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)

The rising incidence of colorectal carcinoma, particularly in the industrial nations of Europe and USA, directs the attention to the aetiological factors of these tumors: nutrition, the association with colorectal adenoma, familiarly genetic disorders as familiar adenomatous polyposis and hereditary non polyposis colorectal cancer. Some aspects of molecular biology are discussed. Furthermore, right and left part of the colon (divided by the Cannon-Boehm point) and the neoplasms of these sections of the colon are different in embryology, function and morphology. The cancers of the right colon develop without polypoid changes, those of the left part in majority via the adenoma-carcinoma sequence. It is possible to demonstrate differences between these two localizations in the DNA-content (diploid tumors on the right side), in the lost of allels (especially distal tumors), in proliferation activity (lower in right side tumors) and in the expression of oncofetal antigens. Besides, there are some histological differences between neoplasms of the right and left colon (production of mucin, "Crohns like lymphoid reaction" histological grading). In our own material of 262 patients with resected colon carcinoma we have investigated the distribution of carcinoma in the right and left colon, furthermore the T-classification, histological grading and the proportion of mucinous carcinoma in the different tumor localizations.
 ...
PMID:[Tumor genesis and prognostic factors in colorectal carcinoma with special consideration of tumor localization]. 1067 92

Intraductal papillary-mucinous tumour is clinicopathologically characterized by papillary growth and mucin production within the pancreatic duct system. The category includes a wide range of dysplasia, ranging from adenoma to carcinoma, the latter designated as intraductal papillary-mucinous cancer. In general, the tumor renders a favorable prognosis after complete resection. However, intraductal papillary-mucinous tumor with overt invasion outside the gland has been reported to have a poor prognosis, as is the case with the usual type of duct cell cancer of the pancreas. We experienced two cases of intraductal papillary-mucinous cancer with obstructive jaundice due to impaction of thick mucus protruding from the pancreas via a "spontaneous" biliopancreatic fistula. Preoperative examinations of both patients showed a large intraductal papillary-mucinous tumor in the head of the pancreas with fistula formation between the intrapancreatic portion of the common bile duct and the main pancreatic duct. Histopathological investigation of the two resected specimens suggested that the fistula may not have developed from invasion by papillary or tubular adenocarcinoma, but from compression and destruction of the intercalating tissues by abundant mucinous secretion. The first patient died of peritoneal carcinomatosis with clinicopathologic features of pseudomyxoma peritonei 6 years after surgery. The second patient is alive and has been well for 2 years postoperatively. Review of the world literature showed that half of the patients with intraductal papillary-mucinous cancer plus biliopancreatic fistula had no stromal invasion around the fistula, indicating that the fistula might have been caused by mechanical pressure. However, the other half of the cases did have stromal invasion around the fistula. Two-thirds of these cases, including our own patients, had foci of mucinous carcinoma in the stroma around the fistulization, implying that mucinous lakes in the stroma may have served as part of the "waterway" from the pancreatic duct to the bile duct, assisted by increased pressure by mucus production. Since intraductal papillary-mucinous cancer with biliopancreatic fistula has a comparatively favorable prognosis, surgical resection should be considered.
 ...
PMID:Biliopancreatic fistula associated with intraductal papillary-mucinous pancreatic cancer: institutional experience and review of the literature. 1102 Sep 5

Several studies have been demonstrated the value of c-ErbB-2 and Bcl-2 in predicting the biological behaviour of tumors. The aim of this study was to investigate Bcl-2 and c-ErbB-2 expression in colorectal carcinomas and the correlation between their presence and other clinicopathologic parameters. Eighty-six colorectal carcinomas and 17 adenomas were stained with Bcl-2 and c-ErbB-2 immunohistochemically. Staining patterns were assessed semi-quantitatively and correlated with tumor size, Duke s classification, tumor differentiation, mucinous characteristic and anatomic locations. We detected Bcl-2 expression in 10 of 17 adenomas (58.8 %) and 31 of 86 carcinomas (36.04 %). Positive staining in normal mucosa was observed only in the compartment of cryptic cells. However neither the difference in the rates of Bcl-2 positivity in adenoma and carcinoma groups, nor the correlation with other mentioned clinicopathological parameters, were found statistically significant. Bcl-2 expression was found to be significantly high in mucinous carcinomas. Expression of c-ErbB-2 was observed in 12 of 86 (13.95 %) carcinomas. It was not detected in adenomas and normal mucosa. Although the incidence of c-ErbB-2 in nonmucinous carcinoma was higher than that of mucinous carcinoma, this was not significant. In addition we were unable to show any significant relation between c-ErbB-2 expression and other clinicopathologic features. Our result suggest that c-ErbB-2 protein expression in colorectal carcinomas, is not very frequent event. There is no correlation between c-ErbB-2 expression and malignant potential of colorectal carcinomas. Higher expressions of Bcl-2 in adenomas than carcinomas suggest us a possible role of Bcl-2 in early carcinogenesis of colon. However since we were unable to find any significant correlation between Bcl-2 expression and other parameters the impact of this gene on biological behavior is still unclear for us.
 ...
PMID:Expression of Bcl-2 and c-ErbB-2 in colorectal neoplasia. 1134 16

