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1. Concurrent occurrence of gastric adenocarcinoma and duodenal neuroendocrine cell carcinoma: a composite tumour or collision tumours ?

Author

Takahiro Fujimori, Yoshikazu Kuroda, Hirokazu Fukui, F. Tabata, Tsutomu Chiba, Moriatsu Takada, M. Sakane, J. Imura, Yoshihiko Ueda, Hitoshi Kawamata, and R. Kashiwagi

Subjects
Male, Pathology, medicine.medical_specialty, Case Reports, Adenocarcinoma, Biology, Polymerase Chain Reaction, Neoplasms, Multiple Primary, Carcinoembryonic antigen, Duodenal Neoplasms, Stomach Neoplasms, Pancreatic cancer, medicine, Carcinoma, Humans, Polymorphism, Single-Stranded Conformational, Neuroendocrine cell, Duodenal Neoplasm, Stomach, Gastroenterology, Chromogranin A, Sequence Analysis, DNA, Middle Aged, Genes, p53, medicine.disease, digestive system diseases, Carcinoma, Neuroendocrine, medicine.anatomical_structure, Mutation, biology.protein
Abstract

BACKGROUNDNeuroendocrine cell (NEC) carcinoma is occasionally accompanied by adenocarcinoma but the relationship between these two morphologically distinct tumours is unclear. Two hypotheses have arisen regarding the mechanism for the association of adenocarcinoma and NEC carcinoma. One is that both are derived from a common multipotential epithelial stem cell. The second hypothesis is that adenocarcinoma and NEC carcinoma arise from a multipotential epithelial stem cell and a primitive NEC, respectively.AIMSTo elucidate the relationship between the two histologically distinct tumours, adenocarcinoma of the stomach and NEC carcinoma of the duodenum.PATIENT/METHODSWe present a case in which the tumour extended across the pyloric ring, the gastric portion of which revealed adenocarcinoma while the duodenal portion showed argyrophil NEC carcinoma. The two histologically distinct lesions of the tumour were examined by immunohistochemistry and genetic analysis of p53.RESULTSThe gastric region was negative for chromogranin A staining but positive for carcinoembryonic antigen (CEA) staining. In contrast, the duodenal region was positive for chromogranin A but negative for CEA. All tumour regions showed a point mutation in p53 gene at exon 7 (GGC (glycine)→GTC (valine) at codon 245). The distal portion of the duodenal tumour showed an additional point mutation inp53 gene at exon 5 (GCC (alanine)→GTC (valine) at codon 129).CONCLUSIONSThe two histologically distinct tumours, adenocarcinoma of the stomach and NEC carcinoma of the duodenum, appear to be derived from a common epithelial cell.

Published
2001
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2. Methylation of the oestrogen receptor gene in non-neoplastic epithelium as a marker of colorectal neoplasia risk in longstanding and extensive ulcerative colitis

Author

Yuko Ono, Yasuo Ohkura, Kazuaki Kitajima, Toshihiro Kusaka, Kazuhito Ichikawa, Shigehiko Fujii, Mikio Fujita, Tsutomu Chiba, Jun Takeda, Takahiro Fujimori, Shigeki Tomita, J. Imura, and Keiichi Tominaga

Subjects
Genetic Markers, Male, Risk, Pathology, medicine.medical_specialty, Time Factors, Colorectal cancer, Rectum, Biology, Intestinal mucosa, medicine, Humans, Colitis, Intestinal Mucosa, Aged, Colorectal Cancer, Chi-Square Distribution, Gastroenterology, Case-control study, Methylation, DNA Methylation, Middle Aged, medicine.disease, Prognosis, Ulcerative colitis, medicine.anatomical_structure, Receptors, Estrogen, Case-Control Studies, DNA methylation, Colonic Neoplasms, Cancer research, Disease Progression, Colitis, Ulcerative, Female
Abstract

