The multicentric occurrence of squamous epithelial dysplasia and squamous cell carcinoma in the esophagus

Morita, Masaru; Kuwano, Hiroyuki; Yasuda, Mitsuhiro; Watanabe, Mamoru; Ohno, Shinji; Saito, Takao; Furusawa, Motonosuke; Sugimachi, F.A.C.S. Keizo

doi:10.1002/1097-0142(19941201)74:11<2889::aid-cncr2820741102>3.0.co;2-k

Cited by 36 publications

(23 citation statements)

References 18 publications

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“…38) In early esophageal cancers, neoplastic cells proliferate in the basal and parabasal compartments of the epithelium, the early stage of which is called dysplasia or carcinoma in situ by pathologists. [40][41][42] Our immunohistochemical study demonstrated that p73 and p21 expressions were conserved in superficially located cancer cells, including early intraepithelial and mucosal cancers and intraepithelial extension. Intraepithelial extension is defined as an intraepithelial carcinoma contiguous to invasive carcinoma, and it coexists in about 30% of squamous cell carcinomas of the esophagus.…”

Section: Discussionmentioning

confidence: 69%

Synergistic decline in expressions of p73 and p21 with invasion in esophageal cancers

et al. 2003

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The significance of the p73 gene, a homologue of the p53 gene, in esophageal cancers is not fully understood. In order to clarify the role of p73 expression in esophageal cancers, p73 expression was immunohistochemically investigated in 106 surgically resected esophageal cancers and the results were compared with various clinicopathological factors. In normal esophageal epithelium, the expression of p73 was observed only in the nuclei of basal cells. In esophageal cancers, p73 immunoreactivity was observed in all intraepithelial lesions except one cancer, and was reduced with cancer invasion, to 78% and 64% at superficial invasion and deep invasion sites, respectively. However, p73 expression was not correlated with any other clinicopathological factor. The expressions of p53 and p21 were also investigated in esophageal cancer. To evaluate the status of the p53 gene mutation immunohistochemically, two monoclonal antibodies (DO7 and PAb240) were used. There seemed to be an inverse correlation between p73 expression and p53 mutation. Moreover, the expression of p21 was highly correlated with p73 expression irrespective of the p53 mutation status. In human esophageal cancers, p73 expression decreased with increasing degree of tumor invasion, and its decreased expression in local advanced tumor caused down-regulation of p21 expression, which might reflect tumor progression. (Cancer Sci 2003; 94: 612-617) sophageal cancers have relatively high mortality rates, despite recent progress in cancer diagnosis and treatment.1) In Japan, long-term follow-up data of a total 11 642 esophagectomized cases show that the prognosis still remains poor, with a mean 5-year survival rate of approximately 36%, even if the esophagectomy is curative.2) Moreover, lymph node metastasis frequently occurs in esophageal cancers compared with other gastrointestinal malignancies, resulting in a poor outcome even for esophageal cancer patients detected at an early stage. 3,4) About 40% of esophageal carcinomas with submucosal invasion have already metastasized to the lymph node, 3) and only 60% of esophageal cancer patients with submucosal invasion survive for 5 years. 2)Recent advances in molecular biology have elucidated that various oncogenes and tumor suppressor genes are closely related to the development and progression of esophageal carcinomas.5-11) Inactivation of the INK4a locus or p16 is the most frequent genetic abnormality in esophageal cancers and occurs in the majority of esophageal cancers at the early stage of carcinogenesis.12, 13) Loss or down-regulation of p16 expression in esophageal cancers is attributed to genetic changes such as homozygous deletion or point mutation in addition to epigenetic hypermethylation of the gene.11) Amplification of the cyclin D1 gene is also a well-known genetic change in esophageal cancers and its overexpression is closely related with the invasiveness of cancer cells and the patient's outcome. 5,9) Furthermore, p53 gene mutation is detected in more than half of esophageal carcinomas and a large ...

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Section: Discussionmentioning

confidence: 69%

Synergistic decline in expressions of p73 and p21 with invasion in esophageal cancers

et al. 2003

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“…16 These findings support the concept of field carcinogenesis in the UADT and suggest the presence of common environmental or genetic factors or both associated with the occurrence of cancer.…”

Section: Surgerymentioning

confidence: 99%

Risk factors for esophageal cancer and the multiple occurrence of carcinoma in the upper aerodigestive tract

Morita¹,

Saeki²,

Mori³

et al. 2002

Surgery

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“…Conversely, it is generally agreed that esophageal squamous cell carcinoma originates from dysplastic lesions in the esophageal epithelium. Kuwano et al [11][12][13] and others 14,15 repeatedly described a definite relationship between squamous dysplasia and carcinoma in the esophagus, referring to the multicentric occurrence of esophageal carcinomas. As for the malignant potential of dysplastic lesions in the esophagus, no significant differences between squamous dysplasia and carcinoma were demonstrated in DNA ploidy by Itakura et al, 16 nor in cell proliferative activity by Sugimachi et al 17 These findings support the fact that severe dysplasia in the esophagus should be managed as an extremely early cancerous lesion.…”

Section: Discussionmentioning

confidence: 99%

Multicentric Occurrence of Esophageal Cancer After Gastrectomy: A Preliminary Report

Kitabayashi¹,

Nakano²,

Saitô³

et al. 2001

Surgery Today

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The effect of gastrectomy on the subsequent development of esophageal cancer was investigated, focusing on its multicentric occurrence. We retrospectively evaluated 28 patients who underwent subtotal esophagectomy for intrathoracic esophageal cancer between 1985 and 1999. They were divided into two groups according to whether or not they had previously undergone a gastrectomy: group 1, comprising 7 patients who had undergone gastrectomy and group 2, comprising 21 patients who had not. Clinical profiles of the patients were obtained from the medical records and the whole resected esophagus was histopathologically examined. The interval between gastrectomy and esophagectomy in group 1 was significantly shorter in the patients who had undergone gastrectomy for gastric cancer than in those who had undergone gastrectomy for a peptic ulcer, and also in the patients for whom anastomosis had been performed by Billroth I compared with Billroth II. The patients in group 1 were significantly younger than those in group 2. The multiple occurrence of esophageal cancer was found in 4 of 5 patients (80%) in group 1, and in 2 of 18 patients (11%) in group 2, with significantly higher frequency being seen in group 1. More than two coexisting cancer lesions apart from the primary tumor were detected in all four patients. Histological examination of all the coexisting cancer lesions showed well-differentiated squamous cell carcinoma confined within the superficial mucosal layer. No significant differences were noted in the location of the coexisting lesions between the oral and anal side of the primary tumors. Squamous dysplasia was randomly observed, especially around the cancer lesions. These findings suggest that gastrectomy precipitated subsequent chronic gastroesophageal reflux which in turn induced the development of squamous dysplasia and carcinoma at multiple locations in the esophagus.

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The multicentric occurrence of squamous epithelial dysplasia and squamous cell carcinoma in the esophagus

Cited by 36 publications

References 18 publications

Synergistic decline in expressions of p73 and p21 with invasion in esophageal cancers

Synergistic decline in expressions of p73 and p21 with invasion in esophageal cancers

Risk factors for esophageal cancer and the multiple occurrence of carcinoma in the upper aerodigestive tract

Multicentric Occurrence of Esophageal Cancer After Gastrectomy: A Preliminary Report

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