Normal colon of Sprague-Dawley rats

Shetye, Jayant; Rubio, Carlos A.; Mellstedt, Håkan

doi:10.1007/bf00213602

Cited by 3 publications

(1 citation statement)

References 25 publications

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“…However, there was no indication for that claim, since neither ‘artefacts’ nor similar crypt-associated anomalies have been recorded in normal colon mucosa in humans 2 20–22 or in laboratory animals. 23 24 …”

Section: Discussionmentioning

confidence: 99%

Novel histological repertoire of crypt-associated anomalies in inflamed colon mucosa

Rubio

Lang-Schwarz

2022

J Clin Pathol

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AimsStudying crypt branching in ulcerative colitis (UC) and in infectious colitis (IC), we detected previously unreported crypt-associated anomalies (CAAs). The objective was to describe, illustrate and assess the frequency of CAAs in inflamed colon mucosa in patients with UC and IC.MethodsSections from 100 consecutive biopsies with UC, in 50 with IC and in 27 with UC in remission (UCR) were reviewed. The following CAAs were identified: crypt eosinophilia, intracryptal epithelial hyperplasia, intracryptal epithelial budding, intracryptal supernumerary crypts, intracryptal epithelial bridges, crypt rings in rows and off-centre epithelial budding.ResultsThe frequency of crypts with extensive crypt eosinophilia and with intracryptal epithelial budding was significantly higher in UC than in IC and UCR (p<0.05); the frequency in the remaining histological parameters was similar in UC, IC and UCR.ConclusionsCAAs were found interspersed with branching crypts. CAAs persisted in long-lasting UC mucosal inflammation, but declined when the inflammation waned. Since similar anomalies are not present in normal colon mucosa, the results suggest that CAAs had been boosted by the ongoing mucosal inflammation. The development of these previously unreported CAAs in the colon mucosa with inflammation might embody pathological aberrations of cryptogenesis.

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Section: Discussionmentioning

confidence: 99%

Novel histological repertoire of crypt-associated anomalies in inflamed colon mucosa

Rubio

Lang-Schwarz

2022

J Clin Pathol

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Differing proliferative responses in proximal and distal colons of growing rats fed food eaten by adenoma patients

et al. 1996

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Animal dietary studies related to human colorectal carcinogenesis are usually based on AIN-76A diet, which is dissimilar to human food in source, preparation, and content. Our aim was to examine colonic epithelial proliferation in rats fed a diet based on the mean daily food intake of adenoma patients. Foods were prepared as reported by the adenoma patients and dehydrated; 64 Sprague-Dawley rats were fed either "human adenoma" or AIN-76A diet and every eight weeks, eight from each group were sacrificed. Both groups gained weight equally, had no colonic histological changes, but during the study showed progressive lengthening of colonic crypts (P < 0.01) and decreased proliferation (P < 0.05) in distal colons. Compared to controls, rats fed human adenoma diet had significantly longer crypts (P < 0.01) and more labeled cells (P < 0.05) at 32 weeks; overall they had increased proliferation (P < 0.01), most significantly in the distal colon. Thus, food eaten by adenoma patients induced hyperproliferative changes in the rat colon during growth and maturity, especially the distal colon, as found in humans at risk for neoplasia.

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Paneth Cell‐rich Flat Adenoma of the Rectum: Report of a Case

Rubio

Kanter

Björk

et al. 1996

Japanese Journal of Cancer Research

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A patient having familiar adenomatosis polyposis and an ileo‐rectal anastomosis developed a flat mucosal lesion in the rectum. A punch biopsy revealed a villous adenoma with high‐grade dysplasia. The subsequent surgical specimen indicated that the flat villous adenoma was rich in Paneth cells. Special stains included lysozyme muramidase (to visualize Paneth cells), MIB1 proliferation monoclonal antibody and single and multilabel immunohistochemistry for Paneth cells. Other methods included transmission electron microscopy and quantification with an image quantifier (Program Optilab 2.1) of lysozyme‐stained Paneth cells. The subjective evaluation of hematoxylin‐cosin‐stained preparations demonstrated that the Paneth cells were mainly located in the lower half of the villi. Sections labeled with a specific stain (lysozyme muramidase) revealed more Paneth cells in the villi and electron microscopy showed even more in lysozyme‐negative areas. Obviously some migrating dysplastic Paneth cells had retained their characteristic granules on their way towards the tip of the villi. Quantitative studies indicated that the lysozyme muramidase‐positive material accounted for 41% of the adenomatous tissue. MIB1 revealed intense cell proliferation at the base of the adenoma and in the entire slopes of the villi. Despite the wide distribution of Paneth cells in intestinal metaplasia of the stomach, in the normal small intestine and in the large bowel with chronic inflammatory diseases, it is surprising that tumors arising in Paneth cells are extremely rare. The causes of the apparent natural resistance of Paneth cells to tumor development deserve to be investigated. This is the first case of Paneth cell‐rich flat adenoma of the rectum in the literature.

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Normal colon of Sprague-Dawley rats

Cited by 3 publications

References 25 publications

Novel histological repertoire of crypt-associated anomalies in inflamed colon mucosa

Novel histological repertoire of crypt-associated anomalies in inflamed colon mucosa

Differing proliferative responses in proximal and distal colons of growing rats fed food eaten by adenoma patients

Paneth Cell‐rich Flat Adenoma of the Rectum: Report of a Case

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