Biomedical subjects

P Fogar

Publications and source records attributed to P Fogar.

45 records · Page 3Linked to original sources

PubMedDate not supplied

Pancreatic cancer cells invasiveness is mainly affected by interleukin-1beta not by transforming growth factor-beta1.

BACKGROUND: We investigated in vitro whether IL-1beta and TGF-beta1 affect pancreatic cancer cell growth, adhesion to the extracellular matrix and Matrigel invasion. MATERIALS AND METHODS: Adhesion to fibronectin, laminin and type I collagen, and Matrigel invasion after stimulation with saline, IL-1beta and TGF-beta1 were evaluated using three primary and three metastatic pancreatic cancer cell lines. RESULTS: Extracellular matrix adhesion of control cells varied independently of the metastatic characteristics of the studied cell lines, whereas Matrigel invasion of control cells was partly correlated with the in vivo metastatic potential. IL-1beta did not influence extracellular matrix adhesion, whereas it significantly enhanced the invasiveness of three of the six cell lines. TGF-beta1 affected the adhesion of one cell line, and exerted contrasting effects on Matrigel invasion of different cell lines. CONCLUSIONS: IL-1beta enhances the invasive capacity of pancreatic cancer cells, whereas TGF-beta1 has paradoxical effects on pancreatic cancer cells; this makes it difficult to interfere with TGF-beta1 signaling in pancreatic cancer treatment.

Cell Adhesion↗

PubMedDate not supplied

Tumor markers in the diagnosis, monitoring and therapy of pancreatic cancer: state of the art.

The present review focuses on the utility of serum tumor markers in screening, diagnosis, prognosis and monitoring of pancreatic cancer. Serum determination of all tumor markers studied offers no help in screening or early diagnosis of pancreatic cancer. For diagnosis, blood group-related antigens, in particular CA 19-9, are considered the best indicators of this neoplasm. However, as occurs with other glycoproteic tumor markers, the circulating levels of CA 19-9 are significantly influenced by jaundice, probably because its liver metabolism is reduced. Therefore, the finding of elevated CA 19-9 levels in jaundiced patients has to be evaluated with caution. Since pancreatic cancer recurrences are not susceptible to treatment, the clinical role of widespread use of tumor marker determination in follow-up programs is limited and calls for a critical evaluation.

Antigens, Neoplasm↗

PubMedDate not supplied

[Cisapride and sucralfate in dyspepsia associated with duodenogastric reflux gastritis].

The present investigation was undertaken with the aim of evaluating the clinical efficacy on dyspeptic symptoms associated with duodenogastric reflux gastritis of two drugs belonging to two different groups: a prokinetic (cisapride) and a cytoprotective agent (sucralfate). A total of 18 patients with duodenogastric reflux gastritis diagnosed on the basis of symptoms, endoscopy and histology were studied. Nine were given 30 mg of cisapride/daily and 9 4 g of sucralfate/daily for two months according to a randomization list. Pyrosis, epigastric pain, sense of epigastric repletion and foul-tasting mouth were considered on a scale from 0 to 4 attributed by the patient. The total score of dyspeptic symptoms significantly decreased only after cisapride (p less than 0.05). Considering each symptom alone, neither cisapride or sucralfate were able to significantly improve them. Cisapride seems to the better than sucralfate in improving dyspeptic symptoms associated with duodeno-gastric reflux gastritis.

Adult↗

PubMedDate not supplied

CAR-3 and CA 19-9 serum levels in pancreatic cancer: any differences between two epitopes of the same mucin-like glycoprotein?

The aim of this study was to compare the utility of two recently identified tumour markers of pancreatic cancer, CA 19-9 and CAR-3, and to ascertain the roles of some factors influencing both antigens. CA 19-9 and CAR-3 were measured in sera of 18 control subjects, 27 patients with pancreatic cancer, 25 with chronic pancreatitis, and 29 with extra-pancreatic diseases. CA 19-9 and CAR-3 were, respectively, found to be increased in 85 per cent and 44 per cent of patients with pancreatic cancer, 28 per cent and 0 per cent with chronic pancreatitis and 72 per cent and 28 per cent with extra-pancreatic diseases. The ROC curves showed that, for any serum value considered, CA 19-9 is more effective than CAR-3 in discriminating between pancreatic cancer and control subjects and chronic pancreatitis. With the combined use of both antigens the results were no better than those given by CA 19-9 alone. Correlations were found between liver function tests and CA 19-9 levels and between cholestasis indices only and CAR-3 values. Our findings show that CAR-3 is not a sufficiently reliable marker of pancreatic cancer, due to its low sensitivity. Nor does it offer any more information than CA 19-9. Both assays are influenced, at least in part, by the extent of the neoplasia. Cholestasis which can greatly influence a serum glycoproteic marker such as CA 19-9, was found also to affect, to a lesser extent, CAR-3, an epitope on the same mucin molecule.

