Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most pancreatic adenocarcinomas are known to have ras gene (oncogene) mutations. The site of the mutations is localized in codon 12 of K-ras gene. Such high incidence and localization of the ras gene mutations have not been observed in any other human malignancies. Polymerase chain reaction and direct sequencing method enabled us to analyze DNA sequence around codon 12 of K-ras gene in small quantities of specimens obtained from needle biopsies and aspirate samples for pathological diagnosis. All the materials obtained from 12 patients with pancreatic adenocarcinoma showed the mutations, whereas those obtained from 6 patients with chronic pancreatitis showed no mutations. In several cases using the mutations of K-ras gene as a marker, this analysis supplemented conventional pathology and cytology in making the diagnosis of pancreatic adenocarcinoma. The analysis of ras-gene mutations was useful for the clinical diagnosis of pancreatic adenocarcinoma.
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PMID:Clinical application of ras gene mutation for diagnosis of pancreatic adenocarcinoma. 198 26

The incidence of the point mutation of K-ras oncogene at codon 12 in surgical or autopsy specimens of pancreatic carcinoma (PC) is reportedly extremely high ranging from 75 to over 90%, and the K-ras mutation found in PC is almost exclusively present in codon 12. The GGT to GAT transition of the 12th codon is observed in more than 50% of PC of Japanese patients, although the incidences of transition of GGT to CGT, GTT, and GAT are essentially equal in PC of European countries. With this point in mind, the authors attempted to detect K-ras mutations in DNA obtained from pancreatic juice (PJ) collected endoscopically. K-ras mutations at codon 12 were found in 55% of 20 PC patients by PCR and ASO probe hybridization method, and in 80% of 25 PC patients by PCR-RFLP method. On the other hand, K-ras mutations were negative in PJ from chronic pancreatitis with one exception by PCR-RFLP method. Other authors also reported almost the same results. These results suggest that analysis of K-ras oncogene in PJ can be useful for qualitative diagnosis of PC, and would be expected as a novel tool for early detection of PC.
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PMID:[Mutation of the K-ras oncogene in pancreatic carcinoma, and application of its detection in pancreatic juice to diagnose pancreatic carcinoma]. 769 81

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

Most of the recently developed tumor antigens detected by monoclonal antibodies are sugar chains and frequently associated with blood group substance. By immunohistochemical studies, we evaluated mainly the clinical usefulness and significance of the serum assay of CA-50 classified as a type 1 sugar chain, sialyl SSEA-1 as a type 2 sugar chain, and ST-439 with an undetermined structure, as well as their clinicopathological significance. In addition, the value of measurement of CA19-9, ST-439, and SLX in pure pancreatic juice (PPJ) was investigated. Furthermore, the clinical usefulness of K-ras mutation at codon 12 (KRM) in PPJ was studied. The incidence of serum CA19-9 among tumor markers was highest in pancreatic cancer (81%), but relatively high in benign diseases. On the other hand, both serological and immunohistological studies showed that sialyl SSEA-1 and ST-439 were highly specific for the tumor, whereas they appeared in serum or tumor less frequently than CA19-9 or CA-50 carrying the type 1 sugar chain. The accuracy of the tumor markers (CA19-9, sialyl SSEA-1, and ST-439) for pancreatic cancer, was almost equal (77% to 80%) and higher than that of CEA (69%). However, a highly positive correlation between sialyl SSEA-1 and ST-439 was revealed as well as among type 1 sugar chains in malignant diseases. Therefore, we conclude that the combination assay with CA19-9 or a similar tumor marker, sialyl SSEA-1 or ST-439, and CEA would be appropriate for the screening of pancreatic cancer. When the cut off value was set as the M + 2SD of the controls, significantly elevated concentrations of CA19-9 in PPJ were found in the secretory phase in 90% of the patients with pancreatic cancer (PC) and 66% of the patients with chronic pancreatitis (CP). Although increased concentrations of CA19-9 in PPJ have no cancer specificity, measurement of CA19-9 in PPJ can be used as a sensitive marker for some pancreatic disorders. On the other hand, concentrations of ST-439 and SLX in PPJ were significantly increased only in PC, and their incidences were 50% and 40%, respectively. They have a high tumor-specificity, but their incidences were not as high as initially expected.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinical usefulness of tumor markers associated with pancreatic cancer]. 790 65

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

Pancreatic adenocarcinoma is the fifth leading cause of cancer death in the United States. Mutations in the K-ras oncogene occur in 85% of pancreatic adenocarcinomas and have also been identified in 75% of pancreatic ducts with mucinous cell hyperplasia seen in association with chronic pancreatitis. We identified K-ras mutations in 65% of duct lesions associated not only with chronic pancreatitis but also with pancreatic adenocarcinoma and distal common bile duct carcinoma (cholangiocarcinoma). These observations make K-ras a potential candidate for a gene-based diagnostic test. Indeed, K-ras mutations have been demonstrated in the pancreatic secretions of patients with pancreatic carcinoma and pancreatic intraductal neoplasia. We analyzed stool specimens for mutated K-ras sequences using a plaque hybridization assay in patients with pancreatic adenocarcinoma, cholangiocarcinoma, and chronic pancreatitis. K-ras mutations were detected in stool specimens from 6 of 11 patients with pancreatic adenocarcinoma, from 2 of 3 patients with cholangiocarcinoma, and from 1 of 3 patients with chronic pancreatitis. The K-ras mutations found in stool specimens from patients with pancreatic carcinoma were identical to those in the primary cancer in five cases. Mutations found in the stool specimens from one patient with pancreatic cancer, one patient with chronic pancreatitis, and two patients with cholangiocarcinoma were the same as those identified in pancreatic ductal mucinous cell hyperplasia lesions present in the resected pancreas specimens. Our data suggest that the K-ras mutations originating from cells of pancreatic adenocarcinomas and from cells shed by abnormal pancreatic duct epithelium can be detected in the stool. These results support the further exploration of stool K-ras analysis as a potential screening assay for the early detection of pancreatic adenocarcinoma and precursor lesions such as pancreatic ductal mucinous cell hyperplasia.
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PMID:Detection of K-ras mutations in the stool of patients with pancreatic adenocarcinoma and pancreatic ductal hyperplasia. 801 83

