Dysplasia in inflammatory bowel disease: Standardized classification with provisional clinical applications

Riddell, Robert H.; Goldman, Harvey; Ransohoff, David F.; Appelman, Henry D.; Fenoglio, Cecilia M.; Haggitt, Rodger C.; hren, Christer; Correa, Pelayo; Hamilton, Stanley R.; Morson, B. C.; Sommers, Sheldon C.; Yardley, John H.

doi:10.1016/s0046-8177(83)80175-0

Cited by 1,718 publications

(1,010 citation statements)

References 37 publications

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“…Dysplasia was evaluated according to the previously published criteria 14 ( Figure 1). For difficult cases, three gastrointestinal pathologists (XL, RP, and S-YX) reviewed the slides independently and a consensus diagnosis (agreed by at least two pathologists) was used.…”

Section: Histopathological Evaluationmentioning

confidence: 99%

“…Further, the epithelial cells in each non-dysplastic focus (normal, diseased mucosa but negative for dysplasia, and diseased mucosa indefinite for dysplasia) were evaluated for the presence of reactive changes using a semi-quantitative scale as follows: none (no reactive change), mild (slight loss of surface mucin, slightly increased nuclear to cytoplasmic (N/C) ratio, and mild nuclear disarray), moderate (more pronounced loss of mucin with regenerative changes in the lower half of the crypts), and severe (pronounced loss of mucin with regenerative changes involving the entire length of the crypts). 14 In our analysis, the absent and mild reactive change groups were combined as low reactive change group; the moderate and marked reactive change groups were combined as high reactive change group. Representative degrees of inflammation and reactive changes are shown in Figures 2 and 3, respectively.…”

Section: Histopathological Evaluationmentioning

confidence: 99%

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Diagnostic utility of TP53 and cytokeratin 7 immunohistochemistry in idiopathic inflammatory bowel disease-associated neoplasia

et al. 2014

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Long-standing inflammatory bowel disease is associated with increased risk of developing colorectal adenocarcinoma. Significant intra-and inter-observers' variability exists in histologic interpretation of dysplasia in surveillance biopsies. In this study, we evaluated the utility of a panel of immunohistochemical markers in diagnosing inflammatory bowel disease-associated neoplasia. We reviewed 39 colectomy specimens with inflammatory bowel disease-associated neoplasia. In these 39 cases, we identified 172 foci of interest (5 normal, 58 negative for dysplasia, 15 indefinite for dysplasia, 59 low-grade dysplasia, 18 highgrade dysplasia, and 17 invasive adenocarcinoma). They were subjected to immunohistochemistry for TP53 and CK7. Logistic regression was used to evaluate their association with the presence of dysplasia. Receiver operating characteristic curves were used to determine the optimal cutoffs and assess the diagnostic performance of TP53 and CK7. Both TP53 nuclear staining and CK7 immunoreactivity gradually increased in the progression of inflammatory bowel disease-associated neoplasia (Po0.0001). CK7 immunoreactivity increased along with the increase of inflammation severity (P ¼ 0.0002) as well as reactive changes (P ¼ 0.04) in the colonic mucosa. But TP53 nuclear staining was independent of either feature. When both TP5348% and CK7430% as identified from logistic regression and receiver operating characteristic curves were used to diagnose dysplasia, the specificity achieved as high as 95%. When either TP5348% or CK7430% was used to diagnose dysplasia, the sensitivity achieved was 82%. Our results suggested that a combination of CK7 and TP53 immunohistochemistry may be helpful in diagnosing inflammatory bowel disease-associated dysplasia in difficult cases.

