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Abramson Cancer CenterNCI CANCERLIT® Search: Diagnosis-Histopathology-Pathogenesis of Pancreatic Cancer - May 2002
National Cancer Institute®
Last Modified: May 1, 2002
Table of Contents
1
UI - 11894319
AU - Wilson H; Butler LJ; Repetto G; Love J
TI -
Providing care to patients with pancreatic cancer: a retrospective chart
review.
SO - Can Oncol Nurs J 2000 Fall;10(4):134-8
AD - QEII Health Sciences Centre, Halifax.
Pancreatic cancer may be considered rare, yet in Canada it is the fourth
leading cause of death by cancer in the elderly. This study was
conducted in a large tertiary centre to determine the symptoms
experienced by patients and the response by health professionals in
providing supportive care. This paper reports the results of a
retrospective review of health records from patients diagnosed with
pancreatic cancer (n = 99). Results indicate that pain, nausea,
vomiting, and anorexia were frequently reported. There was a lack of
consistency in the documentation of nursing care and little evidence of
an organized, planned approach for care delivery. The role of the
interdisciplinary health care team and its members in managing this
devastating disease and its impact on patient quality of life was
difficult to ascertain. The development of an integrated approach to the
care of patients with pancreatic cancer is presented.
2
UI - 11967685
AU - Wong YT; Brams DM; Munson L; Sanders L; Heiss F; Chase M; Birkett DH
TI -
Gastric outlet obstruction secondary to pancreatic cancer: surgical vs
endoscopic palliation.
SO - Surg Endosc 2002 Feb;16(2):310-2
AD - Department of General Surgery, Lahey Clinic, 41 Mall Road, Burlington,
MA 01805, USA. yewtohwong@hotmail.com
BACKGROUND: Gastric outlet obstruction in patients with pancreatic
cancer has a grim prognosis. Open surgical bypass is associated with
high morbidity, whereas endoscopic duodenal stenting appears to provide
better palliation. METHODS: We reviewed the medical records of patients
with gastric outlet obstruction secondary to pancreatic carcinoma who
1998. The data included stage of disease, American Society of
Anesthesiologists (ASA) class, surgical interventions, complications,
and survival. RESULTS: A total of 250 patients with pancreatic cancer
were identified. Twenty-five of them (10%) had gastric outlet
obstruction. Of these 25, 17 were treated with gastrojejunostomy, six
had duodenal stenting (Wallstent), and two were resectable. There was no
significant difference between the gastrojejunostomy group and the
duodenal stenting group in ASA class or stage of disease. For the
gastrojejunostomy group, median survival was 64 days (range, 15-167) and
postoperative stay in hospital was 15 days (range, 8-39). For the
duodenal stenting group, median survival was 110.5 days (range, 42-212)
and postoperative stay was 4 days (range, 2-6). Ten patients (58.8%) in
the gastrojejunostomy group had delayed gastric emptying. All of the
patients in the duodenal stenting group were able to tolerate a soft
diet the day after stent placement. Thirty-day mortality in the
gastrojejunostomy group was 17.64%; in the duodenal stenting group, it
was 0. CONCLUSION: In pancreatic carcinoma patients with gastric outlet
obstruction, duodenal stenting results in an earlier discharge from
hospital and possibly improved survival.
3
UI - 11910485
AU - Park SJ; Kim SW; Jang JY; Lee KU; Park YH
TI -
Intraoperative transfusion: is it a real prognostic factor of
periampullary cancer following pancreatoduodenectomy?
SO - World J Surg 2002 Apr;26(4):487-92
AD - Department of Surgery, Seoul National University College of Medicine, 28
Yongon-dong, Chongno-gu, Seoul 110-744, Korea.
The purpose of this study was to clarify the prognostic significance of
transfusion following pancreatoduodenectomy for periampullary cancers.
We analyzed 357 periampullary cancers from 1985 to 1997 (ampullary
cancer 130 cases, distal bile duct cancer 141 cases, pancreatic head
cancer 86 cases). A total of 215 (60%) of the 357 patients have received
intraoperative transfusion. The 5-year survival rate of 130 ampullary
cancer patients was 59%; altogether, 76 patients (58%) underwent
intraoperative transfusion. The 5-year survival rate of patients without
intraoperative transfusion was 79%, whereas that of patients with a
transfusion was 47% (p = 0.029). Following multivariate analysis,
intraoperative transfusion was found to be an independent poor
prognostic factor for those with ampullary cancer (relative risk 2.174).