Point mutations in K-ras codon 12 were detected in 7 of 10 specimens (70%) of frozen tissues. To determine when point mutations appear in the oncogenic stage, paraffin-embedded tissues of pancreatic cancer, hyperplastic ductal lesions in pancreatic cancer and in chronic pancreatitis were used. DNA extracted from the paraffin-embedded tissues classified as cancer, atypical and nonatypical hyperplasia of the pancreatic duct epithelium, and normal tissue from pancreatic cancer patients and those classified as atypical hyperplasia of the pancreatic duct epithelium and normal tissue from chronic pancreatitis patients were amplified by the polymerase chain reaction (PCR) method. Point mutations were detected in 8 of 17 cancer cases (47.0%). In 5 of 8 point mutation positive cases, atypical hyperplasias were found in the surrounding tissues. In all 5 of these atypical hyperplasia, point mutations, that is, GGT-GTT (Gly-Val) and GGT-GAT (Gly-Asp), were detected. The same transitions were observed in the cancer of these 5 cases. These results suggest a strong relationship between cancer and atypical hyperplasia surrounding cancer. Although atypical hyperplasia around cancer was histologically very similar to that found in chronic pancreatitis, all 5 atypical and 5 nonatypical hyperplasias in chronic pancreatitis were negative for ras point mutation. Thus, the result argues against an association between chronic pancreatitis and pancreatic cancer.
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PMID:The role of Ras mutation in pancreatic cancer, precancerous lesions, and chronic pancreatitis. 811 25

Pancreatic cancer is detected on the basis of morphological changes delineated by means of various image-diagnostic methods. However, differentiation between chronic pancreatitis and pancreatic cancer, especially at the early stage, is not always simple when based upon the morphological changes alone. Therefore, we attempted to elucidate K-ras mutations in the sediment of pure pancreatic juice (PPJ) containing exfoliated ductal pancreatic cancer cells. PPJ was collected endoscopically from 20 patients with pancreatic cancer (PC) and 18 patients with chronic pancreatitis (CP). Polymerase chain reaction and allele specific oligonucleotide dot blot hybridization for K-ras mutations were performed with the DNA extracted from these samples. A K-ras mutation at codon 12 was identified in the PPJ of 11/20 (55%) of the patients with PC. On the other hand, the same mutation was not identified in the PPJ of any patient with CP. Moreover, K-ras mutations at codons 13 and 61 were not recognized in the PPJ of any patient with either PC or CP. These findings suggested that the presence of a K-ras mutation at codon 12 in PPJ would be useful in confirming the diagnosis of PC.
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PMID:Identification of K-ras oncogene mutations in the pure pancreatic juice of patients with ductal pancreatic cancers. 840 63

Pancreatic adenocarcinomas are known to have a high incidence of K-ras gene mutations. Differential diagnosis of pancreatic cancer and chronic pancreatitis sometimes presents a clinical dilemma. We recently developed a highly sensitive and specific polymerase chain reaction capable of detecting 3-30 copies of mutant K-ras genes harboring codon 12 single base changes in the presence of 300,000 normal copies. Mutant ras genes were detected in DNA purified from pancreatic juice from all 6 cases of pancreatic adenocarcinoma and 1 case of intraductal papillary neoplasms of the pancreas. In 2 of 6 other cases with pancreatic adenocarcinoma, circulating metastatic cells were detected in DNA purified from peripheral blood. Activated ras genes were not found in pancreatic juice of three control cases (chronic pancreatitis and choledocholithiasis) or in the peripheral blood of two patients with insulinomas. Notable conclusions of this study are that there can be significant levels of shed tumor cells in peripheral blood and an even higher number in pancreatic juice. In addition, two different K-ras mutations were found in some patients.
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PMID:Detection of ras gene mutations in pancreatic juice and peripheral blood of patients with pancreatic adenocarcinoma. 849 7

The present study was undertaken to detect K-ras oncogene point mutations at codon 12 in pure pancreatic juice (PPJ) by the hybridization protection assay (HPA) method for the diagnosis of pancreatic cancer (PC). This assay can be carried out within 30 min and can determine not only the presence of a mutation, but also the mutational type of K-ras at codon 12. The minimal ratio of mutant DNA detectable by the HPA was 5-10% of the total DNA. PPJ was collected through a cannula under duodenal fiberscope control from 20 patients with PC and 20 patients with chronic pancreatitis (CP). Analysis of PPJ by the HPA revealed that the incidence of K-ras point mutations at codon 12 was 55% (11/20) in patients with PC and 0% (0/20) in those with CP. Mutational types of K-ras at codon 12 in PC were aspartic acid (Asp) in nine cases, both Asp and cysteine in one case, and arginine in one case. Analysis of K-ras point mutations at codon 12 in PPJ using the HPA method seems promising as a new genetic test for the diagnosis of PC, because the HPA method is simple, and can easily determine the mutational type.
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PMID:Detection of K-ras point mutations at codon 12 in pancreatic juice for the diagnosis of pancreatic cancer by hybridization protection assay: a simple method for the determination of the types of point mutation. 864 83


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