Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum amylase shows the greatest increase among the various pancreatic enzymes that increase at the onset of acute pancreatitis. However, the diagnostic value of the total serum amylase activity has been questioned due to its lack of specificity. To differentiate hyperamylasemia due to pancreatic disease from that due to other causes, the activity of pancreatic amylase should be determined by using a monoclonal antibody that specifically binds to pancreatic or salivary amylase, or by electrophoresis. The most useful and accurate method for distinguishing pancreatic from salivary-type hyperamylasemia is isoamylase analysis by electrophoresis. In patients with acute pancreatitis, increase of Amylase-1 and -2 is accompanied by the appearance of Amylase-4, a minor component of the pancreatic-type isoamylases, and by disappearance of the salivary-type isoenzymes, thereby leaving a pattern of the pancreatic isoenzymes alone. This pancreatitis pattern persists for about 10 days after the onset of illness. Therefore, if such a pattern is found in a patient with clinical findings suggesting acute pancreatitis despite a normal serum amylase level, the patient can be diagnosed as having acute pancreatitis or a recent attack of the disease. However, the existence of an inherited trait of the pancreatitis pattern in some healthy individuals must be borne in mind. Patients with recurrent chronic pancreatitis also show pancreatic-type hyperamylasemia, whereas the pancreatic amylase activity decreases when pancreatic exocrine insufficiency progresses. Hyperamylasemia due to elevated salivary amylase activity is also common in patients with diabetic ketosis or malignancies such as lung cancer (adenocarcinoma). Hyperamylasemia is also found following various types of operation. In most cases, it is salivary-type hyperamylasemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Usefulness of amylase isoenzyme determination for the diagnosis of pancreatic diseases]. 754 79

We studied the expression of p53 gene product in pancreatic adenocarcinomas of the usual ductal type to determine its relationship to cigarette smoking and its usefulness as an independent prognostic indicator. Twenty-six resection specimens of pancreatic adenocarcinoma were examined by immunohistochemistry using an antigen retrieval solution and monoclonal PAb1801 and polyclonal CM1 antibodies on paraffin-embedded material. Specific nuclear p53 expression for both PAb1801 and CM1 was identified in seven cases (27%). In all cases immunoreaction was confined to neoplastic cells. Three of four (75%) tumors from patients who had never smoked showed immunoreaction, whereas only three of 14 (21%) tumors from smokers showed positive staining. Cases with positive staining had shorter mean survival (6.3 mo) than cases that failed to stain (9.8 mo), but the difference was not statistically significant in this small study. There was no statistically significant association between p53 immunoreactivity and other clinicopathologic parameters. Our findings indicate that abnormalities of p53 gene in pancreatic adenocarcinomas may not be directly related to cigarette smoking. Those patients who survived the longest tended to have tumors negative for p53 immunostaining. p53 immunoreaction may be a useful feature in distinguishing adenocarcinoma from chronic pancreatitis in small biopsies.
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PMID:Expression of p53 protein in pancreatic adenocarcinoma. Relationship to cigaret smoking. 764 71

An invasive ductal carcinoma of the pancreas with intratumoral calcification is reported in a 59-yr-old female. The calcification was preoperatively demonstrated by ultrasonography and computed tomography. On the cut surface of the resected specimen of the pancreas tail, calcification was observed in the central part of the ductal adenocarcinoma. Although calcification is not uncommon in chronic pancreatitis or serous cystadenoma, mucinous cystadenoma/adenocarcinoma, solid and cystic tumor, and islet cell tumor, intratumoral calcification is uncommon in an ordinary ductal adenocarcinoma of the pancreas. For differential diagnosis from other conditions associated with calcification, careful examinations are necessary.
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PMID:Ductal adenocarcinoma of the pancreas associated with intratumoral calcification. 764 76

This investigation was undertaken in order to analyse the expression of tumor associated antigen CA 242 in normal pancreas, in chronic pancreatitis and in pancreatic ductal adenocarcinoma, and to find out if the expression of CA 242 in carcinoma specimens would have prognostic significance. The expression of CA 242 was examined in the tissue specimens by the avidin-biotin-immunoperoxidase technique. According to our results, normal pancreas showed no or only weak staining for CA 242, whereas chronic pancreatitis samples stained somewhat intensely. Five out of 39 adenocarcinomas were negative for CA 242, 5 showed weak staining and 29 showed intermediate or intense staining. Positive staining was found mostly in the ductal cells as well as in intraluminal contents. We found no statistically significant difference of CA 242 expression between different grades. The staining intensity and survival had no clear statistical correlation but all carcinoma patients whose survival time was more than twelve months showed an intense staining for CA 242. The results suggests that the expression of tumour associated antigen CA 242 may have prognostic significance in pancreatic adenocarcinoma.
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PMID:Expression of C-242 antigen in pancreatic ductal adenocarcinoma. 765 56

From 1984 to the end of 1993, we performed 51 duodenopancreatectomies with pylorus preservation (27 for chronic pancreatitis and 24 for tumours). We have a complete follow up for 96% of our patients with a mean range of 76 months in the first group and 33 months in the second. There was no per- or postoperative mortality and 15% immediate postoperative morbidity. We observed 5 cases (10%) of anastomotic ulceration. New surgical technics enabled us to avoid this major complication for our last 31 patients. The short and long term benefits of pylorus-preserving duodenopancreatectomy on patients' wellbeing, nutritional status and weight gain were confirmed in 22 patients (82%) with pancreatitis. The mean survival time in patients with tumors (periampullary and head of pancreas adenocarcinoma) is similar to that with the classical Whipple procedure.
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PMID:[Cephalic duodenopancreatectomy with pylorus preservation: for which patients?]. 774 Feb 88