Background: Surveillance colonoscopy is widely recommended in patients with longstanding and extensive ulcerative colitis (UC) in order to detect colorectal neoplasia at an early stage. However, it still remains questionable whether surveillance colonoscopy effectively enables early detection of UC associated neoplasia. There is a great need for sensitive markers to identify individuals at increased risk of neoplasia. The oestrogen receptor (OR) gene shows age related methylation in the colorectal epithelium and is methylated frequently in sporadic colorectal neoplasia, suggesting that OR methylation may predispose to colorectal neoplasia. Aim: To clarify whether analysis of methylation of the OR gene in non-neoplastic epithelium can contribute to prediction of increased neoplasia risk in UC patients. Materials and methods: A total of 165 non-neoplastic colorectal epithelia from 30 patients with longstanding and extensive UC, including 13 UC patients with neoplasia and 17 patients without, were evaluated. Methylation specific polymerase chain reaction was performed to determine the methylation status of the OR gene. Results: Methylation of the OR gene was detected in 54 of 70 (77.1%) non-neoplastic colorectal epithelia in UC with neoplasia but in only 23 of 95 (24.2%) without neoplasia. Methylation of the OR gene was significantly more frequent in non-neoplastic epithelium from UC with neoplasia than in chronic colitic epithelium from UC without neoplasia. Furthermore, in UC with neoplasia, the OR gene was extensively methylated in non-neoplastic epithelia throughout the colorectum compared with those in UC without neoplasia. Conclusion: These results suggest that analysis of OR gene methylation may have potential as a useful marker for identifying individuals at increased risk of neoplasia among those with longstanding and extensive UC.

Published
2005

3. Concurrent occurrence of gastric adenocarcinoma and duodenal neuroendocrine cell carcinoma: a composite tumour or collision tumours ?

Author

H, Fukui, M, Takada, T, Chiba, R, Kashiwagi, M, Sakane, F, Tabata, Y, Kuroda, Y, Ueda, H, Kawamata, J, Imura, and T, Fujimori

Abstract

BACKGROUND: Neuroendocrine cell (NEC) carcinoma is occasionally accompanied by adenocarcinoma but the relationship between these two morphologically distinct tumours is unclear. Two hypotheses have arisen regarding the mechanism for the association of adenocarcinoma and NEC carcinoma. One is that both are derived from a common multipotential epithelial stem cell. The second hypothesis is that adenocarcinoma and NEC carcinoma arise from a multipotential epithelial stem cell and a primitive NEC, respectively. AIMS: To elucidate the relationship between the two histologically distinct tumours, adenocarcinoma of the stomach and NEC carcinoma of the duodenum. PATIENT/METHODS: We present a case in which the tumour extended across the pyloric ring, the gastric portion of which revealed adenocarcinoma while the duodenal portion showed argyrophil NEC carcinoma. The two histologically distinct lesions of the tumour were examined by immunohistochemistry and genetic analysis of p53. RESULTS: The gastric region was negative for chromogranin A staining but positive for carcinoembryonic antigen (CEA) staining. In contrast, the duodenal region was positive for chromogranin A but negative for CEA. All tumour regions showed a point mutation in p53 gene at exon 7 (GGC (glycine)-->GTC (valine) at codon 245). The distal portion of the duodenal tumour showed an additional point mutation in p53 gene at exon 5 (GCC (alanine)-->GTC (valine) at codon 129). CONCLUSIONS: The two histologically distinct tumours, adenocarcinoma of the stomach and NEC carcinoma of the duodenum, appear to be derived from a common epithelial cell.

Published
2001

5. Methylation of the oestrogen receptor gene in non-neoplastic epithelium as a marker of colorectal neoplasia risk in longstanding and extensive ulcerative colitis.

Author

Fujii S, Tominaga K, Kitajima K, Takeda J, Kusaka T, Fujita M, Ichikawa K, Tomita S, Ohkura Y, Ono Y, Imura J, Chiba T, and Fujimori T

Subjects
Aged, Case-Control Studies, Chi-Square Distribution, Colitis, Ulcerative complications, Colitis, Ulcerative immunology, Colonic Neoplasms complications, Colonic Neoplasms immunology, DNA Methylation, Disease Progression, Female, Genetic Markers, Humans, Male, Middle Aged, Prognosis, Receptors, Estrogen metabolism, Risk, Time Factors, Colitis, Ulcerative metabolism, Colonic Neoplasms metabolism, Intestinal Mucosa metabolism, Receptors, Estrogen genetics
Abstract

