Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exocrine pancreatic neoplasms developed in the guppy Poecilia reticulata following a single brief exposure to methylazoxymethanol acetate [(MAM-Ac) CAS: 592-62-1]. Fish 6-10 days old were exposed to concentrations of MAM-Ac up to 100 mg/liter for 2 hours. Exposed specimens were transferred to carcinogen-free water and sampled periodically for tumor development. Pancreatic neoplasms occurred in approximately 9% of histologically examined individuals exposed to 10 mg MAM-Ac/liter or less. Neoplastic lesions were not found in 122 control specimens. The neoplasms included 6 cases diagnosed as adenoma, 7 cases diagnosed as acinar cell carcinoma, and 2 cases diagnosed as adenocarcinoma. Adenomas consisted mainly of well-differentiated acinar cells that were filled with zymogen granules. Two adenomas also contained foci of atypical, less-differentiated acinar cells possessing basophilic, fibrillar cytoplasm. Acinar cell carcinomas occurred in several cellular patterns that ranged from well-differentiated to more anaplastic lesions; however, none exhibited areas of ductular proliferation. Adenocarcinomas, on the other hand, exhibited a glandular growth pattern and contained numerous ductlike structures. Both types of carcinomas appear to arise from primary acinar cells. Thus lesions probably progress from adenomas to acinar cell carcinomas and adenocarcinomas. The findings of carcinogen-induced pancreatic neoplasms in guppies further strengthen the usefulness of small fish species in carcinogen testing and provide an additional model for pancreatic tumors.
 ...
PMID:Exocrine pancreatic neoplasms induced by methylazoxymethanol acetate in the guppy Poecilia reticulata. 347 May 47

Exocrine pancreatic neoplasms developed in the guppy Poecilia reticulata following exposure to the direct-acting carcinogen methylazoxymethanol acetate (MAM-Ac). Fish 6 to 10 d old were exposed to nominal, non-toxic concentrations of 4 and 10 mg MAM-Ac l(-1) for 2 h and then transferred to carcinogen-free water for grow-out. Whole specimens were sampled monthly up to 9 mo post-exposure to follow the histologic progression of the lesions. No neoplasms occurred in 119 control specimens examined. Pancreatic acinar cell adenomas and carcinomas occurred in 42 of 243 (17%) of the specimens exposed to MAM-Ac. As in earlier studies, specimens exposed to the low MAM-Ac concentration exhibited a higher pancreatic neoplasm incidence (27.8%) than those exposed to the high concentration (7.8%). Acinar cell adenomas accounted for 27 of the 42 neoplasms. Adenomas exhibited a high degree of acinar cell differentiation and some contained foci of atypical acinar cells that were less differentiated and more basophilic than were surrounding adenoma cells. Carcinomas occurred in 15 specimens and exhibited a range of cellular patterns. Although no distant metastases were found, carcinomas tended to invade neighboring tissues and organs. The occurrence of carcinogen-induced pancreatic neoplasms in guppies strengthens the usefulness of small fish species in carcinogen testing and provides an additional model for studying pancreatic neoplasia.
 ...
PMID:Exocrine pancreatic carcinogenesis in the guppy Poecilia reticulata. 1255 47

The immunohistochemical features of 16 cases of papillary cystadenocarcinoma of salivary glands using a panel of monoclonal and polyclonal antibodies were evaluated. The specimens were from patients postoperatively diagnosed as papillary cystadenocarcinoma of salivary glands where the age of the patients ranged from 20-70 years, males were more commonly affected than the females and parotid gland was the most commonly affected site. The cytokeratins detected by MoAb KL1 and K8.12 were positive in all cases showing a heterogeneity in intensity of reaction. A coexpression of vimentin with cytokeratin was found in 10 cases. The tumor cells had a coexpression of S-100 protein and neuron specific enolase (NSE). Glial fibrillary acidic protein (GFAP) was positive in one case with multiple expression of cytokeratins, vimentin NSE, S-100 protein. The polymorphic mucin MAM-6 was positive in all cases and MAM-3 in 8 cases showing different intensity of reaction. The tumor cells were positive for lysozyme (8 cases), lactoferrin (10 cases) and alpha-1-antichymotrypsin (10 cases). The immunoreactive c-erbB-2 oncoprotein on the cell surface membrane was detected in 2 cases. The labeling index of proliferating cell nuclear antigen in the tumor cells ranged from 3.8 to 43.2% (mean 14.2 +/- standard deviation 9.8). Histopathological feature and a heterogeneity of multiple expression of tissue markers may suggest that a population of cells in papillary cystadenocarcinoma may be counterparts of modified myoepithelial cells of pleomorphic adenoma that express epithelial, mesenchymal and neuronal differentiation although the role of myoepithelial cells in the genesis of this tumor is not clear. However, disorganized stratification and malignant transformation of ductal cells may be the most likely possibility in the histogenesis of this tumor.
 ...
PMID:Papillary cystadenocarcinoma of salivary-glands - an immunohistochemical study. 2156 64

We performed a medaka bioassay for the carcinogenicity of methylazoxymethaol acetate (MAM-Ac) to examine the sequential histological changes in the liver from 3 days after exposure until tumor development. The medaka were exposed to MAM-Ac at a concentration of 2 ppm for 24 hours, and were necropsied at 3, 7, 10, 14, 21, 28, 35, 42, 49, 60, and 91 days after exposure. MAM-Ac induced four cases of hepatocellular adenoma and one case of hepatocellular carcinoma in 8 fish after 60 or 91 days of exposure. Histological changes in the liver until tumor development were divided into three phases. In the cytotoxic phase (1-10 days), MAM-Ac-exposed hepatocytes showed vacuolar degeneration and underwent necrosis and apoptosis, resulting in multiple foci of hepatocyte loss. In the repopulation phase (14-35 days), the areas of hepatocyte loss were filled with hepatic cysts and the remaining hepatocytes were surrounded by hepatic stellate-like cells (or spindle cells) and gradually disappeared. In the proliferation phase (42-91 days), the original hepatic parenchyma was regenerated and progressively replaced by regenerative hyperplastic nodules and/or liver neoplasms. The medaka retained a strong hepatocyte regenerative ability in response to liver injury. It is considered that this ability promotes the proliferation of initiated hepatocytes in multistep carcinogenesis and influences the development of liver tumor over a short period in medaka.
 ...
PMID:Sequential histological changes in the liver of medaka exposed to methylazoxymethaol acetate. 3323 40