Chromoendoscopy with a Standard-Resolution Colonoscope for Evaluation of Rectal Aberrant Crypt Foci

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Abstract

Colorectal cancer (CRC) is the second most common cause of death worldwide. According to the theory by Vogelstein, colorectal carcinogenesis involves a series of successive changes in the normal colonic mucosa, starting with excessive proliferation and focal disorders of intestinal crypts, followed by adenoma and its subsequent malignant transformation. The first identifiable changes in CRC carcinogenesis are aberrant crypt foci (ACF). ACF are invisible during routine colonoscopy yet are well identifiable in chromoendoscopy using methylene blue or indigo carmine. High-resolution colonoscopes are used for assessment of ACF. The aim of the present study was to evaluate the usefulness of standard-resolution colonoscopy for identification of rectal ACF. The following parameters were evaluated: duration of chromoendoscopy of a given rectal segment, type of ACF, sensitivity and specificity of endoscopy combined with histopathological evaluation. The mean duration of colonoscopy and chromoendoscopy was 26.8 min. In the study population, typical ACF were found in 73 patients (p = 0.489), hyperplastic ACF in 49 (p = 0.328), and dysplastic ACF in 16 patients (p = 0.107). Mixed ACF were observed in 11 individuals (p = 0.073). The sensitivity of the method was found to be 0.96 whereas its specificity 0.99.

Identification of rectal ACF using standard-resolution colonoscopy combined with rectal mucosa staining with 0.25% methylene blue is characterised by high sensitivity and specificity.

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Observation and quantification of aberrant crypts in the murine colon treated with a colon carcinogen: preliminary findings.

R P Bird (1987)

In the present study a methodological approach is taken which quantitates aberrant dysplastic crypts in the unsectioned murine colon. C57BL/6J or CF1 female mice (7-8 weeks old) were injected (i.p.) with azoxymethane (5 mg/kg body wt./week) for 4 weeks. Their colons were excised, cut open on the median axis and fixed flat in buffered formalin. Unsectioned colons were stained with methylene blue. The mucosal side was examined under a light microscope. The aberrant crypts, which are larger and have a thicker epithelial lining, were easily visualized using X 4 or X 10 objectives. CF1 mice, which are more sensitive to developing colon tumors, had a higher number of aberrant crypts/colon than their less sensitive counterparts, C57BL/6J mice (5.0 +/- 0.7 vs. 2.4 +/- 0.7). The usefulness of this observation as a possible measure of neoplastic events is discussed in the animal and human situation.

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Aberrant crypt foci of the colon as precursors of adenoma and cancer.

T Takayama, S Katsuki, Y. Takahashi … (1998)

Aberrant crypt foci of the colon are possible precursors of adenoma and cancer, but these lesions have been studied mainly in surgical specimens from patients who already had colon cancer. Using magnifying endoscopy, we studied the prevalence, number, size, and dysplastic features of aberrant crypt foci and their distribution according to age in 171 normal subjects, 131 patients with adenoma, and 48 patients with colorectal cancer. We also prospectively examined the prevalence of aberrant crypt foci in 11 subjects (4 normal subjects, 6 with adenoma, and 1 with cancer) before and after the administration of 100 mg of sulindac three times a day for 8 to 12 months and compared the results with those in 9 untreated subjects (4 normal subjects and 5 with adenoma). All 20 subjects had aberrant crypt foci at base line. We identified 3155 aberrant crypt foci, 161 of which were dysplastic; the prevalence and number increased with age. There were significant (P<0.001) correlations between the number of aberrant crypt foci, the presence of dysplastic foci, the size of the foci, and the number of adenomas. After sulindac therapy, the number of foci decreased, disappearing in 7 of 11 subjects. In the untreated control group, the number of foci was unchanged in eight subjects and slightly increased in one (P<0.001 for the difference between the groups). Aberrant crypt foci, particularly those that are large and have dysplastic features, may be precursors of adenoma and cancer.

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APC mutations and other genetic and epigenetic changes in colon cancer.

