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Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Pancreatic Cancer - October 2002
National Cancer Institute®
Last Modified: October 1, 2002
- Non-invasive differentiation of pancreatic lesions: is analysis of FDG kinetics superior to semiquantitative uptake value analysis?
- Effect of a fish oil-enriched nutritional supplement on metabolic mediators in patients with pancreatic cancer cachexia.
- Multiple mechanisms confer different drug-resistant phenotypes in pancreatic carcinoma cells.
- Isoattenuating pancreatic adenocarcinoma at multi-detector row CT: secondary signs.
- Expression of human regenerating gene mRNA and its product in normal and neoplastic human pancreas.
- Heat stress-induced loss of eukaryotic initiation factor 5A (eIF-5A) in a human pancreatic cancer cell line, MIA PaCa-2, analyzed by
- Matrix metalloproteinase-2 in pancreatic juice for diagnosis of pancreatic cancer.
- A nested case-control study on risk of pancreatic cancer among workers in the rubber industry.
- Results after pancreatic resection for metastatic lesions.
- [How I treat...advanced cancer of the pancreas with a novel approach directed against new targets]
- The role of imaging for the evaluation of pancreatic cancer resectability.
- [Assessment of 18FDG PET for diagnosis of pancreatic tumors]
- Percutaneous self-expanding metal stents versus endoscopic polyethylene endoprostheses for treating malignant biliary obstruction: randomized
- Genetic disorders in pancreatitis: Implications in the pathogenesis of acute and chronic pancreatitis.
- Quantitative analysis of K-ras gene mutation in pancreatic tissue obtained by endoscopic ultrasonography-guided fine needle aspiration:
- Cystic fibrosis transmembrane regulator (CFTR) DeltaF508 mutation and 5T allele in patients with chronic pancreatitis and exocrine pancreatic
- Pancreatic intraductal sampling during ERCP in patients with chronic pancreatitis and pancreatic cancer: cytologic studies and k-ras-2 codon
- [Does cholestasis change the clinical usefulness of CA 19-9 in pacreatobiliary cancer?]
- Long-term surgical outcome of noninvasive and minimally invasive intraductal papillary mucinous adenocarcinoma of the pancreas.
- Long-term and short-term survivors after pancreatectomy for pancreatic cancer.
- Phase II study of anti-gastrin-17 antibodies, raised to G17DT, in advanced pancreatic cancer.
- Identification of a human insulinoma cDNA encoding a novel mammalian protein structurally related to the yeast dibasic processing protease
- Heparanase expression is a prognostic indicator for postoperative survival in pancreatic adenocarcinoma.
- Immunohistochemical p16INK4a analysis of archival tumors with deletion, hypermethylation, or mutation of the CDKN2/MTS1 gene. A comparison of
- Immunohistochemistry in the differential diagnosis of acinar and endocrine pancreatic neoplasms.
- Apoptosis induced by 5-flucytosine in human pancreatic cancer cells genetically modified to express cytosine deaminase.
- Expression of maspin in pancreatic neoplasms: application of maspin immunohistochemistry to the differential diagnosis.
- [Morphologic and functional study of a human insulin-secreting cell line]
Table of Contents
1
UI - 11926386
AU - Nitzsche EU; Hoegerle S; Mix M; Brink I; Otte A; Moser E; Imdahl A
TI -
Non-invasive differentiation of pancreatic lesions: is analysis of FDG
kinetics superior to semiquantitative uptake value analysis?
SO - Eur J Nucl Med Mol Imaging 2002 Feb;29(2):237-42
AD - Department of Radiology, Albert Ludwigs University, Medical Center,
Freiburg, Germany. enitzsche@uhbs.ch
The diagnostic utility of fluorine-18 2-deoxy-D-glucose positron
emission tomography (FDG PET) for the non-invasive differentiation of
focal pancreatic lesions originating from cancer or chronic pancreatitis
by combined visual image interpretation and semiquantitative uptake
value analysis has been documented. However, in clinical routine some
misdiagnosis is still observed. This is because there is potential
overlap between the semiquantitative uptake values obtained for active
inflammatory lesions and cancer. Therefore, this prospective study was
undertaken to test the hypothesis that analysis of dynamic kinetics of
focal pancreatic lesions based on FDG PET may more accurately determine
the benign or malignant nature of such lesions. Thirty patients (56+/-17
years) were studied dynamically with FDG PET for a period of 60-90 min.
Patients were assigned to one of four groups: control, acute
pancreatitis, chronic pancreatitis or pancreatic cancer. Two observers,
blinded to the clinical data, analysed the time-activity curves of FDG
kinetics based on region of interest analysis. The diagnosis predicted
by FDG PET was compared with the result of histological examination of
the surgical specimen. Analysis of FDG kinetics revealed significant
differences in the shape of the time-activity curve for controls,
pancreatic cancer and inflammatory disease. Surprisingly, there was no
significant difference in the time-activity curve shape for chronic
pancreatitis and acute pancreatitis; this is, however, not a clinical
issue. Furthermore, acquisition time (60 min vs 90 min) did not affect
interpretation of the time-activity curve, so that scanning time may be
regularly shortened to 60 min. Interobserver agreement was 1. Based on
these findings, non-invasive differentiation between pancreatic cancer
and chronic pancreatitis was correctly predicted in all cases, as
confirmed by histology. In addition, the specificity was increased
compared with that obtained from standardised uptake value analysis.
Non-invasive differentiation between pancreatic cancer and chronic
pancreatitis may best be achieved based on a dynamic FDG PET study
including kinetic analysis. This approach yields results superior to
those obtained from a semiquantitative analysis of pancreatic lesions.
2
UI - 11962246
AU - Barber MD; Fearon KC; Tisdale MJ; McMillan DC; Ross JA
TI -
Effect of a fish oil-enriched nutritional supplement on metabolic
mediators in patients with pancreatic cancer cachexia.
SO - Nutr Cancer 2001;40(2):118-24
AD - University Department of Surgery, Royal Infirmary of Edinburgh,
Edinburgh EH3 9YW, UK.
Weight loss in advanced cancer patients is refractory to conventional
nutritional support. This may be due to metabolic changes mediated by
proinflammatory cytokines, hormones, and tumor-derived products. We
previously showed that a nutritional supplement enriched with fish oil
will reverse weight loss in patients with pancreatic cancer cachexia.
