As independent risk factors, cellular atypia may reconfirm the importance of morphological analysis, and the TAM number may indicate the significance of TAM function in gastric adenoma.
A small cell carcinoma of the extrahepatic bile duct in a 75-year-old Japanese man is reported. The patient suffered from obstructive jaundice, and percutaneous transhepatic cholangiography-drainage (PTCD) revealed a massive lesion in the lower common bile duct. Because it was diagnosed as a malignant tumor, pancreaticoduodenectomy was performed. A nodular infiltrating tumor measuring 4.5 x 3.0 x 2.0 cm was located in the intrapancreatic portion of the extrahepatic bile duct. Histologically, the tumor was composed of a dense proliferation of small atypical cells with a little region of high-grade dysplasia in the adjacent epithelium of the common bile duct. Tumor cells were immunoreactive to neuroendocrine markers such as chromogranin A, synaptophysin, CD56, and Leu7. Although carcinoma cells invaded into pancreas and duodenum, there were no histological findings that indicated the carcinoma arose from the mucosa of either the pancreatic duct or duodenum. These results indicated that the tumor was a small cell carcinoma derived from the epithelium of the extrahepatic bile duct; a rare neoplasm with only a few cases reported. A few neuroendocrine cells were recognized in the adjacent epithelium of the extrahepatic bile duct, suggesting that the tumor cells might be derived from them. Using immunohistochemical examination, no p53 abnormality was found. Tumor cells showed positive nuclear staining for p16, while negative for cyclin D1, suggesting that functional retinoblastoma protein (pRB) might be lost in the p16/pRB pathway, as in small cell lung cancer.
Colorectal cancer incidence in the LSS sample during 1950-80 was investigated. A total of 730 incidence cases of colorectal cancer were confirmed from a variety of sources. Sixty-two percent of the cancers were microscopically verified and 12% were ascertained through death certificate only. The risk of colon cancer increased significantly with intestinal dose, but no definite increase of risk was observed for rectal cancer. Relative risk at 1 Sv and excess risk per 10(4) PY-Sv for colon cancer are 1.80 (90% confidence internal 1.37-2.36) and 0.36 (90% confidence interval 0.06-0.77) respectively. City and sex did not significantly modify the dose-response of colon cancer, but the risk decreased with age at the time of bombings (ATB). The relative risk of colon cancer does not vary substantially over time following exposure. A non-linear dose response did not significantly improve the fit. Further, the anatomic location of the tumors indicate that the cecum and ascending, transverse and descending, and sigmoid colon seem equally sensitive to radiation. No difference in the distribution of tumor histological types could be observed by radiation dose.
Primary anorectal malignant melanoma is a fairly uncommon but highly malignant disease. This disease is sometimes mistaken for such benign conditions as either a hemorrhoid or rectal polyp. We herein describe a case of early primary malignant melanoma of the anal canal. In this case, magnetic resonance (MR) imaging was found to be useful for diagnosing the melanotic melanoma. We especially emphasize the usefulness of a fat-saturation MR image in distinguishing melanotic melanoma from other rectal tumors.
Twenty-eight moderately differentiated adenocarcinomas invading beyond the muscularis propria of the colorectum were subclassified as 13 moderate- and 15 poor-subtype tumors based on the histology at the deeply infiltrating sites. Moderately differentiated cancer cells were correlated with liver metastasis and p53 immunoreactivity. Poorly differentiated cancer cells were correlated with lymph node metastases but not to p53 immunoreactivity. The proliferative cell nuclear antigen (PCNA) labeling index (LI), Ki-67 LI and agyrophilic nuclear organizer regions (AgNOR) values determined for the poorly differentiated cancer cells in the poor-subtype tumors were significantly lower than those of moderately differentiated cancer cells in the moderate-subtype tumors. In cells from tumors classified as poor-subtype, poor differentiation was associated with decreased PCNA LI levels, but with unchanged Ki-67 LI and AgNOR values. These results indicate that colorectal adenocarcinoma cells that are histologically subclassified as moderately differentiated have different proliferative and metastatic activities from cancer cells that are poorly differentiated. Moderately differentiated cancer cells are associated with hematogenous metastasis to liver and high proliferative activity, and loss of tubular formation of cancer cells may be fundamentally related to lymph node metastasis and infiltrative growth.
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