Abstract
Familial adenomatous polyposis（FAP）is frequently complicated by gastric lesions, which is common in many FAP pedigrees. Gastric lesions complicated by FAP include histologically different lesion types such as fundic gland polyps, gastric adenomas and gastric cancers. Fundic gland polyps are pathologically classified as hamartoma and is a distinct gastric lesion accompanying FAP with high incidence. There have recently been a few reports of FAP case in which a portion of this fundic gland polyp appeared to develop gastric carcinogenesis by dysplasia during long-term observation. Onset of adenoma is characterized by localization in the pyloric antrum, occurrence in younger people, and a high tendency toward multifocality. However, macroscopic and microscopic findings of gastric adenoma complicated by FAP are not different from those of normal gastric adenoma. This phenomenon of carcinogenesis of gastric adenomas is not considered specific to gastric adenoma in FAP. It has been reported that the complication rate of FAP by gastric cancer is approximately 5％. Most cases develop gastric cancer in the gastric antrum and whose clinical features are not uniform in histological type or depth of tumor invasion. However, the mechanism of gastric carcinogenesis in FAP is still unclear. We report here a 51-year-old female with FAP who developed advanced gastric cancer with multiple hepatic metastase after longterm observation. Gastric cancer arose from the upper gastric body. There was nodetectable adenoma in the vicinity of cancer or dysplasia of fundic gland polyp. However, some areas with atypical cells were found near the cancer. Focusing on these areas, p53 and cytokeratin 7 expressions were observed immunohistochemically and double staining consistently demonstrated two concurrent protein expressions. In this case, p53 and cytokeratin 7 expressions may be associated as the mechanisms of gastric carcinogenesis.
