{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T11:43:30Z","timestamp":1791287010757,"version":"4.1.0"},"reference-count":29,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2020,8,22]],"date-time":"2020-08-22T00:00:00Z","timestamp":1598054400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000066","name":"National Institute of Environmental Health Sciences","doi-asserted-by":"publisher","award":["R44 ES028163"],"award-info":[{"award-number":["R44 ES028163"]}],"id":[{"id":"10.13039\/100000066","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environ and Mol Mutagen"],"published-print":{"date-parts":[[2020,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The etiology of distal site cancers in inflammatory bowel disease (IBD) is not well understood and requires further study. We investigated whether pediatric IBD patients' blood cells exhibit elevated levels of genomic damage by measuring the frequency of mutant phenotype (CD59\u2010\/CD55\u2010) reticulocytes (MUT RET) as a reporter of <jats:italic>PIG\u2010A<\/jats:italic> mutation, and the frequency of micronucleated reticulocytes (MN\u2010RET) as an indicator of chromosomal damage. IBD patients (<jats:italic>n<\/jats:italic> =\u200918 new\u2010onset disease, 46 established disease) were compared to age\u2010matched controls (constipation or irritable bowel syndrome patients from the same clinic, <jats:italic>n<\/jats:italic> =\u200930) and young healthy adults age 19\u201324 (<jats:italic>n<\/jats:italic> =\u200925). IBD patients showed no indication of elevated MUT RET relative to controls (mean\u2009\u00b1\u2009SD = 3.1\u2009\u00b1\u20092.3\u2009\u00d7\u200910<jats:sup>\u22126<\/jats:sup> vs. 3.6 \u00b1\u20095.6 x 10<jats:sup>\u22126<\/jats:sup>, respectively). In contrast, 59 IBD patients where %MN\u2010RET measurements were obtained, 10 exceeded the upper bound 90% tolerance interval derived from control subjects (i.e., 0.42%). Furthermore, each of the 10 IBD patients with elevated MN\u2010RET had established disease (10\/42), none were new\u2010onset (0\/17) (<jats:italic>p<\/jats:italic> =\u2009.049). Interestingly, each of the subjects with increased chromosomal damage was receiving anti\u2010TNF based monotherapy at the time blood was collected (10\/10, 100%), whereas this therapy was less common (20\/32, 63%) among patients that exhibited \u22640.42% MN\u2010RET (<jats:italic>p<\/jats:italic> =\u2009.040). The results clearly indicate the need for further work to understand whether the results presented herein are reproducible and if so, to elucidate the causative factor(s) responsible for elevated MN\u2010RET frequencies in some IBD patients.<\/jats:p>","DOI":"10.1002\/em.22403","type":"journal-article","created":{"date-parts":[[2020,8,6]],"date-time":"2020-08-06T04:55:52Z","timestamp":1596689752000},"page":"901-909","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Assessment of systemic genetic damage in pediatric inflammatory bowel disease"],"prefix":"10.1002","volume":"61","author":[{"given":"Ayesha","family":"Baig","sequence":"first","affiliation":[{"name":"Department of Pediatrics University of Rochester Medical Center  Rochester New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Svetlana L.","family":"Avlasevich","sequence":"additional","affiliation":[{"name":"Litron Laboratories  Rochester New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dorothea K.","family":"Torous","sequence":"additional","affiliation":[{"name":"Litron Laboratories  Rochester New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey C.","family":"Bemis","sequence":"additional","affiliation":[{"name":"Litron Laboratories  Rochester New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lawrence J.","family":"Saubermann","sequence":"additional","affiliation":[{"name":"Department of Pediatrics University of Rochester Medical Center  Rochester New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David P.","family":"Lovell","sequence":"additional","affiliation":[{"name":"St. George's University of London  London Borough of Wandsworth UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James T.","family":"MacGregor","sequence":"additional","affiliation":[{"name":"Toxicology Consulting Services  Bonita Springs Florida USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen D.","family":"Dertinger","sequence":"additional","affiliation":[{"name":"Litron Laboratories  Rochester New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2020,8,22]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra0804647"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1093\/ecco-jcc\/jjv141"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.3748\/wjg.v22.i20.4794"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1002\/ibd.21349"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1002\/em.22348"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1002\/ibd.22957"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S1383-5718(99)00183-7"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1093\/toxsci\/kfs258"},{"key":"e_1_2_8_10_1","doi-asserted-by":"publisher","DOI":"10.1002\/em.21924"},{"key":"e_1_2_8_11_1","doi-asserted-by":"publisher","DOI":"10.1136\/gut.48.4.526"},{"key":"e_1_2_8_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2011.02.013"},{"key":"e_1_2_8_13_1","doi-asserted-by":"publisher","DOI":"10.5694\/j.1326-5377.1978.tb131771.x"},{"key":"e_1_2_8_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.cgh.2012.01.010"},{"key":"e_1_2_8_15_1","doi-asserted-by":"publisher","DOI":"10.1002\/ibd.20211"},{"key":"e_1_2_8_16_1","doi-asserted-by":"publisher","DOI":"10.1053\/j.gastro.2013.07.035"},{"key":"e_1_2_8_17_1","doi-asserted-by":"publisher","DOI":"10.2147\/PHMT.S64943"},{"key":"e_1_2_8_18_1","doi-asserted-by":"publisher","DOI":"10.1001\/jama.2017.16071"},{"key":"e_1_2_8_19_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0016-5085(99)70173-3"},{"key":"e_1_2_8_20_1","doi-asserted-by":"publisher","DOI":"10.1093\/aje\/kws375"},{"key":"e_1_2_8_21_1","doi-asserted-by":"publisher","DOI":"10.1038\/ajg.2009.760"},{"issue":"10","key":"e_1_2_8_22_1","first-page":"2403","article-title":"Oxidative stress and DNA damage: Implications in inflammatory bowel disease","volume":"21","author":"Pereira C.","year":"2015","journal-title":"Inflammatory Bowel Diseases"},{"key":"e_1_2_8_23_1","unstructured":"Remicade\u00ae U.S. Food and Drug Administration approved label. 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