Growth patterns in various macroscopic types of noninvasive intramucosal colorectal carcinoma with special reference to apoptosis and cell proliferation

Tanimoto, Takuya; Tanaka, Shinji; Haruma, Ken; Yoshihara, Masaharu; Sumii, Koji; Kajiyama, Goro; Shimamoto, Fumio

doi:10.1007/bf02237053

Cited by 20 publications

(12 citation statements)

References 39 publications

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“…Previously, we reported the median Ki-67 LI and AI of intramucosal CRC to be 35 and 0.7%, respectively, and the median Ki-67 LI of submucosally invasive CRC to be 44.1% [35, 36]. The median Ki-67 LI of rectal carcinoid tumors (0.62%) was much lower than that of CRC.…”

Section: Discussionmentioning

confidence: 99%

Growth Characteristics of Rectal Carcinoid Tumors

et al. 2000

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Purpose: Tissue growth depends on both cell proliferation and cell death. This study was designed to examine the growth characteristics of rectal carcinoid tumors. Methods: Fifty rectal carcinoid tumors were studied clinicopathologically and experimentally. Expression of Ki-67, TGF-α, p53, and bcl-2 was examined immunohistochemically, and apoptotic cells were identified by the in situ DNA nick end labeling method. EGF receptor expression was examined by a colorimetric in situ mRNA hybridization technique. Results: The median Ki-67 labeling index (LI) in all lesions was 0.62 ± 0.59%. Ki-67 LI was significantly (p < 0.01) higher in lesions larger than 5 mm than in lesions smaller than 5 mm. TGF-α was expressed more frequently (p < 0.01) in lesions larger than 5 mm (100%) than in lesions smaller than 5 mm (65.2%). Ki-67 LI was significantly (p < 0.05) higher in lesions with TGF-α expression than in lesions without TGF-α expression. The in situ hybridization revealed EGF receptor expression in all 46 lesions with intact mRNA (100%), and coexpression of TGF-α and EGF receptor was found in 39 of the 46 (84.8%) lesions. The median apoptotic index (AI) in all lesions was 0.15 ± 0.12%. AI has increased with tumor size and was significantly (p < 0.05) higher in lesions with a higher Ki-67 LI than in lesions with a lower Ki-67 LI. p53 protein was detected in only 1 patient who had liver metastases, and the gene mutation was confirmed by polymerase chain reaction and single-strand conformation polymorphism analysis. bcl-2 expression was absent in all lesions. Conclusions: The Ki-67 LI indicated a low cellular proliferative activity in rectal carcinoid tumors. AI was very low, and was significantly correlated with proliferative rate. Inhibition of apoptosis by mutated p53 or bcl-2 may not have occurred in most of these tumors. TGF-α/EGF receptor autocrine mechanisms may play a possible role in tumor growth, and the cellular proliferative activity may increase as tumors grow larger.

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Section: Discussionmentioning

confidence: 99%

Growth Characteristics of Rectal Carcinoid Tumors

et al. 2000

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“…[1][2][3] Despite this distinctive biological behavior, no characteristic genetic abnormalities have been disclosed in LSTs, except for an infrequent mutation rate of the K-ras oncogene. [4][5][6] Furthermore, these reports focusing on K-ras mutation [4][5][6] included not only LSTs but also small flat tumors in the analyses.…”

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Increased cyclooxygenase-2 expression in large flat colorectal tumors (laterally spreading tumors)

Yamashita

Arimura

Shimizu

et al. 2003

Journal of Gastroenterology

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“…Mutation in p53 and aberrant expression of bcl-2 allow continued tumor proliferation and inhibition of apoptosis. 23 Coexpression of the bcl-2 and mutant p53 proteins was detected in 38% of primary colon cancers. 6 In 62.9% of our patients, both p53 and bcl-2 were either identified or absent.…”

Section: Discussionmentioning

confidence: 99%