Detection of aberrant crypt foci by magnifying colonoscopy

Yokota, Takuya; Sugano, Kazuhiko; Yokoyama, Takanori; Sugihara, Kazuaki; Kondo, Hisashi; Saito, Daisuke; Oguro, Yanao; Yoshida, Shintaro

doi:10.1016/0016-5085(95)26540-6

Cited by 7 publications

(15 citation statements)

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“…A comparison of the results of the different series published shows a common trend, in spite of some differences. In fact, Takayama et al [23], Adler et al [19], and Yokota et al [24] found a higher mean number of ACF in patients with benign and malignant colorectal neoplasia than in patients without endoscopic lesions. The paper by Hurlstone et al [20] on ACF in patients with flat lesions reports similar results, demonstrating that the mean number of ACF increases when patients without lesion, with adenoma, and with carcinoma are considered in succession.…”

Section: Discussionmentioning

confidence: 97%

“…The option to study only rectal ACF, in accordance with studies that applied a similar methodology [19][20][21][22][23][24][25][26], deserves some justification. This decision was founded on investigations in surgical specimens [40,41] and endoscopic studies [23,42] that show that ACF are more frequently detected in the left colon and in the rectum.…”

Section: Discussionmentioning

confidence: 99%

“…The modulation of ACF by chemopreventive agents with proven activity in CRC is also described in animal studies [16][17][18]. With the emergence of magnification and chromoscopy, it is now possible to perform endoscopic in vivo human studies [19][20][21][22][23][24][25][26]. Although there are a number of arguments supporting the preneoplastic nature of ACF, such as an average number that increases with age [23], a higher prevalence in patients with neoplastic lesion of the colon [23], the identification of ACF with carcinoma in situ in a patient with sporadic colon cancer [27], the presence of ACF with dysplasia and APC mutations in patients with familial adenomatous polyposis [28,29], and the occurrence of microsatellite instability in ACF picked from patients with Lynch syndrome [30], the truth is that doubt still persists with regard the preneoplastic nature of ACF, which is unquestionable only in animal models of intestinal cancer.…”

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confidence: 99%

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Aberrant crypt foci: endoscopic assessment and cell kinetics characterization

Figueiredo

Donato

Urbano

et al. 2008

Int J Colorectal Dis

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Background and aims Aberrant crypt foci (ACF) are preneoplastic lesions in animal models of colorectal cancer. The aim of the study is to investigate if ACF are involved in human colorectal carcinogenic process and if they can be helpful in predicting the presence of a colorectal neoplasia. Methods The study included, between 2003 and 2005, 182 patients, 62 with adenoma, 55 with colorectal carcinoma, 53 without colorectal lesions, and 12 with nonneoplastic mucosal polyps. The number of rectal ACF was determined by colonoscopy. Proliferation and apoptosis indexes were evaluated by immunohistochemistry in rectal ACF, in normal rectal mucosa, and in carcinomatous tissue. Results The mean number of rectal ACF in patients with rectal neoplasia was 12.64, significantly higher than in patients with neoplastic lesions elsewhere in the colon (p= 0.01). The apoptosis index in ACF of patients with colorectal carcinoma or adenoma aged 50 years or older was significantly lower than in younger patients (1.3% vs 2.7%, p=0.01) and, in patients with carcinoma, lower than in normal mucosa (1.1% vs 2.1%, p=0.002). The proliferation index was significantly higher in ACF of patients with colorectal neoplasia aged less than 50 years than in normal mucosa (10.9% vs 7.7%, p=0.02). The apoptosis index in ACF foci of patients with carcinoma (1.1%) was significantly lower than in patients without lesions (2.2%) and than in normal mucosa (2%). The mean number of ACF is significantly higher in patients with polyps larger than 1 cm (11.28 vs 6.27, p=0.02). Conclusion Aberrant crypt foci probably precede the appearance of neoplasia and may be helpful in predicting the presence of a colorectal neoplastic lesion.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Aberrant crypt foci: endoscopic assessment and cell kinetics characterization

Figueiredo

Donato

Urbano

et al. 2008

Int J Colorectal Dis

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“…ACFs were first defined in the colons of rodents exposed to carcinogens and identified soon thereafter in human colons (20). ACFs are associated with adenomatous polyp (42) and colorectal cancer formation in humans (20) and have become an accepted biomarker for assessing the efficacy of chemopreventive drugs in various nonhuman colorectal cancer models (43). Whereas polyps are relatively fixed as lesions, ACF seem fluid and can readily change in number over time (44).…”

Section: Discussionmentioning

confidence: 99%

Expression of Vitamin D Receptor and 25-Hydroxyvitamin D3-1α-Hydroxylase in Normal and Malignant Human Colon