The present study examines the effect of this supplement on a number of
mediators thought to play a role in cancer cachexia. Twenty
weight-losing patients with pancreatic cancer were asked to consume a
nutritional supplement providing 600 kcal and 2 g of eicosapentaenoic
acid per day. At baseline and after 3 wk, patients were weighed and
samples were collected to measure serum concentrations of interleukin
(IL)-6 and its soluble receptor tumor necrosis factor receptors I and
II, cortisol, insulin, and leptin, peripheral blood mononuclear cell
production of IL-1 beta, IL-6, and tumor necrosis factor, and urinary
excretion of proteolysis inducing factor. After 3 wk of consumption of
the fish oil-enriched nutritional supplement, there was a significant
fall in production of IL-6 (from median 16.5 to 13.7 ng/ml, P = 0.015),
a rise in serum insulin concentration (from 3.3 to 5.0 mU/l, P =
0.0064), a fall in the cortisol-to-insulin ratio (P = 0.0084), and a
fall in the proportion of patients excreting proteolysis inducing factor
(from 88% to 40%, P = 0.008). These changes occurred in association with
weight gain (median 1 kg, P = 0.024). Various mediators of catabolism in
cachexia are modulated by administration of a fish oil-enriched
nutritional supplement in pancreatic cancer patients. This may account
for the reversal of weight loss in patients consuming this supplement.
3
UI - 12136248
AU - Lage H; Dietel M
TI -
Multiple mechanisms confer different drug-resistant phenotypes in
pancreatic carcinoma cells.
SO - J Cancer Res Clin Oncol 2002 Jul;128(7):349-57
AD - Humboldt University Berlin, Charite Campus Mitte, Institute of
Pathology, Schumannstr. 20/21, 10117 Berlin, Germany.
hermann.lage@charite.de
PURPOSE: Drug-resistant phenotypes of cancer cells may be caused by
complex multimodal mechanisms of resistance. In order to gain further
insighte into these mechanisms, a P-glycoprotein-mediated
multidrug-resistant phenotype induced by daunorubicin-selection and an
alternative drug resistance due to treatment with mitoxantrone were
investigated in pancreatic carcinoma-derived cells. METHODS: For
assessing cross-resistance against various drugs, cell proliferation
assays were performed. Drug accumulation was measured by flow cytometry.
Messenger RNA expression was analyzed by Northern blot and RT-PCR,
whereas protein expression was determined by Western blot. Catalytic
activity of DNA-topoisomerases (Topo) II was determined by the
decatenation assay. RESULTS: In mitoxantrone-selected EPP85-181RNOV
cells a decreased accumulation of mitoxantrone and daunorubicin was
observed in the absence of P-glycoprotein, multidrug resistance protein
or breast cancer resistance protein over-expression. An approximately
twofold decrease of DNA topoisomerase II catalytic activity could be
observed in both drug-resistance-exhibiting cell lines. The reduction of
Topo II catalytic activity was reflected by decreased expression of Topo
IIalpha and IIbeta mRNAs and proteins. CONCLUSIONS: The decreased drug
accumulation in EPP85-181RNOV cells indicates that alternative transport
events are occurring. The decreased catalytic activity and expression of
Topo II indicate that modulation of Topo II catalytic activity
contributes to both drug-resistant phenotypes in pancreatic carcinoma
cells.
4
UI - 12202711
AU - Prokesch RW; Chow LC; Beaulieu CF; Bammer R; Jeffrey RB Jr
TI -
Isoattenuating pancreatic adenocarcinoma at multi-detector row CT:
secondary signs.
SO - Radiology 2002 Sep;224(3):764-8
AD - Department of Radiology, Lucas MRS Center, Stanford University, Calif,
USA. rupert.prokesch@univie.ac.at
PURPOSE: To assess the frequency of isoattenuating pancreatic
adenocarcinoma with multi-detector row computed tomography (CT) and
determine whether there are specific secondary signs that aid in
detection. MATERIALS AND METHODS: Fifty-three patients with pancreatic
adenocarcinoma underwent contrast material-enhanced biphasic
multi-detector row CT with curved planar reformation. Tumors were
initially deemed isoattenuating or hypoattenuating to normal pancreatic
parenchyma on the basis of visual inspection, and the degree of
attenuation was confirmed by calculating the mean attenuation
differences between normal pancreatic parenchyma and tumor
(tumor-pancreas contrast) during the pancreatic phase. Indirect signs of
pancreatic tumor were tabulated in patients with an isoattenuating
tumor. RESULTS: Of the 53 patients, six (11%) had isoattenuating tumors
with a mean tumor-pancreas contrast of 9.25 HU +/- 11.3 during the
pancreatic phase and 4.15 HU +/- 8.5 during the portal venous phase. The
secondary signs of pancreatic tumor in these six patients included an
interrupted pancreatic duct (n = 5), dilated biliary and pancreatic
ducts (n = 1), atrophic distal pancreatic parenchyma (n = 3), and mass
effect and/or convex contour abnormality (n = 3). The mean
tumor-pancreas contrast for the remaining 47 patients was 74.76 HU +/-
35.61 during the pancreatic phase. CONCLUSION: With no visible
tumor-pancreas contrast for isoattenuating tumors, indirect signs such
as mass effect, atrophic distal parenchyma, and an interrupted duct sign
are important indicators for the presence of tumor. Copyright RSNA, 2002
5
UI - 1525759
AU - Kimura N; Yonekura H; Okamoto H; Nagura H
TI -
Expression of human regenerating gene mRNA and its product in normal and
neoplastic human pancreas.
SO - Cancer 1992 Oct 1;70(7):1857-63
AD - Department of Pathology, Tohoku University School of Medicine, Sendai,
Japan.
BACKGROUND. Localization of human regenerating gene (reg) mRNA and its
product was investigated in normal and neoplastic human pancreas with
the in situ hybridization method and immunohistochemical studies.
METHODS. Both reg mRNA and reg protein were observed in acinar cells of
the pancreas, but neither was found in ductal or islet cells.
Immunoreactive reg was observed in an acinar cell carcinoma, a
pancreatoblastoma, a solid and cystic tumor, and 5 of 20 duct cell
carcinomas, but it was not found in 15 endocrine tumors and 2
microcystic adenomas. RESULTS. For comparison with reg,
alpha-1-antitrypsin (AAT), lysozyme, chromogranin A (CMG), CA 19-9,
carcinoembryonic antigen (CEA), cytokeratin, vimentin, and
alpha-fetoprotein (AFP) were assessed in those tumors. An acinar cell
carcinoma and a pancreatoblastoma had positive results for AAT,
lysozyme, cytokeratin, and AFP but negative results for vimentin. An
acinar cell carcinoma showed cells focally immunoreactive for CMG and
CEA. A solid and cystic tumor had strongly positive results for AAT and
vimentin and focally positive results for CMG and pancreatic hormones.
