Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0007097 (carcinoma)
152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to define whether all colonic tumors develop from a single transformed cell, we compared two sites each in 40 early-stage colonic carcinomas by K-ras mutation and DNA ploidy pattern. These 40 colonic carcinomas consisted of 26 protruding-type carcinomas and 14 superficial-type carcinomas. The two sites were selected in every tumor tissue and then DNA ploidy pattern and occurrence of K-ras mutation were detected. In cases of "cancer in adenoma", we compared clonality between cancer cells and adenoma cells. In a cytofluorometrical study, it was shown that diploid patterns were predominantly seen in protruding-type carcinomas (76.9%), whereas many superficial-type carcinomas (64.3%) consisted of aneuploid cells. K-ras mutations were more frequently observed in protruding-type carcinomas: 42.3% in protruding-type compared to 21.4% in superficial-type carcinomas. These findings suggested that superficial-type carcinomas have a different mode of carcinogenesis from that of protruding-type carcinomas. Frequently, each pair of sites of the carcinoma tissue carried the same K-ras mutation, and DNA ploidy patterns were essentially the same. However, we encountered some cancers that showed different K-ras mutations in the cancer tissues. In particular, one case of cancer in adenoma demonstrated different K-ras mutations in the cancer and adenoma tissue. These findings suggest that most colonic cancers develop monoclonally, but there are a few cancers (fewer than 5%) that start multiclonally.
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PMID:A possible multiclonal development in human colonic carcinomas. 779 96

Microsatellites are highly polymorphic, short-tandem repeat sequences dispersed throughout the genome. Instability of these repeat sequences at multiple genetic loci may result from mismatch repair errors and occur in hereditary nonpolyposis colorectal carcinoma and certain sporadic cancers. In non-small cell lung cancer, we found that microsatellite instability was infrequent, affecting only 7 (6.5%) of 108 cases. Despite being observed in all histological subtypes and at different tumor stages, microsatellite instability most commonly affected only one of the six loci tested on five chromosomal arms. In addition, microsatellite instability was associated with extensive, concurrent molecular changes including K-ras and p53 mutations as well as frequent loss of heterozygosity at chromosomal regions 5q, 8p, 9p, 11p, and 17p.
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PMID:Microsatellite instability and other molecular abnormalities in non-small cell lung cancer. 780 35

Intraductal papillary growth of mucin producing hypersecreting, columnar cells characterizes a group of rare pancreatic exocrine neoplasms which we propose to call intraductal papillary-mucinous tumors (IPMT). We analysed the histopathology of 26 IPMT in relation to gastro-enteropancreatic marker expression, genetic changes and biology. Four IPMT showing only mild dysplasia were considered to be adenomas. Nine tumours displayed moderate dysplasia and were regarded as borderline. Severe dysplasia-carcinoma in situ changes were found in 13 IPMT which were therefore classified as intraductal carcinomas. Six of these carcinomas were frankly invasive and two of these had lymph node metastases. The invasive component resembled mucinous non-cystic carcinoma in all but one tumour which showed a ductal invasion pattern. Immunohistochemically, an intestinal marker type was found in most carcinomas, while gastric type differentiation prevailed among adenomas or borderline tumours. K-ras mutations (seven at codon 12 and one at codon 13) were found in 31% of IPMT (2 adenomas, 1 borderline, 5 carcinomas). Nuclear p53 overexpression was detected in 31% of IPMT (6 carcinomas and 2 borderline IPMT) and correlated with p53 mutations (one at exon 8 and the other at exon 5) in two carcinomas. p53 abnormalities were unrelated to K-ras mutation. c-erbB-2 overexpression was observed in 65% of IPMT, with various grades of dysplasia. Twenty-two of 24 patients are alive and well after a mean post-operative follow-up of 41 months. Only two patients, both with invasive cancer at the time of surgery, died of tumour disease. It is concluded that pancreatic IPMT encompass neoplasms which, in general, have a favorable prognosis, but are heterogeneous in regard to grade of dysplasia and marker expression. Adenoma, borderline tumour, intraductal carcinoma and invasive carcinoma can be differentiated. p53 changes but not K-ras mutation or c-erbB-2 overexpression are related to the grade of malignancy. Most IPMT differ in histological structure, marker expression and behaviour from ductal adenocarcinoma.
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PMID:Intraductal papillary-mucinous tumours represent a distinct group of pancreatic neoplasms: an investigation of tumour cell differentiation and K-ras, p53 and c-erbB-2 abnormalities in 26 patients. 782 Mar