Among those with common bile duct cancer, the overall 5-year survival
rate was 33%, and the 5-year survival rates for patients with (n = 87)
or without (n = 54) transfusion were 25% and 38%, respectively, which
did not reach statistical significance (p = 0.0717). For those with
pancreatic head cancer, the overall 5-year survival rate was 16%, and
there was no survival difference between transfused (n = 52) and
untransfused (n = 34) patients. In the present study the reason was not
clear, although intraoperative transfusion was an independent
significant prognostic factor for ampullary cancer. Careful dissection
to minimize intraoperative bleeding is mandatory during
pancreatoduodenectomy for ampullary cancer.
4
UI - 11929809
AU - Lott ST; Chandler DS; Curley SA; Foster CJ; El-Naggar A; Frazier M;
TI -
Strong LC; Lovell M; Killary AM
High frequency loss of heterozygosity in von Hippel-Lindau
(VHL)-associated and sporadic pancreatic islet cell tumors: evidence for
a stepwise mechanism for malignant conversion in VHL tumorigenesis.
SO - Cancer Res 2002 Apr 1;62(7):1952-5
AD - Department of Molecular Genetics, The University of Texas M. D. Anderson
Cancer Center, Houston, Texas 77030-4009, USA.
Germ-line mutation of the von Hippel-Lindau (VHL) gene predisposes to
the development of multifocal, benign lesions, including retinal and
central nervous system hemangioblastomas, pheochromocytomas, and renal
and pancreatic cysts. Progression to malignancy in VHL disease is
associated primarily with the development of renal cell carcinoma (RCC)
and pancreatic islet cell tumors (PICT). Although many reports have
documented the multiple functions of the VHL protein, few have
investigated the intriguing question related to the tissue-specificity
of malignant conversion in VHL disease, a problem not easily explained
by strict genotype-phenotype correlations. We investigated a novel VHL
kindred with a preponderance of PICTs to determine whether loss of
additional genetic loci associated with the sporadic forms of RCC and
PICTs might play a role in malignant conversion in this disease. We
report the high frequency loss of heterozygosity (LOH) of genetic loci
distinct from and mapping proximal to VHL within human chromosome 3p in
the VHL kindred under study. Furthermore, chromosome 3p LOH occurs
subsequent to VHL mutation and cyst formation, and correlates with
malignant progression in VHL-associated PICTs. High frequency LOH was
also observed in sporadic PICTs in regions of 3p associated with LOH in
sporadic clear cell RCC as well as homozygous deletion in lung cancer. A
stepwise model for malignant conversion in VHL disease is herein
proposed.
5
UI - 11416115
AU - Stolzenberg-Solomon RZ; Blaser MJ; Limburg PJ; Perez-Perez G; Taylor PR;
TI -
Virtamo J; Albanes D; ATBC Study
Helicobacter pylori seropositivity as a risk factor for pancreatic
cancer.
SO - J Natl Cancer Inst 2001 Jun 20;93(12):937-41
AD - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and
Genetics and Cancer Prevention Studies Branch, Division of Clinical
Sciences, National Cancer Institute, Bethesda, MD 20892, USA.
rs221z@nih.gov
BACKGROUND: Pancreatic cancer is among the most fatal cancers worldwide
and one for which few preventable risk factors have been established.
Gastric carriage of Helicobacter pylori, particularly
cytotoxin-associated gene-A-positive (CagA+) strains, is known to be a
risk factor for peptic ulcer disease and gastric cancer and may have a
similar etiologic relationship with pancreatic cancer. METHODS: We
investigated the association of H. pylori carriage and exocrine
pancreatic cancer in a nested case-control study within the
Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort of 29 133
male Finnish smokers aged 50-69 years at baseline. Case subjects (n =
121) were matched on date of baseline serum collection, study center,
age, trial intervention, and completion of the dietary questionnaire to
226 control subjects who were alive at the time the matching case
subject was diagnosed and who remained free of cancer, during up to 10
years of follow-up. Levels of immunoglobulin G antibodies to H. pylori
whole-cell and CagA+ antigens from stored baseline serum were measured
by enzyme-linked immunosorbent assay. Smoking-adjusted odds ratios (ORs)
and 95% confidence intervals (CIs) were estimated by use of conditional
logistic regression. Statistical tests were two-sided. RESULTS:
Seroprevalence of H. pylori was 82% and 73% among case and control
subjects, respectively. Compared with seronegative subjects, those with
H. pylori or CagA+ strains were at statistically significantly elevated
risk of pancreatic cancer (OR = 1.87 [95% CI = 1.05 to 3.34]; OR = 2.01
[95% CI = 1.09 to 3.70], respectively). CONCLUSIONS: Our findings
support a possible role for H. pylori carriage in the development of
exocrine pancreatic cancer.