Matusiak

Murillo

Carroll

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

111

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Considerable evidence exists to support the use of vitamin D to prevent and/or treat colorectal cancer. However, the routine use of bioactive vitamin D, 1,25-dihydroxyvitamin D3, is limited by the side effect of toxic hypercalcemia. Recent studies, however, suggest that colonic epithelial cells express 25-hydroxyvitamin D3-1A-hydroxylase, an enzyme that converts nontoxic pro-vitamin D, 25-hydroxycholecalciferol [25(OH)D3], to its bioactive form. Yet, nothing is known as to the cellular expression of 1A-hydroxylase and the vitamin D receptor (VDR) in the earliest histopathologic structures associated with malignant transformation such as aberrant crypt foci (ACF) and polyps [addressing the possibility of using nontoxic 25(OH)D3 for chemoprevention], nor is anything known as to the expression of these proteins in colorectal cancer as a function of tumor cell differentiation or metastasis [relevant to using 25(OH)D3 for chemotherapy]. In this study, we show that 1A-hydroxylase is present at equal high levels in normal colonic epithelium as in ACFs, polyps, and colorectal cancer irrespective of tumor cell differentiation. In contrast, VDR levels were low in normal colonic epithelial cells; were increased in ACFs, polyps, and well-differentiated tumor cells; and then declined as a function of tumor cell de-differentiation. Both 1A-hydroxylase and VDR levels were negligible in tumor cells metastasizing to regional lymph nodes. Overall, these data support using 25(OH)D3 for colorectal cancer chemoprevention but suggest that provitamin D is less likely to be useful for colorectal cancer chemotherapy. (Cancer Epidemiol Biomarkers Prev 2005;14(10):2370-6)

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“…In humans, the lesions may also be detected endoscopically by instilling approximately 100 ml of a 0.5% methylene blue and saline solution, administered intrarectally via an enema at the end of a routine colonic cleansing (17) or administered by spraying the mucosa with the methylene blue solution (104). The ings, and dysplastic ACF appear to be slitlike (16,67,74 (16,55,83).…”

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Review Article: Aberrant Crypt Foci: A Review

Fenoglio‐Preiser

Noffsinger

1999

Toxicol Pathol

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(22,25). This adenomacarcinoma sequence initially envisioned adenomas as representing nonmalignant areas of polypoid neoplasia. More recently, the concept was expanded to include flat and depressed adenomas ( Fig. 1) (35,58). Once the histologic colon-cancer continuum was defined, molecular studies showed that sequential genetic alterations accompany the progression of mucosal changes that ultimately lead to the development of colorectal cancer (Fig. 2). One important finding was that genetic alterations may be present in a colonic mucosa that shows no histologic signs of neoplasia (20).At the same time that these studies progressed in humans, detailed animal investigations, particularly those involving rodents, searched for the earliest morphological precursors of carcinoma development in experimental colon-cancer models. This search led to the description of aberrant crypt foci (ACF) (4), one of the earliest visible events in carcinogen-induced models of colorectal tumorigenesis (4,44,47,48,76,94 (Fig. 4) 2) those resembling hyperplastic polyps, (Fig. 5) and 3) those resembling microadenomas (Fig. 6) (Figs. 4-6). The proliferative index is significantly higher in dysplastic ACE The proliferative compartment can be recognized by counting mitoses. Expansion of the proliferating zone can be demonstrated using antibodies to proliferating cell nuclear antigen (PCNA), (Figs. 4-6), and the protein encoded by hMSH2 (Fig. 7), a mismatch-repair gene. PCNA is a nuclear protein that is a cofactor for DNA polymerase (19,43). Ki-67 is commonly used as a marker of cell proliferation, since it is expressed in actively growing cells during all phases of the cell cycle (24,77). hMSH2 expression is largely confined to the proliferative compartment of the crypt, since the mismatch-repair system is most active during DNA replication (33,37,38). Ki (30,41,55,56,64,66,81,85,88,97,102,103). The high incidence of K-ras mutations in ACF contrasts with the low incidence of K-ras mutations found in small (<5 mm in diameter) adenomatous polyps. The incidence of K-ras mutations only exceeds 10% after adenomatous polyps have grown 10 mm in diameter (87,98 (41). They are present in 67% of ACE Surprisingly, the presence of ras mutations inversely correlates with the presence of dysplasia in FAP-associated ACE Dysplastic ACF often lack ras mutations, whereas most nondysplastic hyperplastic ACF, both of the sporadic and FAP types, have mutations (55). In one study, K-ras mutations were found in 29% of dysplastic ACF and in 81 % of hyperplastic ACF (56). The larger the aberrant crypt focus, the lower the K-ras mutation rate. The rate of K-ras mutation in ACF with more than 150 crypts per focus is 58.6%. The majority of ras mutations involve codon 12 (85). APC MutationsInactivation of the APC gene is a key molecular event in the development of sporadic colorectal epithelial dysplasia (30,51,54,62). In contrast, sporadic ACF do not have a very high frequency of APC gene mutations (30,32). Only approximately 5% of ACF harbor APC mutations (85)....

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Detection of aberrant crypt foci by magnifying colonoscopy

Cited by 7 publications

References 0 publications

Aberrant crypt foci: endoscopic assessment and cell kinetics characterization

Aberrant crypt foci: endoscopic assessment and cell kinetics characterization

Expression of Vitamin D Receptor and 25-Hydroxyvitamin D3-1α-Hydroxylase in Normal and Malignant Human Colon

Review Article: Aberrant Crypt Foci: A Review

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