Two cases of pancreatic cancer accompanied by pseudocyst are reported. Case 1 was a 60-year-old man who was admitted to our hospital complaining of left lower abdominal discomfort. A cystic lesion, about 3 cm in diameter, was found in the pancreatic tail by ultrasonography (US) and computed tomography (CT). No signs of chronic pancreatitis were found. At operation, an elastic, hard, white tumor, about 1 cm in diameter, was felt adjacent to the cystic lesion on the duodenal side. Histologically, this tumor was a duct cell carcinoma with an adjacent pseudocyst upstream of the pancreas. Case 2 was a 57-year-old man who complained of back pain and loss of body weight. US and CT examination revealed a cystic lesion, 11 x 7 cm in size, in the tail of the pancreas. Histological examination of the resected specimen revealed both a duct cell carcinoma, 3 cm in size, in the body of the pancreas and a pseudocyst, 9 cm in size. Pseudocysts accompanying carcinoma are thought to develop from obstruction of the pancreatic duct by the carcinoma, followed by intraductal high pressure and disruption of ductules upstream of the pancreas. Thus, we should pay careful attention to pseudocyst of the pancreas, especially when signs of diffuse chronic inflammation cannot be found, to help identify duct cell carcinoma in the early stage. Further detailed examinations of the cyst fluid or pancreatic juice, such as cytology, tumor marker determinations, or establishment of K-ras codon 12 mutation, are needed.
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PMID:Pancreatic carcinoma accompanied by pseudocyst: report of two cases. 787 78

K-ras mutations in colorectal tumors (53 carcinomas, 21 adenomas) were investigated using oligonucleotide probes specific for mutations at codon 12, 13, or 61 of the K-ras gene by polymerase chain reaction and oligonucleotide hybridization techniques, and the proliferative activities were assessed immunohistochemically by using anti-proliferating cell nuclear antigen (PCNA), counting PCNA labeling index (LI). Point mutations were observed 18.8% in the adenomas, 40.0% in the intramucosal carcinomas and 27.0% in the invasive carcinomas. Fewer incidences of K-ras mutations in the invasive carcinoma suggested carcinomas without K-ras mutation invade rapidly. Clinicopathologically, K-ras mutation-positive carcinomas tended to show the presence of venous invasion (p < 0.005). There were many distant metastases in the K-ras mutation-positive cases (p = 0.07). Moreover, among adenocarcinomas a significant correlation was demonstrated between PCNA LI and the pattern of infiltrating growth (p < 0.05). Our data imply that the K-ras mutation gains access to invasion and metastasis, as well as the ras mutation occurs at the initiation of the carcinoma. The present data suggest that K-ras mutations in colorectal carcinomas are correlated with venous invasion, while cell proliferative activities are related to stromal invasion, and these factors are independent markers for invasion of colorectal carcinomas.
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PMID:[Cell kinetics of colorectal tumors with assessment by K-ras mutation and PCNA labeling index]. 790 93

We examined the point mutations of codons 12, 13 and 61 in K-ras gene by slot blot hybridization analysis following polymerase chain reaction and genotypes of polymorphic N-acetyltransferase (NAT) by Southern blot analysis in 36 colorectal carcinoma tissues obtained at surgery. NAT genotypes of 36 autopsied livers from patients without colorectal carcinoma were also determined to compare the populations of each polymorphic NAT genotype in the patients with or without the neoplasm. Genetically, 44.4% (16 cases), 47.2% (17 cases) and 8.3% (3 cases) of patients with colorectal carcinoma were classified as rapid, intermediate and slow acetylators, respectively. Point mutations of K-ras gene were detected in eight carcinomas out of 16 rapid acetylators, two out of 17 intermediate acetylators and one out of three slow acetylators. In control livers, 52.8% (19 cases), 38.9% (14 cases) and 8.3% (3 cases) were classified as rapid, intermediate and slow acetylators, respectively. The occurrence of K-ras gene point mutations was closely linked to rapid acetylator genotype, although there was no statistical difference of NAT genotypes between the group of patients with colorectal carcinoma and the group of controls.
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PMID:Relation between the occurrence of K-ras gene point mutations and genotypes of polymorphic N-acetyltransferase in human colorectal carcinomas. 791 23

The aim was to determine whether proton magnetic resonance spectroscopy (MRS) could grade human colorectal cells of differing malignant potential. A cell model of tumour development and progression comprising 2 non-tumorigenic adenoma lines and 4 carcinoma lines of increasing tumorigenicity was chosen. A gradual reduction in cellular differentiation and an accumulation of genetic alterations from adenoma to carcinoma characterized the selected cell lines. One-dimensional and 2-dimensional MRS showed that reduced differentiation in the cell model correlated with an increase in the levels of lipid, metabolites, the glycosylation intermediate uridine diphospho-N-acetylglucosamine and cell-surface fucosylation. Mutations involving the K-ras, APC and DCC genes are present both in adenoma- and in carcinoma-derived lines in this model, but the first evidence of an abnormality in the p53 gene was concomitant with the cells' ability to grow as a tumour in athymic nude mice. This genetic change coincided with the detection, by MRS, of UDP-hexose (ribose moiety, 2D MRS cross peak between H2 at 4.38 ppm and HI at 5.99 ppm) and the appearance of an additional fucosyl resonance (cross peak between-CH3 at 1.41 and H5 at 4.30 ppm) in the least tumorigenic of the carcinoma cell lines. An increase in complexity of the fucosylation spectral pattern was observed with further cellular de-differentiation and increased tumorigenicity. Collectively these data support the existence of an adenoma-carcinoma sequence.
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PMID:Correlation of cellular differentiation in human colorectal carcinoma and adenoma cell lines with metabolite profiles determined by 1H magnetic resonance spectroscopy. 792 26