6
UI - 11820412
AU - Lavonius MI; Laine S; Salo S; Sonninen P; Ovaska J
TI -
Role of laparoscopy and laparoscopic ultrasound in staging of pancreatic
tumours.
SO - Ann Chir Gynaecol 2001;90(4):252-5
AD - Department of Surgery, Turku University Central Hospital, Finland.
maija.lavonius@tyks.fi
BACKGROUND AND AIMS: Radiological imaging alone is not reliable enough
in staging of pancreatic cancer. Not only because of poor sensitivity
but also because there is a tendency to overstage tumours. The aim of
the study was to compare the efficiency of spiral computed tomography
(CT), transabdominal ultrasound (US), laparoscopy (LAP) and laparoscopic
ultrasound (LUS) in staging of pancreatic tumours. MATERIAL AND METHODS:
In this prospective study 27 patients underwent pancreatic tumour
staging with CT, US, LAP and LUS. The reference standard was operative
evaluation or in case of disseminated disease laparoscopic assessment.
RESULTS AND CONCLUSIONS: Although LAP was hindered by adhesions in 11%
of the patients the benefit of LAP staging was evident in detecting
peritoneal carcinomatosis. The assessment of the local tumour expansion
of a pancreatic carcinoma was difficult for all staging modalities. LUS
did not change the decision whether to proceed with laparotomy once. In
our experience routine use of laparoscopic staging does not benefit
patients with pancreatic tumour but in selected cases it may prevent
unnecessary laparotomy.
7
UI - 11920612
AU - Missiaglia E; Moore PS; Williamson J; Lemoine NR; Falconi M; Zamboni G;
TI -
Scarpa A
Sex chromosome anomalies in pancreatic endocrine tumors.
SO - Int J Cancer 2002 Apr 1;98(4):532-8
AD - Department of Pathology, Universita di Verona, Italy.
We have investigated the status of sex chromosomes in 40 pancreatic
endocrine tumors (PETs) using 2 complementary techniques: microsatellite
and interphase FISH analysis. Twenty-five tumors were from female and 15
from male patients and included 31 nonfunctioning and 9 functioning PET
(6 insulinomas, 2 glucagonomas and 1 VIPoma). Microsatellite and FISH
analysis showed concordant results in all cases. PETs from females
showed frequent loss of chromosome X (40%) whereas PETs from males
showed relatively frequent loss of chromosome Y (36%) but never loss of
the X chromosome. Statistical analysis showed significant association of
sex chromosome loss with metastases (Spearman correlation test, r = 0.5,
p < 0.001), local invasion (r = 0.33, p < 0.05) and high proliferation
rate measured as Ki-67 index with a 5% cut-off (r = 0.42, p < 0.02). The
analysis also showed that local invasion and metastases were highly
correlated (r = 0.86). Multivariate survival analysis was therefore
carried out including local invasion and loss of sex chromosomes. The
presence of local invasion increased the risk of death almost 9 times
whereas sex chromosome loss was an independent variable associated with
a shorter survival period and an increased risk of death of
approximately 4-fold. Copyright 2002 Wiley-Liss, Inc.
8
UI - 11888712
AU - Reddy SK; Burton AW
TI -
Re: video-assisted thoracoscopic sympathectomy-splanchnicectomy.
SO - J Pain Symptom Manage 2002 Mar;23(3):177; discussion 178
9
UI - 11960385
AU - Ueki T; Walter KM; Skinner H; Jaffee E; Hruban RH; Goggins M
TI -
Aberrant CpG island methylation in cancer cell lines arises in the
primary cancers from which they were derived.
SO - Oncogene 2002 Mar 27;21(13):2114-7
AD - Department of Pathology, The Johns Hopkins Medical Institutions,
Baltimore, Maryland, MD 21205-2196, USA.
A higher prevalence of epigenetic inactivation of tumor suppressor genes
has been reported in cancer cell line populations compared to primary
cancer populations. Cancer-related genes are commonly methylated in
cancer cell lines but it is not known the extent to which tumor
suppressor genes may be artificially methylated in vitro. We therefore
examined 10 pancreatic cancer cell lines and corresponding primary
tumors for aberrant DNA methylation of promoter CpG islands of eight
genes and seven CpG islands. Using methylation-specific PCR (MSP),
methylation was not detected at any of the 15 CpG islands in 15 normal
pancreata or in an immortalized normal pancreatic duct epithelial (HPDE)
cell line. Of 150 loci examined, 49 loci were methylated in both primary
carcinomas and their corresponding cell lines, 95 loci were not
methylated in either cell lines or their corresponding primary
carcinomas. There were four loci methylated only in cell lines while
another two loci were methylated only in primary carcinomas. Overall,
the methylation status of primary carcinomas and their cell lines were
concordant in 96% of cases (144 of 150) (J statistic; J=0.92, P<0.0001).