IPMTs (intraductal papillary-mucinous tumors) of the pancreas have been recognized as a distinct clinical entity. WHO used this term in most recent classification (1996). The present report reviews the WHO classification and recent descriptions of IPMT. Problems regarding the histological diagnosis and differential diagnosis are also discussed. In the WHO classification, IPMTs are classified into three categories: intraductal papillary-mucinous adenoma, intraductal papillary-mucinous tumor with moderate dysplasia and intraductal papillary-mucinous carcinoma. The classification is based on the tissue morphology, such as degree of dysplasia and pattern of proliferation. Some immunohistochemical and molecular markers have been reported for differential diagnosis and estimating the prognosis of IPMT. MUC1, Dpc-4, p53 and Ki-67. In making a differential diagnosis, mucinous cystic tumors are the most problematic. Communication with the pancreatic ducts, the presence of ovarian type stroma and capsular formation are key histological factors for a differential diagnosis between IPMTs and mucinous cystic tumors. The prognosis of IPMTs is favorable in general. However, once massive invasion has occurred, the prognosis is very poor, as in cases of ductal carcinoma. For further studies of IPMT, pathologists and clinicians involved in the diagnosis and treatment of IPMTs need to understand the concept of IPMTs and use the WHO classification.
 ...
PMID:Problems in histological diagnosis of intraductal papillary-mucinous tumor (IPMT). 1149 Aug 51

We investigated the adenoma-carcinoma sequence in intraductal papillary-mucinous neoplasm from the aspect of genetic changes. The formalin-fixed paraffin-embedded tumors and surrounding normal pancreatic tissues from patients with 16 intraductal papillary-mucinous adenoma of the pancreas (IPMA) and 10 intraductal papillary-mucinous carcinoma of the pancreas (IPMC) were provided for DNA extraction after microdissection. SSCP-DNA sequencing analysis demonstrated K-ras mutations at codon 12 in 75% of IPMA and 70% of IPMC, while those at codon 13 were observed neither in IPMA nor IPMC. There were no characteristic K-ras mutation types in IPMA and IPMC and no significant differences in incidence of K-ras mutations between the two categories. The frequencies of p53 mutations analyzed by SSCP-DNA sequencing were not high in IPMA (18.8%) and IPMC (30%), showing no significant difference between them. LOHs of APC in IPMA and IPMC were infrequent (6.3 and 20%, respectively) and showed no significant difference in incidence between the two categories. The LOH frequencies of DCC in IPMA and IPMC were 31.3 and 40%, respectively, and were not statistically different from each other. Taken together, genetic changes such as K-ras, p53, APC and DCC mutations may not be associated with adenoma-carcinoma sequence in intraductal papillary-mucinous neoplasm of pancreas.
 ...
PMID:Genetic alterations in adenoma-carcinoma sequencing of intraductal papillary-mucinous neoplasm of the pancreas. 1237 Jul 56

Pleomorphic adenoma of the breast is a rare, benign tumor accounting for 68 cases in the literature. It is most commonly seen in postmenopausal women and is characterized by an admixture of epithelial and myoepithelial cells embedded in abundant myxomatous stroma. Its clinical and histologic appearance can be challenging and may lead to a misdiagnosis of invasive carcinoma. We report a case of mammary pleomorphic adenoma in an asymptomatic 59-year-old woman and briefly discuss its distinction from mucinous carcinoma through the use of special stains.
 ...
PMID:Pleomorphic adenoma of the breast. A case report and distinction from mucinous carcinoma. 1268 78