Microcystic adenomas had abundant glycogen and strong immunoreactivity
for cytokeratin. Ductal cell carcinomas showed cells focally positive
for AAT, lysozyme, CMG, CA 19-9, and CEA. CONCLUSIONS. The localization
of reg protein was not consist with that of any other proteins examined
in the current study. Thus, reg protein was considered a useful marker
for acinar cell differentiation; however, ectopic expression of reg also
was observed in ductal cell carcinomas. In ductal cell carcinomas,
expression of reg immunoreactivity was considered as one of phenotypic
heterogeneity, as seen in AAT, lysozyme, and CMG immunoreactivity.
6
UI - 11870779
AU - Takeuchi K; Nakamura K; Fujimoto M; Kaino S; Kondoh S; Okita K
TI -
Heat stress-induced loss of eukaryotic initiation factor 5A (eIF-5A) in
a human pancreatic cancer cell line, MIA PaCa-2, analyzed by
two-dimensional gel electrophoresis.
SO - Electrophoresis 2002 Feb;23(4):662-9
AD - Department of Gastroenterology and Hepatology of Medicine, Yamaguchi
University School of Medicine, Ube, Japan.
Alterations of intracellular proteins during the process of heat
stress-induced cell death of a human pancreatic cancer cell line, MIA
PaCa-2, were investigated using two-dimensional gel electrophoresis
(2-DE), agarose gel electrophoresis, and cell biology techniques.
Incubation of MIA PaCa-2 at 45 degrees C for 30 min decreased the cell
growth rate and cell viability without causing chromosomal DNA
fragmentation. Incubation at 51 degrees C for 30 min suppressed cell
growth and again led to death without DNA fragmentation. The cell death
was associated with the loss of an intracellular protein of M(r) 17,500
and pI 5.2 on 2-DE gel. This protein was determined to be eukaryotic
initiation factor SA (eIF-5A) by microsequencing of the N-terminal
region of peptide fragments obtained by cyanogen bromide treatment of
the protein blotted onto a polyvinylidene difluoride (PVDF) membrane.
The sequences detected were QXSALRKNGFVVLKGRP and STSKTGXHGHAKVHLVGID,
which were homologous with the sequence of eIF-5A from Gln 20 to Pro 36
and from Ser 43 to Asp 61, respectively. Furthermore, the result of
sequencing suggested that the protein was an active form of hypusinated
eIF-5A, because Lys 46 could be detected but not Lys 49, which is the
site for hypusination. These results suggest that loss of the active
form of eIF-5A is an important factor in the irreversible process of
heat stress-induced death of MIA PaCa-2 cells.
7
UI - 11961486
AU - Yokoyama M; Ochi K; Ichimura M; Mizushima T; Shinji T; Koide N; Tsurumi
TI -
T; Hasuoka H; Harada M
Matrix metalloproteinase-2 in pancreatic juice for diagnosis of
pancreatic cancer.
SO - Pancreas 2002 May;24(4):344-7
AD - Department of Laboratory Medicine, Okayama University Medical School,
Okayama, Japan. yoko@sk9.so-net.ne.jp
INTRODUCTION: Matrix metalloproteinase-2 (MMP-2) has an activity to
degrade type IV collagen and is associated with invasion angiogenesis of
malignant tumor. AIM: A diagnostic value of MMP-2 in pancreatic juice
was studied in the diagnosis of pancreatic cancer. METHODOLOGY: Using
gelatin zymography, active MMP-2 and proMMP-2 were determined in
pancreatic juice obtained endoscopically from 12 patients with
pancreatic cancer, 11 with chronic pancreatitis, and 7 control subjects.
RESULTS: ProMMP-2 was detected in 12 of 12 patients (100%) with
pancreatic cancer, 6 of 11 (54.5%) with chronic pancreatitis, and 3 of 7
(42.9%) controls. Active MMP-2 was detected in 11 patients (91.6%) with
pancreatic cancer, 2 (18.2%) with chronic pancreatitis, and none of the
control subjects. An activation ratio of MMP-2 (active MMP-2/total
MMP-2) in pancreatic juice is significantly higher in pancreatic cancer
(23.4 +/- 4.4%, mean +/- SE) than in chronic pancreatitis (2.1 +/- 1.7%)
and controls (0%) (p < 0.01). Active MMP-2 was also detected in
pancreatic juice from three cases of small pancreatic cancer (tumor <2
cm in diameter). CONCLUSION: Our observation suggests that detection of
active MMP-2 in pancreatic juice using gelatin zymography may be useful
for the diagnosis of pancreatic cancer.
8
UI - 11961497
AU - Li K; Yu S
TI -
A nested case-control study on risk of pancreatic cancer among workers
in the rubber industry.
SO - Pancreas 2002 May;24(4):417-8
9
UI - 12167582
AU - Hiotis SP; Klimstra DS; Conlon KC; Brennan MF
TI -
Results after pancreatic resection for metastatic lesions.
SO - Ann Surg Oncol 2002 Aug;9(7):675-9
AD - Department of Surgery, Memorial Sloan-Kettering Cancer Center, 1275 York
Avenue, New York, NY 10021, USA. hiotis01@med.nyu.edu
BACKGROUND: Unlike primary pancreatic carcinoma, isolated metastatic
lesions to the pancreas are uncommon. Although the value of surgical
resection is poorly documented, resection may be deemed appropriate in
selected cases. The aim of this study was to review our experience with
the operative management of pancreatic metastases. METHODS: Sixteen
patients who underwent pancreatic resection for the treatment of
metastatic disease were identified from a prospective pancreatic
database. The clinical features of and results after resection were
examined. RESULTS: Renal cell carcinoma was the most frequent primary
histopathology (10 of 16; 62%). In the remaining patients, the primary
histopathology was non-small-cell lung cancer (n = 3), sarcoma (n = 1),
melanoma (n = 1), or transitional cell carcinoma of the bladder (n = 1).
A prolonged disease-free interval (median, 7.5 years) was characteristic
of most patients. Operative procedures performed included eight
pancreaticoduodenectomies, seven distal pancreatectomies, and one total
pancreatectomy. The operative mortality was 6%, and the morbidity was
25%. The overall 2- and 5-year actuarial survival rates were 62% and
25%, respectively. A trend toward improved survival was observed in the
renal cell carcinoma patients, but this finding was not statistically
significant. CONCLUSIONS: Long-term survival after pancreatic resection
for metastatic disease is achievable, and patients with primary renal
cell carcinoma seem to have a more favorable prognosis. Surgical
resection should thus be offered to selected patients with isolated
metastatic disease to the pancreas.