Adult↗

PubMedDate not supplied

Acute phase proteins in chronic pancreatic disease.

In order to evaluate the behaviour of some acute phase proteins in chronic pancreatic disease and to correlate these reactants with different factors, C-reactive protein, ceruloplasmin and alpha-1-antitrypsin were assayed in the sera of 24 control subjects, 26 patients with pancreatic cancer, 22 patients with chronic pancreatitis and 22 patients with a variety of diseases not of pancreatic origin. Alpha-1-antitrypsin, C-reactive protein and ceruloplasmin concentrations were found to be increased in 63%, 50% and 42% of patients with chronic pancreatic disease, respectively. In patients with pancreatic cancer no difference was found between the values of each protein considering the presence or otherwise the absence of liver metastases. Patients with chronic pancreatitis had higher C-reactive protein or alpha-1-antitrypsin values when increased serum amylase or pseudocysts were present. Significant correlations were found between the three acute-phase proteins considering the subjects as a whole; however in the single subjects they were not found to be concomitantly abnormal. Correlations were detected between these proteins and liver function test values. Alpha-1-antitrypsin is probably the most sensitive index in chronic pancreatic disease, while C-reactive protein seems better to reflect the stage of the disease. The variations of the levels of these proteins seem to be, at least in part, independent of each other; they are all partially influenced by the presence of liver damage.

Acute-Phase Proteins↗

PubMedDate not supplied

[Role of serum markers and or various clinical parameters in the diagnosis of pancreatic carcinoma].

This study was performed to ascertain the role of serum markers and simple clinical data in detecting pancreatic cancer and in distinguishing this malignancy from chronic pancreatitis and other gastrointestinal diseases. Serum CA 19-9, tissue polypeptide antigen and carcinoembryonic antigen were measured in 38 control subjects, 37 patients with pancreatic cancer, 39 with chronic pancreatitis and 44 with extra-pancreatic diseases mainly of gastrointestinal origin. Clinical data recorded included age, sex, presence of pancreatic calcifications, weight loss, pain, jaundice, alcohol abuse, diabetes mellitus. Serum markers gave a correct allocation of the subjects in 48.1% of the cases with pancreatic cancer patients correctly predicted in 62.2%. Clinical data correctly diagnosed 74.2% of subjects. Chronic pancreatitis was identified in 84.6% of the cases and pancreatic cancer in 64.9%. The first clinical variables selected were pain and age. The addition of serum markers to clinical data did not enhance accuracy of the results. We conclude that the diagnosis of chronic pancreatic diseases should first be suspected on the basis of accurately recorded simple clinical data; serum markers seem to be only occasionally useful. Since indicative clinical data and serum markers become positive in the advanced phases of pancreatic cancer, early diagnosis of this malignancy still remains an objective to reach.

Adult↗

PubMedDate not supplied

Diabetes mellitus in pancreatic cancer follow-up.

