Eiichi Ikeda
Iwate Medical University
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Publication
Featured researches published by Eiichi Ikeda.
Cytometry | 1996
Kohsuke Sasaki; Akira Kurose; Yasuhiro Miura; Toshihiko Sato; Eiichi Ikeda
We evaluated laser scanning cytometry (LSC) by comparing nuclear DNA ploidy determined by LSC and by flow cytometry (FCM) in 77 samples of human colorectal cancer from 48 patients. Both methods revealed an aneuploid peak in 30 (62.5%) of the cases, although two samples that were aneuploid by LSC were diploid by FCM and two others were diploid by LSC and aneuploid by FCM. The concordance rate for nuclear DNA ploidy was 91.7% in the 48 patients and 87.0% for the 77 samples. The DNA index was also highly correlated between two methods (r2 = 0.97, P < 0.001). We concluded that LSC provides DNA histograms equivalent to FCM for surgical specimens and has potential clinical application in pathology.
Cancer | 1995
Kohsuke Sasaki; Toshihiko Sato; Akira Kurose; Noriyuki Uesugi; Eiichi Ikeda
Background.At least two different evolutional pathways of colorectal cancer, namely the adenoma‐carcinoma sequence and de novo carcinogenesis, have been indicated. However, whether there is a difference between them in affected chromosomes and genes has not yet been elucidated. Chromosomal examination is expected to provide a clue to an answer to this question. In this study, the relation of aberrations in chromosome 18 to type of colorectal cancer was examined.
Human Pathology | 1996
Kohsuke Sasaki; Toshihiko Sato; Akira Kurose; Eiichi Ikeda
Wild-type p53 protein is a critical participant in G1 cell cycle arrest through the induction of waf1/cip1/sdi1 gene product p21, but mutant p53 proteins have lost transcriptional activity. To know whether the view obtained from studies using cultured cells is adaptable to human solid tumors, the authors immunohistochemically stained p21 and p53 in formalin-fixed, paraffin-embedded tissue sections from 67 cases of colorectal carcinoma. Of these, 54 cancers showed positive staining of p53, whereas p21-positive cells were identified in 46 tumors. However, the proportion of cells positive for these proteins varied considerably among cases, and moreover wide variation in p21 immunoreactivity was noted within the same tumor. Although there was an inverse relationship between p21 and p53 staining in tumors, namely, p21-positive cells were p53 negative and vice versa, an intermingling of tumor cells expressing concomitantly both genes was noted in 34 (51%) of 67 tumors. In these tumors, both proteins were usually moderately stained, but tumor cells intensely coexpressing both were found in one sample. This study supports the notion that although p21 expression is regulated by p53 under physiological conditions, it can be regulated by an additional pathway(s) in solid malignant tumors.
Oncology | 1999
Toshihiko Sato; Atsunori Oga; Eiichi Ikeda; Takeshi Todoroki; Tomoko Furuya
We measured DNA content by flow cytometry and determined the number of chromosomes 7, 17 and 18 by fluorescence in situ hybridization using DNA probes in 38 sporadic colorectal adenocarcinomas including 14 early cancers. Based on DNA ploidy and the copy number of chromosome 18, colorectal cancers were divided into two groups. In early cancers (mucosal and submucosal adenocarcinomas), monosomy 18 with DNA hypotriploidy was detected exclusively in 6 sessile tumors without adenoma portions. Seven of the remaining 8 tumors in which adenoma portions coexisted manifested disomy 18 and DNA diploidy or near diploidy. These tumors were considered to occur along the adenoma-carcinoma sequence. In contrast, monosomy 18 was accompanied by DNA diploidy or near diploidy in advanced cancers penetrating the muscularis propria. In advanced cancers, DNA hypertriploidy was linked with disomy 18 and chromosomes 7 and 17 were trisomic or tetrasomic. Observations indicate at least two different cytogenetic pathways in colorectal carcinogenesis. According to these findings, two thirds of advanced cancers were estimated to originate from adenoma, and the others were not.
International Journal of Oncology | 2004
Xiu Ping Liu; Toshihiko Sato; Atsunori Oga; Kenzou Ikemoto; Shigeto Kawauchi; Eiichi Ikeda
Oncology Reports | 2007
Xiuping Liu; Shigeto Kawauchi; Atsunori Oga; Toshihiko Sato; Kenzou Ikemoto; Eiichi Ikeda
Surgery Today | 1998
Hajime Iizawa; Eiichi Ikeda; Toshihiko Sato; Yoichi Ohta
Jpn J Gastroenterol Surg, Nihon Shokaki Geka Gakkai zasshi | 1995
Ichiro Hirai; Eiichi Ikeda; Hajime Iizawa; Toshihiko Sato; Kenji Okabe; Takuya Ishida; Youichi Ohta
Jpn J Gastroenterol Surg, Nihon Shokaki Geka Gakkai zasshi | 2006
Naoki Sakurai; Junichiro Yamauchi; Hisashi Shibuma; Eiichi Ikeda; Shunichi Sasou
Jpn J Gastroenterol Surg, Nihon Shokaki Geka Gakkai zasshi | 2005
Naoki Sakurai; Junichiro Yamauchi; Norimasa Fukushima; Hisashi Shibuma; Eiichi Ikeda; Shunichi Sasou