10
UI - 12233216
AU - Polus M; Bours V; Jerusalem G; Sautois B; Fillet G
TI -
[How I treat...advanced cancer of the pancreas with a novel approach
directed against new targets]
SO - Rev Med Liege 2002 Jul;57(7):428-32
AD - Service d'Oncologie medicale, CHU, Sart Tilman.
A better knowledge of fundamental mechanisms of carcinogenesis allows
the development of novel therapeutic tools specifically targeting the
cancer cell. Our understanding of cellular and molecular mechanisms
controlling cellular cycle and cell survival is an important step for
new anti-cancer treatments. This review will focus on new therapeutic's
strategies in advanced pancreatic cancer.
11
UI - 12096319
AU - Saftoiu A; Ciurea T
TI -
The role of imaging for the evaluation of pancreatic cancer
resectability.
SO - Rom J Gastroenterol 2002 Mar;11(1):78-9; discussion 79-80
12
UI - 12216484
AU - Granov AM; Tiutin LA; Ryzhkova DV; Kostenikov NA; Fadeev NP; Savello VE;
TI -
Pavlovskii AV; Tlostanova MS; Efimenko AV; Stanzhevskii AA
[Assessment of 18FDG PET for diagnosis of pancreatic tumors]
SO - Vestn Rentgenol Radiol 2002 Mar-Apr;(2):18-22
AD - Central Research Institute of X-ray and Radiation Studies, Ministry of
Health of the Russian Federation, Saint Petersburg.
The paper examines the informational value of positron emission
tomography (PET) using 18FDG in the diagnosis of malignant of neoplasms
of the pancreas and in the estimation of the extent of a metastatic
involvement. Forty-four patients (26 males and 18 females whose age
ranged from 28 to 60 years) with histologically verified cancer of the
pancreas were examined. The study was conducted in the whole body mode
on an Ecat Exact 47 positron emission tomograph following 70-90 minutes
of administration of 18FDG, 370-420 MBk. To assess the findings, the
differential accumulation ratio (DAR) of formation/liver was calculated.
The mean DAR in patients with benign and malignant pancreatic tumors was
1.17 +/- 0.064 and 4.90 +/- 0.3 (p < 0.05). There was a false positive
case in a patient with an exacerbation of chronic pancreatitis in the
study. A relationship was observed between the level of tumor tissue
18FDG capture and the degree of malignancy. PET scanning in the whole
body mode estimates the extent of a tumorous process. The authors' data
show that the liver was most commonly involved in a metastatic process
(96.6%). Hence, 18FDG PET is a highly informative technique in the
diagnosis of malignant pancreatic tumors and in the estimation of the
extent of a metastatic process and permits a differential diagnosis
between benign and malignant tumors.
13
UI - 12354980
AU - Pinol V; Castells A; Bordas JM; Real MI; Llach J; Montana X; Feu F;
TI -
Navarro S
Percutaneous self-expanding metal stents versus endoscopic polyethylene
endoprostheses for treating malignant biliary obstruction: randomized
clinical trial.
SO - Radiology 2002 Oct;225(1):27-34
AD - Department of Gastroenterology, Institut de Malalties Digestives,
Hospital Clinic, Villarroel 170, 08036 Barcelona, Spain.
PURPOSE: To compare percutaneous self-expanding metal stents with
conventional endoscopic polyethylene endoprostheses for treatment of
malignant biliary obstruction by means of a prospective randomized
clinical trial. MATERIALS AND METHODS: Patients with biliary obstruction
due to inoperable primary carcinoma of the pancreas, gallbladder, or
bile ducts or regional lymph node metastases were included. Evaluated
outcomes included technical and therapeutic success rates, morbidity and
30-day mortality rates, hospital stay length and readmission, biliary
reobstruction, and overall survival rates. Data were analyzed according
to both the intention-to-treat principle and the treatment actually
administered. Univariate (Kaplan-Meier method) and multivariate (Cox
model) analyses were performed. RESULTS: After randomization, 28
patients were assigned to receive a percutaneous self-expanding metal
stent and 26 patients to receive a 12-F endoscopic polyethylene
prosthesis. The technical success rates of both implantation procedures
were similar (percutaneous, 75% [21 of 28 patients]; endoscopic, 58% [15
of 26 patients]; P =.29), whereas therapeutic success was higher in the
percutaneous group (71% [20 of 28 patients] vs 42% [11 of 26 patients];
P =.03). However, major complications were more common in the
percutaneous group (61% [17 of 28 patients] vs 35% [nine of 26
patients]; P =.09) but did not account for differences in 30-day
mortality rates (percutaneous, 36% [10 of 28 patients]; endoscopic, 42%
[11 of 26 patients]; P =.83). Overall median survival was significantly
higher in the percutaneous group than in the endoscopic group (3.7 vs
2.0 months; P =.02). Cox regression analysis enabled identification of
placement of the percutaneous self-expanding metal stent as the only
independent predictor of survival (relative risk, 2.19; 95% CI: 1.11,
4.31; P =.02). CONCLUSION: Placement of a percutaneous self-expanding
metal stent is an alternative to placement of an endoscopic polyethylene
endoprosthesis in patients with malignant biliary obstruction.
14
UI - 12324754
AU - Mossner J; Teich N
TI -
Genetic disorders in pancreatitis: Implications in the pathogenesis of
acute and chronic pancreatitis.
SO - Surgery 2002 Sep;132(3):421-3
AD - University of Leipzig, Medizinische Klinik und Poliklinik II, Germany.
15
UI - 12358243
AU - Tada M; Komatsu Y; Kawabe T; Sasahira N; Isayama H; Toda N; Shiratori Y;
TI -
Omata M
Quantitative analysis of K-ras gene mutation in pancreatic tissue
obtained by endoscopic ultrasonography-guided fine needle aspiration:
clinical utility for diagnosis of pancreatic tumor.
SO - Am J Gastroenterol 2002 Sep;97(9):2263-70
AD - Department of Gastroenterology, Faculty of Medicine, University of
Tokyo, Japan.
OBJECTIVES: Endoscopic ultrasonography-guided fine needle aspiration
(EUS-FNA) has become established in the diagnosis of pancreatic cancer.