Background: Surveillance colonoscopy is widely recommended in patients with longstanding and extensive ulcerative colitis (UC) in order to detect colorectal neoplasia at an early stage. However, it still remains questionable whether surveillance colonoscopy effectively enables early detection of UC associated neoplasia. There is a great need for sensitive markers to identify individuals at increased risk of neoplasia. The oestrogen receptor (OR) gene shows age related methylation in the colorectal epithelium and is methylated frequently in sporadic colorectal neoplasia, suggesting that OR methylation may predispose to colorectal neoplasia., Aim: To clarify whether analysis of methylation of the OR gene in non-neoplastic epithelium can contribute to prediction of increased neoplasia risk in UC patients., Materials and Methods: A total of 165 non-neoplastic colorectal epithelia from 30 patients with longstanding and extensive UC, including 13 UC patients with neoplasia and 17 patients without, were evaluated. Methylation specific polymerase chain reaction was performed to determine the methylation status of the OR gene., Results: Methylation of the OR gene was detected in 54 of 70 (77.1%) non-neoplastic colorectal epithelia in UC with neoplasia but in only 23 of 95 (24.2%) without neoplasia. Methylation of the OR gene was significantly more frequent in non-neoplastic epithelium from UC with neoplasia than in chronic colitic epithelium from UC without neoplasia. Furthermore, in UC with neoplasia, the OR gene was extensively methylated in non-neoplastic epithelia throughout the colorectum compared with those in UC without neoplasia., Conclusion: These results suggest that analysis of OR gene methylation may have potential as a useful marker for identifying individuals at increased risk of neoplasia among those with longstanding and extensive UC.

Published
2005
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6. Development of colonic neoplasia in p53 deficient mice with experimental colitis induced by dextran sulphate sodium.

Author

Fujii S, Fujimori T, Kawamata H, Takeda J, Kitajima K, Omotehara F, Kaihara T, Kusaka T, Ichikawa K, Ohkura Y, Ono Y, Imura J, Yamaoka S, Sakamoto C, Ueda Y, and Chiba T

Subjects
Animals, Cell Transformation, Neoplastic genetics, Colitis, Ulcerative chemically induced, Colitis, Ulcerative pathology, Colonic Neoplasms genetics, Colonic Neoplasms pathology, Cytoskeletal Proteins metabolism, Dextran Sulfate, Disease Models, Animal, Genes, ras, Genetic Predisposition to Disease, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Knockout, Mutation, Trans-Activators metabolism, beta Catenin, Colitis, Ulcerative complications, Colonic Neoplasms etiology, Genes, p53
Abstract

Background: Several animal models for human ulcerative colitis (UC) associated neoplasia have been reported. However, most neoplasias developed in these models have morphological and genetic characteristics different from UC associated neoplasia., Aims: To establish a new colitis associated neoplasia model in p53 deficient mice by treatment with dextran sulphate sodium (DSS)., Methods: DSS colitis was induced in homozygous p53 deficient mice (p53(-/-)-DSS), heterozygous p53 deficient mice (p53(+/-)-DSS) and wild-type mice (p53+/+-DSS) by treatment with 4% DSS. Numbers of developed neoplasias were compared among the experimental groups, and macroscopic and microscopic features of the neoplasias were analysed. Furthermore, K-ras mutation and beta-catenin expression were assessed., Results: p53(-/-)-DSS mice showed 100% incidence of neoplasias whereas the incidences in p53(+/-)-DSS and p53+/+-DSS mice were 46.2% and 13.3%, respectively. No neoplasias were observed in the control groups. The mean numbers of total neoplasias per mouse were 5.0 (p53(-/-)-DSS), 0.62 (p53(+/-)-DSS), and 0.2 (p53+/+-DSS). The number of neoplasias per mouse in the p53(-/-)-DSS group was significantly higher than that in the other DSS groups. The incidences of superficial type neoplasias were 91.7% in p53(-/-)-DSS mice, 75.0% in p53(+/-)-DSS mice, and 33.3% in p53+/+-DSS mice. The K-ras mutation was not detected in any of the neoplasias tested. Translocation of beta-catenin from the cell membrane to the cytoplasm or nucleus was observed in 19 of 23 (82.6%) neoplasias., Conclusions: The p53(-/-)-DSS mice is an excellent animal model of UC associated neoplasia because the morphological features and molecular genetics are similar to those of UC associated neoplasia. Therefore, this model will contribute to the analysis of tumorigenesis related to human UC associated neoplasia and the development of chemopreventive agents.

Published
2004
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