Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Telomerase activity was measured in pancreatic juice obtained by endoscopic retrograde pancreatography from 34 patients (12 with ductal carcinoma, 12 with pancreatic adenoma, and 10 with pancreatitis). The activity in pancreatic juice was expressed as the number of cells of a human pancreatic cancer cell line, MIA PaCa-2, that exhibit an activity equal to that expressed in 1 microg of protein from pancreatic juice. A telomerase ladder was detected in the pancreatic juice obtained from a majority of the patients with ductal adenocarcinoma. The median value of relative telomerase activity in the carcinoma samples was 9.38 (25th percentile, 3.14; 75th percentile, 95.8), a value significantly higher than that derived from patients with either pancreatitis or pancreatic adenoma (P < 0.0001). When a threshold value of relative telomerase activity of 3.00 was used, 75% (9 of 12) of the samples obtained from patients with ductal carcinoma were positive. We conclude that telomerase activity in pancreatic juice differentiates adenocarcinoma from adenoma and pancreatitis and may serve as a useful diagnostic tool.
 ...
PMID:Telomerase activity in pancreatic juice differentiates ductal carcinoma from adenoma and pancreatitis. 981 50

The authors describe the case of a 70-year-old man with primary adenocarcinoma of the fourth segment of the duodenum. Due to the infrequency of the condition there was diagnostic and therapeutic uncertainty. After the endoscopic and bioptic diagnosis three months elapsed before an incorrectly indicated derivation operation and only after another month the tumour was resected. The exhausted patient developed postoperative pancreatitis with subsequent multiorgan failure to which he succumbed. The disease should be suspected even if the symptomatology is poor. The patient suffered only from nausea and anaemia. From the diagnostic aspect endoscopic examination is most useful for the oral segment of the duodenum and double contrast examination for the aboral one. The method of treatment is duodenopancreatectomy for the upper part and segmental resection for the distal part of the duodenum.
 ...
PMID:[Primary carcinoma of the duodenum]. 982 54

Only 15% of primary malignant tumors are confined to the gland at the time of presentation. Fine-needle aspiration (FNA) is valuable in confirming the malignant nature of these unresectable lesions. Benign pancreatic lesions and metastatic neoplasms can also be evaluated by fine-needle aspiration. We undertook a retrospective study to evaluate the efficacy of FNA in assessing pancreatic masses. Three hundred and sixty-four radiologically guided FNAs of the pancreas performed between 1986-1996 were reviewed. Surgical material was also evaluated when available and compared to the FNA material. There were 223 men and 141 women. Their ages ranged from 23-90, with a mean of 64 yr. Two hundred and twelve patients (58%) had primary malignant tumors, 183 had adenocarcinomas, 15 had mucinous cystadenocarcinomas, 12 had neuroendocrine tumors, and 2 had pleomorphic giant-cell carcinomas. Ninety-one (43%) had available surgical material which showed adenocarcinoma. Ninety-one patients (25%) had benign aspirates, including 53 showing benign ductal epithelium, 23 showing pancreatitis/inflammation. 10 showing pseudocysts, and 7 showing serous cystadenomas. Surgical material was available in 24 (26%) of these patients. Two of these showed adenocarcinoma. Sixteen aspirates (4%) were suspicious for malignancy, 13 (81%) of which showed adenocarcinoma on follow-up biopsies. Twenty-two aspirates (6%) showed metastatic neoplasms. Twenty-three (6%) had unsatisfactory specimens. Ten (43%) of these had follow-up biopsies, 3 of which were malignant. FNA of primary benign and malignant pancreatic masses is highly sensitive (98%) and specific (100%). Eighty-one percent of the suspicious lesions showed adenocarcinoma on follow-up biopsy. FNA of metastatic neoplasms to the pancreas is also very accurate. This technique can be useful in avoiding unnecessary surgery.
 ...
PMID:Pancreatic masses: a multi-institutional study of 364 fine-needle aspiration biopsies with histopathologic correlation. 983 31