We conclude that most of the DNA methylation of tumor suppressor genes
observed in cancer cell lines is present in the primary carcinomas from
which they were derived.
10
UI - 11959898
AU - Nilsson HO; Stenram U; Ihse I; Wadstrom T
TI -
Re: Helicobacter pylori seropositivity as a risk factor for pancreatic
cancer.
SO - J Natl Cancer Inst 2002 Apr 17;94(8):632-3
11
UI - 11964041
AU - Barth PJ; Ebrahimsade S; Hellinger A; Moll R; Ramaswamy A
TI -
CD34+ fibrocytes in neoplastic and inflammatory pancreatic lesions.
SO - Virchows Arch 2002 Feb;440(2):128-33
AD - Institute of Pathology, Philipps University Marburg, Germany.
barthp@post.med.uni-marburg.de
Besides its function as a matrix-producing cell, the CD34+ fibrocyte has
been reported to be an antigen-presenting cell capable of priming naive
T cells in situ. Therefore, it has been claimed that the CD34+ fibrocyte
may play an important role in host response to tissue damage. The
objective of the present study was to analyze the presence and
distribution of CD34+ fibrocytes and smooth muscle actin (SMA) reactive
myofibroblasts in relation to the underlying pancreatic disease. We
investigated a total of 12 pancreatic adenocarcinomas, 7 endocrine
tumors of the pancreas, and 8 cases of chronic pancreatitis; in 11
cases, normal pancreatic tissue was available. The stroma of normal
pancreatic tissue harbored diffusely scattered CD34+ fibrocytes. Chronic
pancreatitis was characterized by an increased number of stromal CD34+
fibrocytes paralleled by a gain of SMA reactive myofibroblasts which
were not observed in the normal pancreatic stroma. The stroma of
pancreatic ductal adenocarcinomas and endocrine tumors was devoid of
CD34+ fibrocytes or showed at least a focal loss of this cell type,
whereas SMA reactive myofibroblasts were detected in both endocrine
tumors and adenocarcinomas. We conclude that detection of CD34+
fibrocytes may constitute an adjunctive tool in distinguishing chronic
pancreatitis from ductal adenocarcinoma since the absence of this cell
population strongly favors a neoplastic process. Moreover, CD34+
fibrocytes and myofibroblasts appear to be involved in stromal
remodeling associated with chronic pancreatitis and ductal
adenocarcinoma.
12
UI - 11950919
AU - Klein WM; Hruban RH; Klein-Szanto AJ; Wilentz RE
TI -
Direct correlation between proliferative activity and dysplasia in
pancreatic intraepithelial neoplasia (PanIN): additional evidence for a
recently proposed model of progression.
SO - Mod Pathol 2002 Apr;15(4):441-7
AD - Department of Pathology, The Johns Hopkins Medical Institutions,
Baltimore, Maryland 21205, USA.
A growing body of morphological, clinical, and genetic observations
suggests a progression model for pancreatic ductal adenocarcinoma. In
this model, pancreatic ducts progress through a series of architectural
and cytological changes that define degrees of pancreatic
intraepithelial neoplasia (PanIN). Expressed in dividing cells, Ki-67
has been extensively used as a proliferation marker. Its expression in
different grades of PanIN has not been well studied. A total of 76
PanINs from 41 patients were histologically graded according to recently
established criteria. These PanINs were then immunolabeled with a
monoclonal antibody against Ki-67 (Mib-1). Normal ducts and invasive
ductal adenocarcinomas were also labeled with the antibody. In 15 normal
ducts, only 0.41% of the epithelial cells expressed Ki-67.
Ki-67-labeling indices in the increasing grades of PanIN were as
follows: PanIN-1A, 0.69%; PanIN-1B, 2.33%; PanIN-2, 14.08%; and PanIN-3,
22.01%. Fifteen invasive ductal adenonocarcinomas showed an average
labeling index of 36.99%. The difference in Ki-67 labeling among these
groups was statistically significant (P <.0005, Kruskal-Wallis test).
This pattern of proliferation provides additional evidence supporting
the recently proposed pancreatic progression model. It also correlates
well with known molecular changes, such as activating point mutations in
the K-ras oncogene and the loss of DPC4 and p16 gene expression. Ki-67
staining may be useful as an adjunct in the diagnosis of precancerous
lesions in the pancreas and may provide a reliable way to identify
lesions at high risk for the subsequent development of infiltrating
carcinoma.
