.209Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {false},
 hidden = {false},
 folder_uuids = {9ecde1f2-fbc7-413d-b8a2-7f450155961e},
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 abstract = {It is well appreciated that microbial metabolism of drugs can influence treatment efficacy. Microbial β-glucuronidases in the gut can reactivate the excreted, inactive metabolite of irinotecan, a first-line chemotherapeutic for metastatic colorectal cancer. Reactivation causes adverse drug responses, including severe diarrhea. However, a direct connection between irinotecan metabolism and the composition of an individual's gut microbiota has not previously been made. Here, we report quantitative evidence of inter-individual variability in microbiome metabolism of the inactive metabolite of irinotecan to its active form. We identify a high turnover microbiota metabotype with potentially elevated risk for irinotecan-dependent adverse drug responses. We link the high turnover metabotype to unreported microbial β-glucuronidases; inhibiting these enzymes may decrease irinotecan-dependent adverse drug responses in targeted subsets of patients. In total, this study reveals metagenomic mining of the microbiome, combined with metabolomics, as a non-invasive approach to develop biomarkers for colorectal cancer treatment outcomes.},
 bibtype = {article},
 author = {Guthrie, Leah and Gupta, Sanchit and Daily, Johanna and Kelly, Libusha},
 journal = {npj Biofilms and Microbiomes}
}

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