The combination of pathological diagnosis and analysis for mutant K-ras
gene was investigated to improve the accuracy of diagnosis. METHODS:
EUS-FNA was performed in 34 patients with pancreatic masses (26
adenocarcinomas and eight chronic pancreatitis). Mutant ras gene was
analyzed semiquantitatively in the specimens obtained by EUS-FNA as well
as in pancreatic juice obtained by ERCP. RESULTS: Mutant gene was
detected at high amounts (more than 2% of total ras genes) in 20 of 26
(77%) specimens of EUS-FNA and in 12 of 19 (63%) of pancreatic juice in
cases with pancreatic carcinoma. Cytological diagnosis of malignancy by
EUS-FNA was found in 16 of 26 (62%) patients with pancreatic cancer.
Accurate diagnosis of the carcinoma was 21 of 26 (81%) by combined
cytology and molecular method of EUS-FNA, and increased to 23 of 26
(88%) by adding molecular analysis of pancreatic juice. In contrast,
mutant gene was absent or low level despite suspicious cytology in
patients with benign pancreatic lesion. CONCLUSION: Quantitative
analysis of mutant ras gene supplemented conventional cytology of
EUS-FNA and ERCP. Detection of mutation at high amounts may represent
pancreatic cancer, whereas its absence increased the possibility of
benign lesion.
16
UI - 11115825
AU - Malats N; Casals T; Porta M; Guarner L; Estivill X; Real FX
TI -
Cystic fibrosis transmembrane regulator (CFTR) DeltaF508 mutation and 5T
allele in patients with chronic pancreatitis and exocrine pancreatic
cancer. PANKRAS II Study Group.
SO - Gut 2001 Jan;48(1):70-4
AD - Grup de Recerca d'Epidemiologia Clinica i Molecular del Cancer, Institut
Municipal d'Investigacio Medica, Universitat Pompeu Fabra, Barcelona,
Universitat Autonoma de Barcelona, Spain. nuria@imim.es
BACKGROUND: An increased risk of chronic pancreatitis has been described
among carriers of the cystic fibrosis transmembrane regulator (CFTR)
mutation. In addition, patients with cystic fibrosis may have a higher
risk of exocrine pancreatic cancer. AIMS: To determine the prevalence of
the DeltaF508 mutation and 5T allele, the most common CFTR disease
related variants, and to assess their association with lifestyle factors
in an unselected series of patients with chronic pancreatitis or
pancreatic cancer. SUBJECTS: Patients recruited to the multicentre
PANKRAS II study with a diagnosis of chronic pancreatitis and pancreatic
cancer from whom normal DNA was available. METHODS: The DeltaF508
mutation and 5T allele were analysed using polymerase chain reaction
amplified normal DNA. Information on clinical and lifestyle factors was
obtained through personal interviews. RESULTS: Among patients with
pancreatitis, no DeltaF508 alleles were found and the prevalence of the
5T allele was 10.5%, similar to that described in the general
population. Among patients with pancreatic cancer, the prevalence of the
DeltaF508 mutation and the 5T allele was 2.4% and 5.5%, respectively. 5T
allele carriers with cancer consumed significantly less alcohol than
non-carriers (p=0.038). CONCLUSIONS: Our findings do not support the
view that the DeltaF508 mutation and 5T allele confer a higher risk of
chronic pancreatitis or pancreatic cancer. Nevertheless, our data
suggest that interactions between CFTR polymorphism and environmental
factors may play a role in the pathogenesis of these diseases. Our study
emphasises the need for a multinational study to conclusively establish
the role of CFTR variants as genetic susceptibility factors for chronic
pancreatitis and pancreatic cancer.
17
UI - 11677475
AU - Pugliese V; Pujic N; Saccomanno S; Gatteschi B; Pera C; Aste H; Ferrara
TI -
GB; Nicolo G
Pancreatic intraductal sampling during ERCP in patients with chronic
pancreatitis and pancreatic cancer: cytologic studies and k-ras-2 codon
12 molecular analysis in 47 cases.
SO - Gastrointest Endosc 2001 Nov;54(5):595-9
AD - Center for Gastrointestinal Endoscopy, the Department of Oncology,
University of Genoa, Italy.
BACKGROUND: A preoperative tissue diagnosis of pancreatic cancer is
desirable but difficult to obtain. METHODS: Pancreatic brush cytology,
salvage cytology, and collection of pancreatic juice were attempted
prospectively during ERCP in 34 patients with pancreatic cancer and 11
with chronic pancreatitis. K-ras-2 codon 12 was analyzed for presence
and type of point mutations. RESULTS: Brush cytology coupled with
salvage cytology had a sensitivity of 74%. The addition of cytologic
analysis of pancreatic juice did not substantially improve sensitivity
(76%). K-ras-2 was mutated in both cancer (87%) and pancreatitis (40%).
The specificity for cytology was 100% and for K-ras-2 mutations 60%.
Combining cytology with mutation analysis increased sensitivity to 93%
but reduced the positive predictive value. The negative predictive value
never exceeded 75%. None of the patients with chronic pancreatitis had
cancer develop (median follow-up 60 months). CONCLUSIONS: Pancreatic
ductal brushing with salvage cytology is useful in the diagnosis of
cancer, whereas cytologic analysis of pancreatic juice can be abandoned.
At present, K-ras-2 mutation is not useful for differentiating
pancreatic cancer from chronic pancreatitis or the identification of
patients with chronic pancreatitis at risk for malignant transformation.
18
UI - 11921523
AU - Mery CM; Duarte-Rojo A; Paz-Pineda F; Gomez E; Robles-Diaz G
TI -
[Does cholestasis change the clinical usefulness of CA 19-9 in
pacreatobiliary cancer?]
SO - Rev Invest Clin 2001 Nov-Dec;53(6):511-7
AD - Departamento de Gastroenterologia, Instituto Nacional de Ciencias
Medicas y Nutricion Salvador Zubiran.
BACKGROUND: CA 19-9 is used for diagnosis of gastrointestinal neoplasia,
mainly pancreatic and biliary cancer. False positive results have been
described in cholestasis. OBJECTIVE: To establish the clinical value of
CA 19-9 in the diagnosis of pancreatic and biliary cancer in patients
with and without cholestasis. METHODS: Five hundred forty-eight medical
records of patients with serum CA 19-9 determination performed from
May-1996 to June-1998 were reviewed. Cases were grouped by final
diagnosis; malignancy was established by histology or clinical and
radiological characteristics. ROC curves were used to calculate ideal
cut-off values (ICV) for the test. Cholestasis was defined as
bilirrubinemia above 3 mg/dL. RESULTS: Thirty percent of serum
determinations were done in patients with non-pancreatic and
non-hepatobiliary benign diseases (only 1.3% with values > or = 100
U/mL). CA 19-9 levels were higher in pancreatic and hepatobiliary
malignancy compared to benign diseases of the same origin, as well as in
pancreatic cancer when compared with hepatobiliary cancer. ICV for
differentiation of malignant hepatobiliary diseases was set around 100
U/mL, with increased specificity when compared with the usual cut-off
value (37 U/mL). Cholestasis increased the values of the antigen in
malignant and benign diseases and modified the efficacy of the test by
increasing sensitivity while decreasing specificity. The ICV for
determining resectability in pancreatic tumors was 224 U/mL.