Several recently developed techniques have been applied to the study of endometrial lesions. These include the evaluation of K-ras abnormalities in patients with endometrial hyperplasia to identify those at high risk to develop carcinoma, the analysis of p53 abnormalities to distinguish between endometrial hyperplasia and carcinoma, the use of p53 for predicting clinical outcome in patients with endometrial carcinoma, and PCNA immunostaining of endometrial lesions with secretory activity. However, these studies should be regarded at this juncture as auxiliary, at best, to the cytological and histopathologic examination of human endometrial disorders.
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PMID:New concepts in the diagnosis and prognosis of endometrial carcinoma. 793 50

The bad prognosis of exocrine pancreas carcinoma manifests itself by a high incidence of recidivation, early metastasis formation and a low 5-year survival rate of 1-2% on an average has not essentially been improved in recent times although progress is evident in diagnosis as well as in surgical, radiological and cytostatic therapy. The unfavourable course of illnesses is due to the symptomless early phase rather than the existing diagnostic potential. Thus, a recording, standardization and definition of pancreatic duct atypias is a necessity for optimizing the pattern of examinations. Topographically, the structure of pancreatic parenchyma may be classified by 1) interlobular ducts; 2) intralobular ducts; 3) intercalated ducts; 4) centroacinar cells, and 5) acinar cells. Based on this matrix, entities of varying diagnostic relevance may be derived, i.e. 1) orthological histiomorphological tissue formations; 2) hyperplastic epithelial changes; 3) metaplastic epithelial formations; and 4) atypical hyperplasias. Beyond this, there are numerous indications of a redifferentiation of numerous pancreatic cell types, primarily of acinar cells. The close relationships between ductal and acinar cells may be subsumed as a terminal ductulo-acinar intercalated duct complex. Against the background of chronic pancreatitis and corresponding length of history (< 6.5 years), cancer may develop in up to 16% of cases. On the molecularbiological level, point mutations of the K-ras gene, a mutation or deletion of the p53 suppressor gene and an excess production of the c-erbB-2 protooncogene are found in a great number of pancreatic carcinomas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lesions of the pancreatic duct epithelium and histogenesis of exocrine pancreatic carcinomas]. 794 29

High molecular weight DNA isolated from 14 primary tumour tissues of human oral carcinoma patients was analysed for transforming activity by NIH3T3 co-transfection assay using pSV2neo gene as a selectable marker, followed by nude mouse tumorigenicity assay. Ten of the patient tumour tissues demonstrated molecular lesions in myc, ras or/and EGF-R genes, whereas 4 patients did not show tumour associated aberrations in these oncogenes. The G418-resistant transfected cells from 12 of 14 individual patients demonstrated transforming potential by colony formation in soft agar and tumour induction in nude mice within 25-80 days. DNAs from the transfected cells, consequent nude mice tumours and corresponding cell lines, contained human Alu sequences. Southern blot hybridisation with ras, myc, EGF-R oncogenes demonstrated the presence of human H-ras oncogene in one of the 12 sets of nude mice tumours. In contrast, DNA from the other 11 sets of nude mice tumours indicated absence of c-myc, N-myc, L-myc, H-ras, K-ras, N-ras and EGF-R genes on Southern analysis. Further, DNAs from five first cycle tumorigenic transformants were subjected to a second cycle of transfection, and induced tumours in nude mice with a shorter latency period of 21-50 days. The secondary transformants contained discrete human Alu sequences; however, the DNA did not hybridise with myc/ras/EGF-R probes. A genomic library was constructed from a second cycle nude mice tumour, using EMBL-3 as the vector. Four human Alu sequence positive clones were isolated on screening 2 x 10(5) plaques, and one of the recombinant clones subjected to fine restriction mapping using 16 restriction enzymes. The lack of association of the nude mice tumour DNA with myc/ras/EGF-R showing aberrations in the primary human tumour, implies activation of an alternative potent transforming gene(s) in the chewing tobacco-related oral carcinomas in India.
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PMID:Detection and cloning of potent transforming gene(s) from chewing tobacco-related human oral carcinomas. 795 Aug 42


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