Roger Wolff, Hans M. Albertsen, Martha Slattery … (2007)

Relationships between adenomatous polyposis coli (APC) mutations, BRAF V600E mutations, and the CpG island methylator phenotype (CIMP) in colon cancer have not been explored. In addition, controversies exist about the proportion of tumors with APC mutations in the mutation cluster region (MCR); how commonly APC, Ki-ras, and p53 mutations occur in the same tumor; and whether APC mutations occur in sporadic microsatellite-unstable tumors. The APC gene was therefore sequenced in 90 colonic adenocarcinomas previously evaluated for CIMP, microsatellite instability, BRAF, Ki-ras, and p53. APC mutations were inversely related to BRAF mutations (P = 0.0003) and CIMP (P = 0.02) and directly related to p53 and Ki-ras mutations (P = 0.04). Slightly more than half of APC mutations occurred outside of the MCR, and frameshift mutations were more likely than nonsense mutations to occur in the MCR (21 of 28 versus 12 of 40, P = 0.0003). APC mutations were found in sporadic microsatellite-unstable tumors and were more likely to be frameshifts in short nucleotide repeats (P = 0.007). The occurrence of APC, Ki-ras, and p53 mutations together in the same tumor was uncommon (11.1%). In conclusion, an analysis restricted to the MCR will miss more than half of APC mutations as well as mischaracterize their mutational spectrum. The conventional wisdom that most colon cancers contain APC, Ki-ras, and p53 mutations is incorrect. Microsatellite instability may precede acquisition of APC mutations in sporadic microsatellite-unstable tumors. The relationships of APC mutations to other genetic and epigenetic alterations add to the already impressive genetic heterogeneity of colon cancer.

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Author and article information

Contributors

Hong Wang: Role: Editor

Journal

Journal ID (nlm-ta): PLoS One

Journal ID (iso-abbrev): PLoS ONE

Journal ID (publisher-id): plos

Journal ID (pmc): plosone

Title: PLoS ONE

Publisher: Public Library of Science (San Francisco, CA USA )

ISSN (Electronic): 1932-6203

Publication date (Electronic): 17 February 2016

Publication date Collection: 2016

Volume: 11

Issue: 2

Electronic Location Identifier: e0148286

Affiliations

[1 ]Department of Oncologic and General Surgery, University Hospital in Olsztyn, Poland

[2 ]Department of Maritime & Hyperbaric Medicine Department, Military Institute of Medicine Gdynia, Poland

[3 ]Academy of Physical Education in Cracow, Department of Physical Education and Sport, Cracow, Poland

[4 ]Centre for Diagnosis and Treatment of Gastrointestinal Diseases, Gdańsk, Poland

[5 ]2nd Department of General, Gastroenterologic and Gastrointestinal Oncologic Surgery, Medical University of Lublin, University Hospital No.1, Lublin, Poland

[6 ]Department of General, Oncologic, Metabolic and Thoracic Surgery, Military Institute of Medicine, Military Hospital in Warsaw, Poland

[7 ]Unit for Laboratory Diagnostics, University Hospital in Olsztyn, Poland

[8 ]Department of Histology and Embryology with Unit of Experimental Cytology, Medical University of Lublin, Poland

Rutgers, the State Univesity of New Jersey, UNITED STATES

Author notes

Competing Interests: The authors have declared that no competing interests exist.

Conceived and designed the experiments: MK KP. Performed the experiments: MK PS AP. Analyzed the data: MK PS DM TA MO KZ WK KP IK AP. Contributed reagents/materials/analysis tools: MK PS DM TA MO KZ WK KP IK AP. Wrote the paper: MK PS DM TA MO KZ WK KP IK AP. Editor: DM.

‡ These authors also contributed equally to this work.

* E-mail: nauka.autograf@ 123456gmail.com

Article

Publisher ID: PONE-D-15-39884

DOI: 10.1371/journal.pone.0148286

PMC ID: 4757420

PubMed ID: 26886097

SO-VID: a1511b2e-766c-4cdc-b317-8ba96422469d

License:

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

History

Date received : 13 October 2015

Date accepted : 15 January 2016

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Figures: 0, Tables: 0, Pages: 7

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The authors have no support or funding to report.

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Data Availability All relevant data are within the paper and its Supporting Information files.

Chromoendoscopy with a Standard-Resolution Colonoscope for Evaluation of Rectal Aberrant Crypt Foci

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Abstract

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Most cited references 18

Observation and quantification of aberrant crypts in the murine colon treated with a colon carcinogen: preliminary findings.

Aberrant crypt foci of the colon as precursors of adenoma and cancer.

APC mutations and other genetic and epigenetic changes in colon cancer.

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