The aim of this study was to assess the behavior of fasting serum glucose, C-peptide levels and OGTT in pancreatic cancer follow-up. We studied 49 patients with pancreatic cancer (stage I = 8 pts; II = 16 pts; III = 12 pts; IV = 13 pts). At diagnosis 13/49 patients had fasting serum glucose levels of above 140 mg/dL. Of the remaining 36 pts, 22 underwent OGTT, which indicated diabetes mellitus in 9/22 (41%) and impaired glucose tolerance in 7/22 (32%) cases. C-peptide basal values were within the normal range (0.8-2.0 micrograms/L) in 14/49 (28%), above 2.0 micrograms/L in 6/49 (13%) and below 0.8 micrograms/L in 29/49 (59%) of the cases. No significant correlation was found between tumor stage or size and the presence of diabetes or of a reduced glucose tolerance. Twenty-four patients underwent curative resection (group 1) and 16 palliative resection, while the remaining nine did not undergo surgery (group 2). Group 1 and 2 patients had a follow-up of 2 to 40 months (mean = 14 months) and from 1 to 7.5 months (mean = 3.5 months) respectively. In group 1 patients no significant difference was found between pre- and post-operative fasting serum glucose levels. However, in 11/15 (73%) patients who underwent OGTT before and after surgery, an improvement in glucose tolerance was observed after tumor resection. In group 2 patients, a significant increase in fasting serum glucose levels was found during follow-up. In neither of the groups studied were significant variations found in C-peptide levels during the follow-up, although a slight increase was observed in patients who did not undergo surgery. In conclusion, the reduced glucose tolerance or frank diabetes mellitus, which frequently occurs during the onset of pancreatic cancer, does not seem to be related to tumor stage or size. Curative resection ameliorates glucose intolerance, while tumor persistence can enhance serum glucose levels.

Adult↗

PubMedDate not supplied

C-peptide pattern in patients with pancreatic cancer.

The pathogenetic mechanism underlying glucose intolerance in pancreatic cancer is still unclear. We studied the pattern of three glucose regulating hormones (C-peptide, glucagon and GH) in pancreatic cancer patients with (N = 34) and without (N = 8) hyperglycemia, and compared the findings made with those from subjects with other hyperglycemic conditions of well-known origin [type I diabetes mellitus (8 cases) and diabetes mellitus secondary to chronic pancreatitis (13 cases) or liver cirrhosis (4 cases)]. In hyperglycemic pancreatic cancer patients, C-peptide was absent in 26% of the cases, reduced in 24%, elevated in 29% and within the normal range in the remaining 21%. In normoglycemic pancreatic cancer this hormone was reduced in two cases (25%) and within the normal range in all the others. GH was within the normal range in all cases: glucagon was below the normal range in some hyperglycemic pancreatic cancer patients (41%) or within the normal range in all the remaining patients. No correlations were found between the three hormones when findings from subjects were considered all together. However, in pancreatic cancer C-peptide and glucagon presented consensual variations. C-peptide, glucagon and GH levels were not related to tumor volume; glucagon was found to be associated with liver metastases. C-peptide was correlated with serum ALT and ALP. We may conclude that hyperglycemia associated with pancreatic cancer may be caused by different mechanisms. In some cases a reduced secretion of both insulin and glucagon was observed, as occurs in chronic pancreatitis. In the majority of patients, beta cell function appears normal, and the hyperglycemic state may depend on an altered peripheral sensitivity to insulin due to the pancreatic pathology itself or to consensual liver involvement.

Adult↗

PubMedDate not supplied

Neural cell adhesion molecule (N-CAM) in gastrointestinal neoplasias.

BACKGROUND: The neural adhesion molecule N-CAM, a membrane bound glycoprotein, seems to play an important role in the development of normal tissue architecture and in contact-dependent inhibition of cell growth. MATERIALS AND METHODS: We evaluated the behaviour of circulating N-CAM in patients with pancreatic cancer (24 cases) and chronic pancreatitis (15 cases) and compared it with that of 20 controls, 6 patients with colon adenoma, 31 with colorectal cancer or 21 with gastric cancer and ascertained the influence of tumor stage and grade on the findings. RESULTS: N-CAM levels were significantly lower in patients with pancreatic cancer and chronic pancreatitis than in the other groups studied. High levels were found only in few colorectal carcinoma patients (4/31). No correlation was found between tumor stage and N-CAM levels when pancreatic and colorectal cancer were considered. However, low N-CAM levels were found in 50% of advanced, but not in early gastric cancer. When pancreatic, colorectal and gastric cancer were considered, poorly differentiated (G3) had lower levels of N-CAM than well (G1) or moderately (G2) differentiated tumors. The variations found in circulating N-CAM were comparable to those in CEA but not to those in CA 19-9. CONCLUSIONS: a) perhaps because of its higher aggressiveness, pancreatic cancer is associated with low serum N-CAM levels unlike other gastrointestinal neoplasias; b) the association between aggressiveness and reduced N-CAM levels is borne out by the correlation found with the grade of differentiation; c) the reduced levels found in chronic pancreatitis suggest that this molecule plays a role in stromaparenchymal interactions, which might be altered in the presence of fibrotic phenomena.

Adult↗