CONCLUSIONS: CA 19-9 is a valuable test for diagnosis of malignant
pancreato-hepatobiliary disease. Given that cholestasis modifies the
operational characteristics of the test, a cut-off value has to be
tailored for each patient depending on the clinical setting, so to
maintain the usefulness of the marker.
19
UI - 12045867
AU - Nakagohri T; Asano T; Kenmochi T; Urashima T; Ochiai T
TI -
Long-term surgical outcome of noninvasive and minimally invasive
intraductal papillary mucinous adenocarcinoma of the pancreas.
SO - World J Surg 2002 Sep;26(9):1166-9
AD - Second Department of Surgery, Chiba University School of Medicine, 1-8-1
Inohana, Chuo-ku, Chiba 260-8670, Japan. tnakagor@east.ncc.go.jp
The objective of this study was to clarify the long-term outcome after
surgical resection in patients with noninvasive and minimally invasive
intraductal papillary mucinous adenocarcinoma. We performed a
retrospective review of the clinicopathological features and outcome in
patients who underwent pancreatic resection for noninvasive and
minimally invasive intraductal papillary mucinous adenocarcinoma between
invasive structures were pathologically observed in five cases. The mean
age of patients with either noninvasive (n = 16) or minimally invasive n
= 5) adenocarcinoma was 61 years. Of the patients with minimally
invasive adenocarcinoma, 4 had abdominal pain. Conversely, 7 patients
with noninvasive adenocarcinoma had no complaint. The mean size of
noninvasive and minimally invasive tumors was 2.5 cm (range 0.8 to 4.0)
and 3.3 cm (range 2.5 to 4.5), respectively. The overall 5-year and
10-year survival rates for all 21 patients were 89% and 47%,
respectively. Disease recurred in 3 patients; 2 patients with minimally
invasive adenocarcinoma and 1 with noninvasive adenocarcinoma.
Recurrence sites were peritoneum = 2) and main pancreatic duct of the
remnant pancreas (n = 1); 5 disease-free patients died of unrelated
causes. The remaining 13 patients are alive and disease free 3 to 12
years after surgery. Noninvasive and minimally invasive intraductal
papillary mucinous adenocarcinoma had a favorable prognosis after
surgical treatment.
20
UI - 10817437
AU - Yamaguchi K; Noshiro H; Shimizu S; Morisaki T; Chijiiwa K; Tanaka M
TI -
Long-term and short-term survivors after pancreatectomy for pancreatic
cancer.
SO - Int Surg 2000 Jan-Mar;85(1):71-6
AD - Department of Surgery and Oncology, Graduate School of Medical Sciences,
Kyushu University, Fukuoka, Japan.
yamaguch@mailserver.med.kyushu-u.ac.jp
Out of 63 Japanese patients with pancreatic carcinoma who underwent
surgical resection, 8 short-term survivors who died within 3 months
after resection and 6 long-term survivors who were alive for more than 3
years after resection were compared regarding 26 clinicopathological
parameters. The 8 short-term survivors were significantly older than the
6 long-term survivors (63.7 versus 47.8 years, P = 0.0099). The mean
peripheral lymphocyte count was significantly smaller in the short-term
survivors than in the long-term survivors (1,212 versus 2,115 /microl, P
= 0.0459). Operative blood loss was significantly larger in the
short-term survivors than in the long-term survivors (2,393 versus 1,043
g, P = 0.0157). The surgical margin was affected by malignant cells in 7
of the 8 short-term survivors, but in only 2 of the 6 long-term
survivors (P = 0.0362). Of the 8 short-term survivors, 5 were in
comprehensive stage IV and 3 in stage III, while 3 of the 6 long-term
survivors were in stage III, two in stage II, and one in stage I (P =
0.0487). All the 8 short-term survivors were of the comprehensive
curability C, while 3 of the 6 long-term survivors were of A, one B and
the other two C (P = 0.0239). Multiple regression analysis of these 6
profound factors showed that the peripheral lymphocyte count was an
independent significant parameter to differentiate the short-term and
long-term survivors. These findings suggest that, although the
aggressive nature of pancreatic cancer has been accepted, the clinical
course after pancreatectomy would also depend upon the immunological
state of the patient.
21
UI - 12377966
AU - Brett BT; Smith SC; Bouvier CV; Michaeli D; Hochhauser D; Davidson BR;
TI -
Kurzawinski TR; Watkinson AF; Van Someren N; Pounder RE; Caplin ME
Phase II study of anti-gastrin-17 antibodies, raised to G17DT, in
advanced pancreatic cancer.
SO - J Clin Oncol 2002 Oct 15;20(20):4225-31
AD - Department of Medicine, Royal Free Hospital National Health Service
Trust, London, United Kingdom.
PURPOSE: The prognosis for advanced pancreatic cancer remains poor.
Gastrin acts as a growth factor for pancreatic cancer. We describe the
first study of the antigastrin immunogen G17DT in pancreatic cancer. Our
aims were to determine the antibody response, safety, tolerability, and
preliminary evidence of efficacy of G17DT in advanced pancreatic cancer.
PATIENTS AND METHODS: Thirty patients with advanced pancreatic cancer
were immunized with three doses of either 100 micro g or 250 micro g of
G17DT. RESULTS: In the whole group, 20 (67%) of 30 patients produced an
antibody response. The 250- micro g dose resulted in a significantly
greater response rate of 82% compared with 46% for the 100- micro g
group (P =.018). The most significant side effects, seen in three
patients, were local abscess and/or fever. The median survival for the
whole group from the date of the first immunization was 187 days; median
survival was 217 days for the antibody responders and 121 days for the
antibody nonresponders. The difference in survival between the antibody
responders and nonresponders was significant (P =.0023). CONCLUSION:
Patients with advanced pancreatic cancer are able to mount an adequate
antibody response to G17DT. The 250- micro g dose is superior to the
100- micro g dose, and it appears to be generally well tolerated.