MIB-1 antibody staining discriminates the cells in phases other than G0 of the cell cycle. The current study examined the proliferative activity assessed by MIB-1 antibody in colorectal adenoma, primary lesions of colorectal carcinoma (CRC) to investigate the relation between the histologic atypia, the proliferative, infiltrative, and metastatic activities. The MIB-1 antibody positive rate was immunohistologically determined in primary lesions in 311 patients, 22 having adenoma or carcinoma in situ, 207 invasive CRC without distant metastasis, and 82 invasive CRC with distant metastasis. The MIB-1 antibody positive rate was significantly higher in cases of adenoma with severe atypia and carcinoma in situ, showing a close relation between histologic atypia and proliferative activity. Among invasive CRC, the positive rate in poorly differentiated adenocarcinoma and mucinous carcinoma is significantly lower than in well differentiated and moderately differentiated adenocarcinomas. The positive rate was significantly lower in carcinomas with subserosa or deeper invasion than in carcinomas with submucosa or muscularis propria invasion, showing no distinct relation between the proliferative activity and the infiltrative activity. The positive rate of primary lesion was significantly lower in cases with metachronous liver or lung metastasis than in synchronous cases, indicating that metachronous hematogenous metastasis occurs even in cancers with low proliferative activity. The MIB-1 antibody positive rate showed a close relation between histologic atypia and proliferative activity in mucosal colorectal tumors although its relation with infiltrative activity was unclear in invasive CRC. It was apparent that metachronous hematogenous cancer metastasis might take place even in cases with low proliferative activity.
 ...
PMID:Proliferative, infiltrative, and metastatic activities in colorectal tumors assessed by MIB-1 antibody. 1453 89

Hereditary non-polyposis colorectal cancer (HNPCC) accounts for approximately 2 to 4% of the total colorectal cancer burden. For economic reasons a diagnostic "stepladder" is recommended. After evaluation of the family history, diagnostic microsatellite instability (MSI) analysis has found its place as a valuable screening tool for HNPCC. Immunohistochemical analysis can help to pinpoint the affected gene. The detection of a mutation in one of the responsible mismatch repair gene confirmed the diagnosis HNPCC. Here we demonstrate our experience of some important pitfalls that will be discussed in this study. In MSI testing, one potential source for false-negative results is intralesional heterogeneity. We demonstrate examples of a flat adenoma and a carcinoma, which required laser microdissection to correctly determine the microsatellite status. In these lesions manual microdissection, the most frequently applied method, was not sufficient. However, the number of cells obtained by using laser microdisssection can fall below a necessary minimum, which can also cause false-negative results of MSI analysis, as shown here in a mucinous carcinoma. In addition, evaluation of immunohistochemically stained tissue slides requires experience to avoid false-positive or false-negative interpretation. A case with two synchronous colorectal cancers revealed loss of MSH2 expression in one carcinoma, whereas the second carcinoma stained positively leading to a false-negative interpretation. In some cases, false-positive results can be obtained, if a perinuclear-staining pattern is interpreted as positive. In summary, there are several potential pitfalls in the molecular screening for HNPCC. Therefore the importance of correct interpretation of clinical data, immunohistochemistry, and microsatellite analysis in combination, performed by a pathologist with experience in molecular genetics is essential. In addition, laser microdissection of tumor areas that have been chosen by a pathologist is highly recommended in cases that cannot be resolved with manual microdissection.
 ...
PMID:Challenges and pitfalls in HNPCC screening by microsatellite analysis and immunohistochemistry. 1550 69