Often the diagnosis of pancreas cancer needs to be established from limited cytology specimens or small biopsies. Most ductal adenocarcinomas are histologically well to moderately differentiated and mimicked closely by pancreatitis, and therefore the microscopic diagnosis can be difficult. In addition, there appears to be significant heterogeneity in the outcome of the patients with pancreatic cancer, which cannot be predicted accurately by current prognosticators such as the grade and stage of the tumor. Therefore, there is need for methods that can be used as adjuncts to routine diagnostic and prognostic parameters. This study was designed to test the utility of the fluorescent in situ hybridization (FISH) method in identifying the molecular alterations, particularly the ones that have been detected with relatively high frequency in pancreas cancer. Formalin-fixed and paraffin-embedded tissues of 10 cases were enumerated for chromosome 7, 8, 17, 18, and 20 copy numbers by using alpha-satellite probes, and for c-myc by using a gene-specific probe. The number of signals per nucleus (reflecting chromosomal copy number and status of c-myc amplification) were counted in more than two areas containing 50-500 cells. Because of tumor heterogeneity, monosomy (loss of one chromosome copy) was defined arbitrarily as one signal in >25% of nuclei. C-myc amplification was defined as more than two gene copies in >20% of the cells. The most frequent signal losses were found in chromosomes 8 (four of 10 cases) and chromosome 17 (four of 10), followed by 20 (three of 10) and 18 (two of 10). No loss of chromosome 7 was detected. In contrast, gains in chromosome copy number were identified in only one of 10 tumors, which showed gain of both chromosome 7 and 18. Amplification of c-myc gene was detected in two of 10 cases, but neither of the two had aneuploidy for chromosome 8, where the c-myc gene is located. In addition, loss in c-myc signal was observed in one case that also showed loss of chromosome 8 copy number. FISH can be used to detect chromosomal changes in pancreatic cancer; abundance of lytic enzymes in this organ is not an impediment for the applicability of this technique. Therefore it can potentially be used in the future as an adjunct to the conventional diagnostic and prognostic markers. This study confirms that loss of chromosomes, particularly chromosomes 17 and 18, which carry the p53 and DCC genes, are common in pancreas cancer. Chromosome 20 is also frequently lost. In addition, in this study, alterations of chromosome 8, which is seen commonly in prostatic adenocarcinoma but has not been previously documented in pancreatic cancer, also was detected in five of 10 tumors. Furthermore, amplification of the c-myc gene, which is located in chromosome 8, was found in the two of the remaining five cases. Further studies are needed to confirm this high incidence of chromosome 8 and c-myc alterations and their possible role in the pathogenesis of pancreatic adenocarcinoma.
 ...
PMID:Utility of fluorescence in situ hybridization in pancreatic ductal adenocarcinoma. 1009 Apr 7

The role of MR imaging in the assessment of pancreatic adenocarcinoma is in identification, characterization and staging of the neoplastic lesion. Technique optimization is required in order to obtain high qualities images competitive with spiral CT. The choice of imaging protocol is strictly related to the available equipment as well as fast imaging capabilities. Contrast-enhanced study using breath-hold sequences is required if working at high field strength with high gradient performance; on mid-low field strength nonbreath-hold acquisition techniques, using respiratory compensation techniques, can be implemented. The use of fat saturation pulses may increase the sensitivity of MR in detecting pancreatic lesions. Other advantages of MR imaging are represented by the availability of additional noninvasive techniques for the evaluation of the biliary tree (MR-cholangiopancreatography) and splanchnic vessels (MR-angiography). Lesion identification is based on TIw sequences where the lesion appears hypointense compared with the surrounding pancreas; increased lesion-pancreas contrast is obtained when fat suppression is used. On dynamic studies following gadolinium injection, pancreatic tumors are hypovascular compared with surrounding normal pancreatic gland. Problems in correctly defining the size of the lesions may be encountered in patients presenting with inflammatory changes of the pancreatic parenchyma surrounding the carcinoma (epineoplastic pancreatitis). For lesion characterization MRI is not able to characterize focal pancreatic lesions, allowing a differential diagnosis between pancreatic cancer and focal hypertrophic chronic pancreatitis. Even the use of MR-cholangiopancreatography is not helpful for characterizing focal pancreatic masses. MR imaging is accurate in local staging (assessment of peripancreatic fat infiltration) thanks to the higher contrast resolution, but in vascular staging and in the evaluation of lymphnodal involvement it suffers the same limitations as computed tomography. Future perspective are represented by the use of magnetic resonance angiography for the evaluation of vascular encasement and the use of specific contrast agents for lymphadenopathy. Identification of hepatic metastases with MRI has been proven to be high, with sensitivity and specificity comparable to CT. The use of liver-specific contrast agents (either positive or negative) is becoming almost routine and it is proving to further improve the diagnostic value of MRI.
 ...
PMID:[MR imaging of pancreatic neoplasms]. 1023 72