Differential diagnosis of pancreatic cancer and chronic pancreatitis is sometimes difficult and cytological examination of brushings or aspirated material collected during endoscopic retrograde cholangiopancreatography (ERCP) remains disappointing. As point mutations in codon 12 of the c-Ki-ras 2 gene are found in most pancreatic adenocarcinoma and not in chronic pancreatitis, this study analysed prospectively the presence of these mutations in brushing samples collected during ERCP in 45 patients (26 males, 19 females) showing a dominant stricture of the main pancreatic duct at pancreatography: 24 with pancreatic adenocarcinoma, 16 with chronic pancreatitis, and five intraductal mucin hypersecreting neoplasms. Twenty of 45 patients presented equivocal ERCP findings that did not permit a definite diagnosis. Ki-ras mutations at codon 12 were detected using a rapid and sensitive method based on polymerase chain reaction mediated restriction fragment length polymorphism analysis and confirmed by direct sequencing of polymerase chain reaction products. Results were compared with those provided by routine brush cytology. A definitive diagnosis was established for each patient. Mutations were detected in 20 of 24 patients with pancreatic adenocarcinoma (83%), but in none of the chronic pancreatitis patients and intraductal mucin hypersecreting neoplasms, irrespective of their location. By contrast, only 13 of 24 pancreatic adenocarcinoma (54%) were detected by conventional cytological examination, which yielded four false negative and seven non-contributive results. Sensitivity, specificity, and accuracy of molecular biological and cytological methods were 83%-76%, 100-83%, and 90%-58%, respectively. Notably the mutations could be detected in six patients with small tumour size (< or = 2 cm). In conclusion, Ki-ras analysis performed on pancreatic brushing samples is an efficient procedure, more accurate than cytology in the diagnosis of pancreatic adenocarcinoma, and highly specific in the differentiation between neoplastic and chronic inflammatory ductal changes, especially in patients showing inconclusive ERCP findings.
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PMID:Detection of c-Ki-ras gene codon 12 mutations from pancreatic duct brushings in the diagnosis of pancreatic tumours. 779 31

Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique was used to analyze c-Ki-ras codon 12 mutation in 27 fine needle aspiration biopsy (FNAB) specimens of the pancreas and its adjacent organs for the diagnosis of pancreatic adenocarcinoma. C-Ki-ras codon 12 mutation was present in 14 out of 15 cases of pancreatic adenocarcinoma, the positive rate was 93.33% (14/15); whereas no mutation was detected in those obtained from 12 patients with chronic pancreatitis, pancreatic cyst, gallbladder carcinoma, carcinoma of ampulla of Vater and gastric lymphoma. The results of this study verifies the PCR-RFLP technique as a practical, sensitive, rapid and reliable method for the detection of c-Ki-ras codon 12 mutation in the diagnosis of pancreatic adenocarcinoma.
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PMID:[Gene diagnosis of pancreatic adenocarcinoma]. 787 57

Heat shock proteins (hsp) are involved in degradation or chaperoning nascent and abnormal proteins to various subcellular locations. p53 tumour suppressor gene overexpression and mutation occur frequently in pancreatic cancers. Mutant p53 proteins produced in cancers of other sites have been found to form complexes with hsp 70. Consequently, binding to hsp 70 may be used to indicate the presence of mutant p53 proteins. The presence of hsp 70 was investigated by immunohistochemistry in core biopsies of 42 adenocarcinomas of the pancreas (well differentiated, N = 1 and moderate to poorly differentiated, N = 41). Four cases of islet cell tumours were included in the study. These neoplasias were compared with biopsies of chronic pancreatitis (N = 9) and normal pancreas (N = 5). The majority of adenocarcinomas, 24/42 (57%), showed expression of both hsp 70 and p53. None of the islet cell tumours or cases of chronic pancreatitis showed p53 and hsp 70 coexpression. Only 1 (20%) of the normal pancreas showed concurrent nuclear immunostaining for p53 and cytoplasmic immunostaining for hsp 70. The high proportion of pancreatic adenocarcinoma showing immunoreactivity for both hsp 70 and p53 may indicate high mutation rate of the p53 gene in this tumour. Further studies using molecular techniques are required to elucidate the nature of both hsp and p53 genes in pancreatic cancers.
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PMID:Overexpression of heat shock protein (hsp) 70 associated with abnormal p53 expression in cancer of the pancreas. 794 33

The c-fos gene product is a 55 kd nuclear protein bound to a cellular protein, p39. Expression of the c-fos oncogene is complex in that increased expression occurs in cultured cells during undifferentiated growth but decreased during terminal differentiation. We studied c-fos gene expression by streptavidin-biotin-peroxidase immunohistochemistry in pancreatic adenocarcinoma (N = 20), chronic pancreatitis (N = 9) and normal pancreas (N = 5). One islet cell tumour was included in the study. There was positive staining for c-fos oncoprotein in 15 of the 20 (75%) adenocarcinomas examined (9/12 moderate to poorly differentiated, 6/8 poorly differentiated). The single islet cell tumour investigated was also positive. Only 2 of 9 (22%) cases of chronic pancreatitis and 2 of 5 (40%) normal pancreata were positive. Stromal immunoreactivity was noted in all cancer cases while 5 of 9 (56%) chronic pancreatitis and 3 of 5 (60%) normal pancreas cases showed such staining. In conclusion, c-fos oncoprotein overexpression occurs more frequently in pancreatic cancers compared to chronic pancreatitis and normal pancreas. These findings are consistent with in vitro cell line studies of other cancers which showed increased expression of c-fos during undifferentiated growth.
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PMID:Immunohistochemical localisation of the c-fos oncoprotein in pancreatic cancers. 794 35

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


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