Histopathological studies of superficial‐type early colorectal carcinoma

Wada, Ryo; Matsukuma, Susumu; Abe, Hiroshi; Kuwabara, Noriyuki; Suda, Koichi; Arakawa, Atsushi; Kitamura, Shigehiro

doi:10.1002/(sici)1097-0142(19960101)77:1<44::aid-cncr9>3.3.co;2-7

Cited by 22 publications

(27 citation statements)

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“…At the same time, P53-positive rates were rare in serrated polyps. P53 overexpression appears to become more frequent as tumors progress to higher grades of neoplasia, in agreement with previous studies (36,37).…”

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confidence: 92%

Protein expression of Fragile Histidine Triad and cyclooxgenase-2 in serrated neoplasia of the colorectum

et al. 2017

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Section: ------------------------------------------------------------supporting

confidence: 92%

Protein expression of Fragile Histidine Triad and cyclooxgenase-2 in serrated neoplasia of the colorectum

et al. 2017

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“…Some reports have suggested that flat colorectal carcinomas develop either through a polypoid intermediate by ulceration and sloughing off of a polyp or through formation of a flat adenoma intermediate (9,10). However, contrasting models have posited that flat carcinomas arise de novo without an adenomatous intermediate (2,11,12,34,35). To distinguish between these conflicting models, we used endoscopy to visualize and serially follow tumor growth patterns from initiation through progression to invasive carcinoma.…”

Section: Resultsmentioning

confidence: 99%

Flat Colorectal Cancers Are Genetically Determined and Progress to Invasion without Going through a Polypoid Stage

Uronis

Herfarth²,

Rubinas

et al. 2007

Cancer Research

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Growing evidence suggests that flat colorectal cancers (CRC) account for 10% to 20% of all CRCs and that these are frequently associated with more advanced pathologies. However, controversy exists as to the origin and progression of flat CRCs compared with the more common polypoid-type morphology. We report using the azoxymethane mouse model for human CRC that KK/HIJ and I/LNJ mice develop different frequencies of flat and polypoid tumors; 83% of colon tumors in I/LNJ mice are flat compared with only 19% in KK/HIJ mice, indicating a strong genetic predisposition to the development of specific CRC morphologies. Like polypoid tumors, all flat tumors show a significant increase in the level of nuclear B-catenin (CATNNB1), supported by similar frequencies of mutations in the phosphorylation domain-coding region (codons 32-41) of Catnnb1. However, in contrast to previous reports, tumors bearing higher ''oncogenic potential'' do not cluster in codon 41 of Catnnb1. There are no differences between flat and polypoid tumors in the frequency of mutations in codons 12 and 13 of Kras or codon 624 of Braf. Similarly, there are no differences between tumor morphologies in their location along the proximal-to-distal colonic axis or in the relative quantity of intratumor stromal myofibrobasts as marked by the expression of A-smooth muscle actin. Using a combination of serial colonoscopic and histologic analyses, we definitively show that flat CRCs do not develop de novo but progress through a flat adenomatous stage to invasive carcinoma without transit through an intermediary polypoid stage. [Cancer Res 2007;67(24):11594-600]

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“…The tenor of de novo carcinoma theory is that many lesions of small colorectal early cancers of the superficial type with nonpolypoid form (Kuramoto and Oohara, 1989;Shimoda et al, 1989), flat elevation or depressed type are carcinomas without any adenomatous remnants (Kudo et al, , 2000. Genetic studies also support the view that there are at least two pathways that lead to the development of colonic cancer, including polyp-cancer sequence and de novo Tsujitani et al, 1996;Wada et al, 1996). While two opposing theories were confirmed by histopathological studies, the relative importance of the two theories associated with development of colorectal carcinoma is still fraught with uncertainty.…”

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confidence: 99%

A case–cohort study for the disease natural history of adenoma–carcinoma and de novo carcinoma and surveillance of colon and rectum after polypectomy: implication for efficacy of colonoscopy

et al. 2003

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The disease natural history of colorectal neoplasm regarding two opposing theories, adenoma -carcinoma sequence and de novo carcinoma theory, is controversial and rarely quantified. The aims of this study are therefore to estimate the dwelling times of adenoma -carcinoma sequence by adenoma size and histological type, taking de novo carcinoma into account. The efficacy of polypectomy was therefore estimated making allowance for two pathways. A case -cohort design, underpinning a cohort with 13 908 subjects (including 10 496 normal subjects, 2652 polyps, 760 colorectal cancers) who underwent the first examination of colonoscopy between 1979 and 1998, was devised to estimate parameters associated with two opposing theories by randomly selecting 305 normal subjects, 300 patients with polyps, and 116 colorectal cancers from the cohort. All the 2652 polyps were linked to national cancer registry to ascertain 25 invasive carcinomas after polypectomy. For the five-state model associated with adenoma size, dwelling times of small (0.6 -1 cm) and large adenoma (41 cm) are 7.75 and 5.27 years for the model without considering de novo, and 17.48 and 15.90 years for the model taking de novo carcinoma into account. Similar findings are observed for the model associated with histological type. The estimated proportions of de novo carcinoma are 31.87% from the model by adenoma size and 27.81% from the model by histological type. Compared to size less than 5 mm, patients with adenoma size between 6 and 10 mm and patients with adenoma size larger than 1 cm have 2.17-fold (0.67 -10.74) and 4.25-fold (1.23 -14.70), respectively, for the risk of malignant transformation. There are similar findings for the model by histological type. The estimates of overall efficacy of colonoscopy in reducing CRC is 73% for the model allowing for de novo carcinoma and 88% for the model without considering de novo carcinoma theory. The efficacy of diminutive adenoma and small adenoma increases with follow-up years, whereas the efficacy of large adenoma decreases with follow-up years. In conclusion, about 30% of cancers arising from de novo sequence are demonstrated. This finding, together with the adenoma -carcinoma sequence associated with adenoma size and histological type, is important for the estimation of dwelling times, the efficacy of colonoscopy, and the surveillance of polyp after polypectomy.

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Histopathological studies of superficial‐type early colorectal carcinoma

Cited by 22 publications

References 0 publications

Protein expression of Fragile Histidine Triad and cyclooxgenase-2 in serrated neoplasia of the colorectum

Protein expression of Fragile Histidine Triad and cyclooxgenase-2 in serrated neoplasia of the colorectum

Flat Colorectal Cancers Are Genetically Determined and Progress to Invasion without Going through a Polypoid Stage

A case–cohort study for the disease natural history of adenoma–carcinoma and de novo carcinoma and surveillance of colon and rectum after polypectomy: implication for efficacy of colonoscopy

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