Antibody responders demonstrate significantly greater survival than
antibody nonresponders. Phase III studies are currently underway in
order to determine efficacy.
22
UI - 2154467
AU - Smeekens SP; Steiner DF
TI -
Identification of a human insulinoma cDNA encoding a novel mammalian
protein structurally related to the yeast dibasic processing protease
Kex2.
SO - J Biol Chem 1990 Feb 25;265(6):2997-3000
AD - Howard Hughes Medical Institute, Chicago, Illinois.
We have identified a human insulinoma cDNA (PC2) that encodes a protein
homologous to the precursor processing Kex2 endoprotease of yeast by
using a polymerase chain reaction to detect and amplify conserved
sequences within the catalytic site. The 638-residue amino acid sequence
of PC2 begins with a cleavable signal peptide, indicating that it enters
the secretory pathway, and contains a 282-residue domain that is
homologous to the catalytic modules of both Kex2 and the related
bacterial subtilisins. Within this region 49 and 27% of the amino acids
are identical to those in the aligned Kex2 and subtilisin BPN'
sequences, respectively, and the catalytically essential Asp, His, and
Ser residues are all conserved. Northern blot analysis revealed the
presence of 2.8- and 5.0-kilobase hybridizing bands in mRNA from the
insulinoma. The PC2 protein also shows great similarity to the
incomplete NH2-terminal sequence of the human furin gene product, a
putative membrane-inserted receptor-like molecule. We propose that PC2
is a member of a family of mammalian Kex2/subtilisin-like proteases that
includes members involved in a number of specific proteolytic events
within cells, including the processing of prohormones.
23
UI - 11953884
AU - Rohloff J; Zinke J; Schoppmeyer K; Tannapfel A; Witzigmann H; Mossner J;
TI -
Wittekind C; Caca K
Heparanase expression is a prognostic indicator for postoperative
survival in pancreatic adenocarcinoma.
SO - Br J Cancer 2002 Apr 22;86(8):1270-5
AD - Department of Medicine II, Leipzig University, Philipp-Rosenthal-Str.
27, 04103 Leipzig, Germany.
Pancreatic ductal adenocarcinoma has a median survival of less than 6
months from diagnosis. This is due to the difficulty in early diagnosis,
the aggressive biological behaviour of the tumour and a lack of
effective therapies for advanced disease. Mammalian heparanase is a
heparan-sulphate proteoglycan cleaving enzyme. It helps to degrade the
extracellular matrix and basement membranes and is involved in
angiogenesis. Degradation of extracellular matrix and basement membranes
as well as angiogenesis are key conditions for tumour cell spreading.
Therefore, we have analysed the expression of heparanase in human
pancreatic cancer tissue and cell lines. Heparanase is expressed in cell
lines derived from primary tumours as well as from metastatic sites. By
immunohistochemical analysis, it is preferentially expressed at the
invading edge of a tumour at both metastatic and primary tumour sites.
There is a trend towards heparanase expression in metastasising tumours
as compared to locally growing tumours. Postoperative survival
correlates inversely with heparanase expression of the tumour reflected
by a median survival of 34 and 17 month for heparanase negative and
positive tumours, respectively. Our results suggest, that heparanase
promotes cancer cell invasion in pancreatic carcinoma and could be used
as a prognostic indicator for postoperative survival of patients.
Copyright 2002 Cancer Research UK
24
UI - 10937052
AU - Geradts J; Hruban RH; Schutte M; Kern SE; Maynard R
TI -
Immunohistochemical p16INK4a analysis of archival tumors with deletion,
hypermethylation, or mutation of the CDKN2/MTS1 gene. A comparison of
four commercial antibodies.
SO - Appl Immunohistochem Mol Morphol 2000 Mar;8(1):71-9
AD - Nuffield Department of Pathology & Bacteriology, University of Oxford,
John Radcliffe Hospital, United Kingdom. joseph.geradts@ndp.ox.ac.uk
The MTS1/CDKN2/p16 gene encoding the p16INK4a tumor-suppressor protein
is commonly inactivated by homozygous deletion or hypermethylation of
the promoter in a wide range of human malignancies. In select tumor
types, including pancreatic adenocarcinomas, intragenic mutations are
found in a significant percentage of cases. The immunoreactivity of
mutant p16 proteins has not been comprehensively studied. Moreover, the
immunohistochemical properties of commercially available antibodies have
not been described in detail. We studied 35 pancreatic adenocarcinomas
with a molecularly defined p16 status (16 homozygous deletions, 3
hypermethylated cases, and 16 tumors with an intragenic mutation in one
allele associated with loss of the second allele). In addition, we
studied nine cell lines (three homozygous deletions, three
hypermethylated lines, and three intragenic mutations). Paraffin
sections of the tumors and cell blocks were reacted with four different
anti-p16 antibodies: polyclonal and monoclonal (clone G175-405)
antibodies from PharMingen, monoclonal antibody DCS-50 from Oncogene
Science, and monoclonal antibody ZJ11 from Neo-Markers. Optimal staining
conditions were established for each antibody. The pancreatic carcinomas
with homozygous p16 deletions were largely devoid of nuclear staining
(admixed nonneoplastic cells served as internal positive controls); only
one adenocarcinoma each reacted with DCS-50 and the polyclonal antibody,
and five were positive with ZJ11, suggesting that nonspecific nuclear
staining can occur under certain conditions. Antibody DCS-50 produced
nuclear staining in all three hypermethylated carcinomas, whereas
G175-405 stained none of them. Three of the four antibodies produced
nuclear immunoreactivity in 7 to 14 of the 16 carcinomas carrying p16
mutations; G175-405 showed only weak reactivity in one case. Cytoplasmic
staining was present in all carcinomas and cell lines and with all
antibodies and therefore cannot be considered specific; it was strongest
with G175-405. Thus, we found antibody G175-405 to be the most specific,
and monoclonals DCS-50 and ZJ11 the least specific for wild-type p16.
However, the former tends to give stronger cytoplasmic background
staining. For tumor types in which p16 mutations are uncommon, the
PharMingen polyclonal antibody may be a suitable alternative.
25
UI - 10981872
AU - Skacel M; Ormsby AH; Petras RE; McMahon JT; Henricks WH
TI -
Immunohistochemistry in the differential diagnosis of acinar and
endocrine pancreatic neoplasms.