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Section: Histopathological Evaluationmentioning

confidence: 99%

Section: Histopathological Evaluationmentioning

confidence: 99%

Diagnostic utility of TP53 and cytokeratin 7 immunohistochemistry in idiopathic inflammatory bowel disease-associated neoplasia

et al. 2014

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“…The degree of dysplasia was rated as suggested by Riddell et al (none, low grade, and high grade). 12 …”

Section: Histomorphologymentioning

confidence: 99%

Genomic instability and oncogene amplifications in colorectal adenomas predict recurrence and synchronous carcinoma

et al. 2011

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Individual colorectal adenomas have different propensities to progress to invasive disease. In this study, we explored whether these differences could be explained by gene copy number alterations. We evaluated 18 adenomas of patients without synchronous or subsequent carcinoma (6.5 years follow-up), 23 adenomas of carcinoma patients, and 6 related carcinomas. All samples were measured for their DNA ploidy status. Centromere probes for chromosomes 17 and 18, as well as gene-specific probes for SMAD7, EGFR, NCOA3, TP53, MYC, and RAB20 were assessed by multicolor fluorescence in situ hybridization. An increased genomic instability index of CEP17, SMAD7, and EGFR, as well as TP53 deletions and MYC amplifications defined adenomas of patients with synchronous carcinoma (Po0.05). Diploid NCOA3 signal counts were associated with longer adenoma recurrence-free surveillance (P ¼ 0.042). In addition, NCOA3, MYC, EGFR, and RAB20 amplifications, as well as TP53 deletions correlated with increased DNA stem line values and/or aneuploidy in adenomas (Po0.05). Furthermore, aberrations of NCOA3, MYC, and RAB20 were associated with histopathologically defined high-risk adenomas (Po0.05). RAB20 amplifications were also correlated with high-grade dysplastic adenomas (P ¼ 0.002). We conclude that genomic instability in colorectal adenomas is reflected by EGFR, MYC, NCOA3, and RAB20 amplifications that do correlate with histomorphological features and are indicative for adenoma recurrence and the presence of synchronous carcinomas.

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“…The emergence and maintenance of CC is a complex process characterized by disordered cell division and death and the histological progression occurs in a step-wise fashion: negative, to indefinite dysplasia to dysplasia to cancer [11]. The rate of proliferation and apoptosis is determined by the histologic activity of inflammation [22].…”

Section: Discussionmentioning

confidence: 99%

“…Unlike SCRC that arises from a focal dysplastic lesion, an adenoma, and evolves through the adenoma-carcinoma sequence, the majority of CC arises from focal or multifocal dysplastic mucosae in areas of inflammation and the cancer evolves through inflammation-dysplasia-carcinoma sequence [10][11][12]. As in HNPCC, CC most commonly develops in younger patients, is often mucinous or signet cell and is characterized by multiple lesions; although reported to occur more commonly in the left colon, some studies reported higher incidences in the proximal colon [13,14].…”

Section: Introductionmentioning

confidence: 99%

Ulcerative colitis and cancer

Kulaylat

Dayton

2010

Journal of Surgical Oncology

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Patients with ulcerative colitis (UC) are at an increased risk for the development of colorectal cancer (CRC). Unlike sporadic CRC, the cancer in UC patients arises from a focal or multifocal dysplastic mucosa in areas of inflammation. The clinical features of UC-associated cancer are similar to those found in patients with hereditary non-polyposis colorectal cancer. As with other varieties of CRC, UC-associated cancer exhibits a variety of genetic and molecular changes/abnormalities. These abnormalities are however clustered in areas of mucosae with histological abnormalities. The magnitude and timing of these changes are however significantly different. Surveillance and identification of patients at risk for cancer are a challenging problem.

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Dysplasia in inflammatory bowel disease: Standardized classification with provisional clinical applications

Cited by 1,718 publications

References 37 publications

Diagnostic utility of TP53 and cytokeratin 7 immunohistochemistry in idiopathic inflammatory bowel disease-associated neoplasia

Diagnostic utility of TP53 and cytokeratin 7 immunohistochemistry in idiopathic inflammatory bowel disease-associated neoplasia

Genomic instability and oncogene amplifications in colorectal adenomas predict recurrence and synchronous carcinoma

Ulcerative colitis and cancer

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