Hereditary pancreatitis is a rare condition characterized by acute and chronic pancreatitis transmitted in an autosomal dominant fashion. There also is an epidemiologic link to pancreatic cancer in some affected families. Failure of a secondary brake mechanism responsible for inactivation of prematurely activated cationic trypsin in acinar cells seems to be the fundamental defect in type I hereditary pancreatitis (R117H cationic trypsin), and also may explain the pathogenesis of type II hereditary pancreatitis (N211 cationic trypsin). The diagnosis is made based on clinical history and, in certain cases, by molecular diagnostic testing for these gene defects. Medical management of acute and chronic hereditary pancreatitis currently does not differ from that of nonhereditary AP. As in nonhereditary pancreatitis, the surgical approach must be tailored to the individual problem, with an understanding that disease restricted to the head of the gland is atypical and that residual acinar tissue continues to drive the disease state. Although diagnosis and management of pancreatic adenocarcinoma are similar in this cohort, the increased age-accumulated risk suggests that thoughtful screening protocols eventually may be clinically and cost-effective.
 ...
PMID:Hereditary pancreatitis. Gene defects and their implications. 1047 Mar 21

In this article, we report the identification of a new autoantigen in type 1 diabetes originating from the exocrine pancreas. This antigen is a pancreatic enzyme termed bile salt-dependent lipase (BSDL). We show that antibodies present in the sera of newly diagnosed type 1 diabetic patients recognize BSDL and more specifically the COOH-terminal mucin-like region of the protein. Therefore, we engineered the COOH-terminal peptide of BSDL and demonstrated that autoreactivity was linked to specific glycosylation sites by at least two glycosyltransferases: the Core 2 beta(1-6)N-acetylglucosaminyltransferase and the alpha(1-3) fucosyltransferase FUT7. We next examined the prevalence of circulating anti-BSDL antibodies in type 1 diabetic patients and found 73.5% positivity (25 sera among 34 patients tested) at onset, whereas only 8.4% of normal individuals (7 of 83) were positive. Within a cohort of first-degree relatives of diabetic patients followed prospectively until development of diabetes, 6 of 19 (31.6%) were also positive. Interestingly, two prediabetic individuals were already positive for anti-BSDL antibodies (Abs), while islet cell cytoplasmic Abs and antibodies to GAD65, IA-2, and insulin were not detected. Anti-BSDL autoantibodies were weakly or not detected in patients suffering from pancreatitis or pancreatic adenocarcinoma or in patients with Graves' disease. Although autoreactivity to BSDL in prediabetic and newly diagnosed diabetic patients might reflect cross-reactivity, our results strongly suggest that in addition to pancreatic beta-cells, acinar cells may be also affected in type 1 diabetes.
 ...
PMID:Circulating antibodies against an exocrine pancreatic enzyme in type 1 diabetes. 1058 Apr 19