KOC (K homology domain containing protein overexpressed in cancer) is a novel oncofetal RNA-binding protein highly expressed in pancreatic carcinomas. Recently, Corixa Corporation developed a monoclonal antibody specific for KOC that can be used with standard immunohistochemical techniques. The purposes of this study were 1) to assess KOC mRNA expression in pancreatic carcinoma, 2) to determine the pattern of KOC immunoexpression among benign, borderline, and malignant pancreatic epithelial lesions, and 3) to evaluate the utility of the KOC antibody in distinguishing between these entities. mRNA was isolated from fresh pancreatic tissues (19 carcinomas, 2 normal pancreas, 1 chronic pancreatitis) and amplified using standard RT-PCR techniques. Fifteen of 19 (79%) carcinomas overexpressed KOC mRNA relative to non-neoplastic tissue samples and expression increased progressively with tumor stage: the mean copy number of KOC mRNA transcripts was 1.5, 11.1, 31, and 28 for stage I, II, III, and IV carcinomas, respectively, compared with 0.9 and 1 for normal pancreatic tissue and chronic pancreatitis, respectively. Immunostains using the KOC antibody were performed on 50 surgical resection specimens (38 invasive adenocarcinomas, 3 intraductal papillary-mucinous neoplasms, 2 mucinous cystic neoplasms, 7 chronic pancreatitis). KOC staining was present in 37 of 38 (97%) carcinomas: the staining reaction was moderate or strong in 36 of 38 (94%) and present in >50% of the tumor cells in 35 of 38 (92%) cases. Severe dysplasia of the ductal epithelium, present in 19 foci of intraductal papillary mucinous carcinoma, mucinous cystadenocarcinoma, and grade 3 pancreatic intraepithelial neoplasia (PanIN3) showed strong or moderate staining in 15 (79%) cases, whereas foci of mild and moderate dysplasia (intraductal papillary-mucinous neoplasms and mucinous cystic neoplasms with adenoma and/or moderate dysplasia, PanIN1, and PanIN2) were uniformly negative for this marker in 25 and 22 cases, respectively. In the normal pancreas, weak background staining of acini was present in 12 of 50 (24%) cases but was easily distinguishable from the type of staining identified in neoplastic epithelium, and benign ducts and ductules were negative in all cases. Four of 38 (11%) foci of chronic pancreatitis, present in the 7 resections performed for chronic pancreatitis as well as 31 foci of peritumoral chronic pancreatitis, showed weak staining in <10% of the ductules. We conclude that KOC is a sensitive and specific marker for carcinomas and high-grade dysplastic lesions of the pancreatic ductal epithelium. Therefore, immunostains directed against KOC may be of diagnostic utility in the evaluation of pancreatic lesions, particularly when biopsy material is limited.
 ...
PMID:KOC (K homology domain containing protein overexpressed in cancer): a novel molecular marker that distinguishes between benign and malignant lesions of the pancreas. 1564 75

Most pancreatic neoplasia are of ductal lineage, characterized by tubule (gland), cyst, papilla, or mucin formation and expression of mucin-related glycoproteins and oncoproteins (eg, MUC1, CA19-9, CEA, DUPAN), as well as some subsets of cytokeratin (eg, CK19). Mutations of k-ras oncogene and DPC4 are also common in ductal neoplasia and generally not seen in nonductal tumors. A variety of pancreatic neoplasia fall under the heading of ductal neoplasia. Invasive ductal adenocarcinoma (DA) is the most important and constitutes the vast majority (>85%) of pancreatic tumors. DA is characterized by insidious infiltration and rapid dissemination, despite its relatively well-differentiated histologic appearance. In some variants of DA such as undifferentiated or sarcomatoid, evidence of ductal differentiation may be lacking or only focal. The presumed precursors of DA are microscopic intraductal proliferative changes that are now termed pancreatic intraepithelial neoplasia (PanIN). PanINs comprise a neoplastic transformation ranging from early mucinous change (PanIN-1A) to frank CIS (PanIN-3). A similar (in situ) neoplastic spectrum also characterizes intraductal papillary mucinous neoplasms and mucinous cystic neoplasms, which are cystic ductal-mucinous tumors with varying degrees of papilla formation, and may be associated with invasive carcinoma. As such, these can be regarded as mass-forming preinvasive neoplasia. Some intraductal papillary mucinous neoplasms are associated with invasive carcinoma of the colloid type. Colloid carcinoma of the pancreas appears to be a clinicopathologically distinct tumor with indolent behavior. Whereas most ductal pancreatic neoplasia are characterized by some degree of mucin formation, serous tumors, of which serous (microcystic) adenoma is the sole example, lack mucin formation, presumably because they recapitulate centroacinar ducts. They are typically benign tumors. It is recognized now that pancreatic carcinoma, like other malignant processes, is a genetic disease produced by progressive mutations in cancer-related genes. These alterations can be categorized as "early" such as k-ras mutation, HER-2/neu, PSCA, MUC5, and fascin overexpression; "intermediate" such as p16 inactivation, MUC1, and cyclin D1 overexpression; and finally as "late" such as p53 and DPC4 inactivation, BRCA2 mutation, and overexpression of ki-67, 14-3-3sigma, and mesothelin. Ductal neoplasia is the most important category among pancreatic tumors. It is important to appreciate the different types of ductal tumors because they vary greatly in their clinicopathologic characteristics and prognosis. Understanding the molecular mechanisms of ductal carcinogenesis will help develop more efficient prevention and therapy of these tumors.
 ...
PMID:Ductal neoplasia of the pancreas: nosologic, clinicopathologic, and biologic aspects. 1618 79


<< Previous 1 2 3 4 5 6 Next >>