SO - Appl Immunohistochem Mol Morphol 2000 Sep;8(3):203-9
AD - Department of Anatomic Pathology, Cleveland Clinic Foundation, Ohio
44195, USA. mskacel@pol.net
Histologic differential diagnosis of acinar cell carcinoma (ACC), mixed
acinar-endocrine cell carcinoma (MAEC), and pancreatic endocrine tumors
(PET) can be difficult but is important because of differences in their
clinical behavior. This study investigates the utility of
immunohistochemistry (IHC) in this differential diagnosis using
immunohistochemical stains that are available in most laboratories. IHC
was performed on paraffin-embedded tissue in ACC (n = 6), MAEC (n = 2),
and PET (n = 13), using synaptophysin (SYN), chromogranin (CHR),
chymotrypsin (CHY), and alpha-1-antitrypsin (AAT). Electron microscopy
(EM) was performed in all cases to confirm the diagnosis. Long-term
follow-up and death of disease (DOD) was known in all patients. The ACCs
stained as follows: CHY (4/6), AAT (3/6), SYN (4/6); CHR was negative in
all cases. Both cases of MAEC stained with CHY, AAT, and SYN (2/2); CHR
was negative. PET stained as follows: SYN (13/13), CHR (8/13), CHY
(4/13), AAT (5/13). In the ACC/ MAEC group, six of eight patients were
DOD at mean follow-up of 11 months. Among the PET, two of 16 patients
were DOD at mean follow-up of 37 months. Considerable immunophenotypic
overlap exists between ACC, MAEC, and PET. Consequently, one can neither
confirm nor rule out a diagnosis of ACC or MAEC using generally
available immunohistochemical stains alone. These findings support a
role for EM in the evaluation of exocrine and endocrine pancreatic
neoplasms.
26
UI - 11360677
AU - Zhang SN; Yuan SZ; Zhu ZH; Wen ZF; Huang ZQ; Zeng ZY
TI -
Apoptosis induced by 5-flucytosine in human pancreatic cancer cells
genetically modified to express cytosine deaminase.
SO - Acta Pharmacol Sin 2000 Jul;21(7):655-9
AD - Department of Gastroenterology, Sun Yat-Sen Memorial Hospital, Sun
Yat-Sen University of Medical Sciences, Guangzhou 510120, China.
AIM: To elucidate the pattern of 5-flucytosine (5-FC)-induced apoptosis
and its role in gene therapy of human pancreatic cancer. METHODS: The
human pancreatic cancer SW1990 cells (CEA-producing) were infected with
recombinant adenoviruses (Adex1CEA-prCD or Adex1CEA-prZ). Expression of
CD gene protein was examined by western blot. Apoptosis induced by 5-FC
in human pancreatic cancer SW1990 cells genetically modified to express
cytosine deaminase was observed by means of electron microscopy, DNA
electrophoresis, and flow cytometry analysis techniques. RESULTS: The
SW1990 cells infected with Adex1CEA-prCD were treated with 5-FC at 100
mumol.L-1 for 48 h, and cell apoptosis was observed. Typical apoptosis
morphological feature appeared and DNA ladder could be demonstrated on
DNA electrophoresis. Apoptosis peak was also showed by flow cytometry.
Apoptotic cells accounted for 34.6% of the cell population. Cells in G1,
S, and G2/M phase of cell cycle were 64%, 11%, and 7%, respectively.
CONCLUSION: The apoptosis induced by 5-FC may be a primary mechanism in
CD gene therapy of pancreatic cancer.
27
UI - 11893038
AU - Oh YL; Song SY; Ahn G
TI -
Expression of maspin in pancreatic neoplasms: application of maspin
immunohistochemistry to the differential diagnosis.
SO - Appl Immunohistochem Mol Morphol 2002 Mar;10(1):62-6
AD - Department of Diagnostic Pathology, Samsung Medical Center, Sungkyunkwan
University School of Medicine, Seoul, Korea.
Maspin is a unique member of the serpin family, which inhibits tumor
invasion and metastasis of the human breast and prostate cancers.
Immunohistochemical evaluation of the maspin expression in pancreatic
neoplasms has never been performed. The authors examined the expression
of maspin in various pancreatic neoplasms to investigate its usefulness
as an adjunct diagnostic marker. Formalin-fixed, paraffin-embedded
tissue sections from 107 pancreatic neoplasms were immunostained with
anti-maspin antibody using an EnVision+ System. Maspin was expressed in
all ductal adenocarcinomas, of which 78.9% (30/38) were high expressors
and 21.1% (8/38) were low expressors. All 13 intraductal papillary
mucinous tumors and 11 of the 13 mucinous cystic tumors reacted to
maspin with stronger expressions in carcinomatous lesions. In contrast,
acinar cell carcinoma, pancreatic endocrine tumors,
solid-pseudopapillary tumors, and serous cystadenomas demonstrated no
maspin expression. In addition, nonneoplastic pancreatic parenchyma and
chronic pancreatitis lacked expression. The current study suggests that
maspin may be of importance in the pathobiology of pancreatic neoplasms
with epithelial origin, especially pancreatic tumors that are composed
of mucin-producing cells. It may be useful in separating ductal
adenocarcinoma from acinar cell carcinoma, pancreatic endocrine tumor,
solid-pseudopapillary tumor, and chronic pancreatitis, especially in
needle biopsy specimens.
28
UI - 3022894
AU - Thivolet C; Chatelain P; Haftek M; Durand A; Pugeat M
TI -
[Morphologic and functional study of a human insulin-secreting cell
line]
SO - C R Acad Sci III 1986;303(10):381-6
Monolayer cell cultures were obtained from a human insulinoma (HIN)
after collagenase digestion. HIN cells were initially plated on
extracellular matrix (ECM) secreted by bovine corneal endothelial cells.
Capsular integrity from cell clusters quickly interrupted and cell began
to migrate as adhesive sheets onto ECM. After 2 months on ECM cell
attachment and proliferation occurred on plastic allowing cloning of
cells by limiting dilution. 9 clones were successfully cultured for 7
months with 20 subsequent passages. Immunoreactivity for insulin by
indirect immunofluorescence typical secretory granules by electron
microscopy and stable amounts of immunoreactive insulin in culture media
suggest that HIN cells are beta cell related. One clone HIN D8 when
challenged for half an hour with either 30 mM glucose, 1 mM isobutyl
Methylxanthine 4 mM Tolbutamide, 10(-6) M glucagon responded
respectively with a 1.5, 2, 3 and 1.5 fold increase in insulin output.
Population doubling time of HIN D8 was 42 hrs. Establishment of such
insulin secreting cell lines provides a valuable tool for d
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