When the radiologist is faced with a well-circumscribed tumoral mass in the pancreas, knowing when to direct the patient toward nonsurgical biopsy instead of surgical biopsy and staging is critical. Lymphoma does not require surgical staging or a palliative Whipple's procedure before chemotherapy or radiation therapy. A better overall prognosis with nonsurgical treatment is additional impetus to search for secondary signs of primary pancreatic lymphoma. In patients with primary pancreatic lymphoma, no marked pancreatic ductal dilatation is present even with ductal invasion. Adenocarcinoma commonly dilates the more distal pancreatic duct when more proximal ductal invasion has taken place. Lymph node involvement below the level of the renal veins was another finding not seen with adenocarcinoma. Clinical and imaging findings are otherwise not specific in the differentiation of pancreatic lymphoma and pancreatic cancer, but a bulky homogeneous tumoral mass without alteration of Wirsung's duct or the peripancreatic vessels should suggest the diagnosis. In patients with diffuse infiltration of the pancreatic gland without clinical signs of pancreatitis, the radiologist should be alert to the possibility of pancreatic lymphoma.
 ...
PMID:Imaging findings in pancreatic lymphoma: differential aspects. 1070 7

Recently, there has been a great deal of interest in the role of cytokines in acute pancreatitis. Serum levels of IL-1, IL-6, and TNF-alpha have been demonstrated to be elevated in acute pancreatitis. We hypothesized that cytokines may be produced primarily by pancreatic parenchymal cells. Reasoning that ductal epithelium is the cell type most likely to be exposed to noxious stimuli in common causes of pancreatitis, such as ERCP and passage of a gallstone, we examined the response of well differentiated pancreatic ductal adenocarcinoma cell lines to stimuli known to stimulate cytokine production in other cells. CAPAN-1 and CAPAN-2 cells were incubated with endotoxin or TNF-alpha. The supernatant was assayed for production of IL-1, IL-6, and IL-8 by ELISA. The cells were assayed for activation of the transcription factor NF-kappaB by electrophoretic mobility shift assay. There was no detectable production of IL-1 by either cell line. CAPAN-1 cells had concentration-dependent production of IL-6 and IL-8 in response to both endotoxin and TNF-alpha. CAPAN-2 cells had concentration-dependent production of IL-6 and IL-8 in response to TNF-alpha. They had low level expression of IL-8 that was unaffected by any concentration of LPS, and no detectable production of IL-6 in response to LPS. These findings suggest that pancreatic duct cells may take an active part in the pathogenesis of acute pancreatitis through the production of cytokines.
 ...
PMID:Cytokine production by CAPAN-1 and CAPAN-2 cell lines. 1079 56

Because of the dismal prognosis of advanced ductal pancreatic adenocarcinoma, recent investigational strategies have focused on improved detection and therapeutic intervention in early-stage pancreatic cancer. The obvious cost constraints of screening populations at risk but with a low tumor yield will restrict screening protocols to only the highest risk groups (hereditary pancreatitis = age 50, certain hereditary pancreatic cancer kindreds). The vast majority of patients, either lacking or exhibiting an inherited predisposition to pancreatic cancer, will continue to present with disease not resectable for cure. The authors believe that the best hope for these patients lies in the further delineation of the integrative pathophysiology driving tumor growth; this would facilitate the future development of a computer program or other modality that would predict the dominant pathways driving the growth and spread of each tumor based on its "molecular profile." This article reviews the authors' current knowledge regarding the growth factors, receptors, and molecular alterations driving uncontrolled proliferation, local invasion, and metastatic spread of these tumors. The current and potential contributions of studies in cohorts with an inherited predisposition to pancreatic cancer to this pathophysiologic model are also discussed. The future strategy for incorporating this information into a working pathophysiologic road map with clinical relevance is subsequently outlined.
 ...
PMID:Growth factors, receptors, and molecular alterations in pancreatic cancer. Putting it all together. 1087 26


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>