13
UI - 11950922
AU - Schleger C; Verbeke C; Hildenbrand R; Zentgraf H; Bleyl U
TI -
c-MYC activation in primary and metastatic ductal adenocarcinoma of the
pancreas: incidence, mechanisms, and clinical significance.
SO - Mod Pathol 2002 Apr;15(4):462-9
AD - Institute of Pathology, Universitatsklinikum Mannheim, Germany.
christiane.schleger@path.ma.uni-heidelberg.de
Amplification and overexpression of c-MYC is a common event in various
neoplasias. Recently, comparative genomic hybridization (CGH) of primary
pancreatic adenocarcinomas revealed a distinct high-level amplification
of 8q23-qter, suggesting that c-MYC located on 8q24 may be a candidate
oncogene. To evaluate the biological significance and prognostic value
of c-MYC activation in pancreatic carcinoma, we performed interphase
fluorescence in situ hybridization (FISH) and immunohistochemistry on a
series of 69 primary pancreatic adenocarcinomas, 19 corresponding lymph
node metastases, and 5 pancreatic intraductal lesions. Dual color FISH
using a probe for c-MYC (8q24) and a centromeric probe for chromosome 8
revealed amplification of c-MYC in 32.3% and 29.4% of primary and
metastatic tumors, respectively. Immunostaining identified c-MYC protein
overexpression in 43.5% of primaries and 31.6% of metastases. Low
concordance between positive FISH and immunostaining (13.4%) suggests
multiple independent regulatory pathways of c-MYC activation.
Statistical evaluation revealed significant correlation (alpha = 0.033)
between c-MYC protein overexpression and histopathological tumor grade
but absence of correlation with tumor stage or lymph node status.
Analysis of pancreatic intraductal lesions showed c-MYC amplification
and protein overexpression in two of five cases in which invasive
carcinoma exhibited identical aberrations. We conclude that deregulation
of c-MYC protein is common in pancreatic cancer and that it may be
involved in early neoplastic development and progression rather than in
locoregional spread of invasive cancer.
14
UI - 11964083
AU - Rudroff C; Seibold S; Kaufmann R; Zetina CC; Reise K; Schafer U;
TI -
Schneider A; Brockmann M; Scheele J; Neugebauer EA
Expression of the thrombin receptor PAR-1 correlates with tumour cell
differentiation of pancreatic adenocarcinoma in vitro.
SO - Clin Exp Metastasis 2002;19(2):181-9
AD - Second Department of Surgery, University of Cologne, Germany.
c.rudroff@netcologne.de
Patients with pancreatic cancer frequently suffer from thrombosis due to
excess thrombin generation. Yet, the effects of thrombin on pancreatic
cancer are still poorly understood. The thrombin receptor PAR-1 is
responsible for cellular effects of thrombin. PAR-1 plays an important
role in the progression of different solid tumours in vitro. In breast
cancer the level of PAR-1 expression correlates with invasiveness. Our
aim was to correlate PAR-1 mRNA and protein expression level with the
grade of differentiation of pancreatic tissue and cancer cell lines.
PAR-1 protein was not detectable in the epithelium of healthy pancreas.
Analysis of PAR-1 protein expression by immunofluorescence staining of
pancreatic cancer cell lines revealed a correlation to the grade of
differentiation. Quantitative analysis of PAR-1 protein expression by
Western Blot analysis confirmed these observations. Analysis of PAR-1
mRNA expression showed low levels in healthy pancreas compared to
pancreatic cancer tissue and the pancreatic cancer cell line MIA PaCa-2.
The level of PAR-1 mRNA differed up to 25 fold between the respective
pancreatic cancer cell lines. The eminent differences in PAR-1
expression, both protein and mRNA, between healthy pancreatic tissue and
pancreatic cancer in vivo and in vitro emphasise the putative role of
PAR-1 in pancreatic cancer progression.
15
UI - 11836587
AU - Ueda T; Oda T; Kinoshita T; Konishi M; Nakahashi C; Takahashi S; Hasebe
TI -
T; Fukao K; Ochiai A
Neovascularization in pancreatic ductal adenocarcinoma: Microvessel
count analysis, comparison with non-cancerous regions and other types of
carcinomas.
SO - Oncol Rep 2002 Mar-Apr;9(2):239-45
AD - Pathology Division, National Cancer Center Research Institute East,
Kashiwa, Chiba, Japan.
Although neovascularization is regarded as an essential factor for tumor
growth, it is unclear whether pancreatic adenocarcinoma is also
influenced by this process. Furthermore, the reported microvessel count
(MVC) data can not be compared due to the diversity of evaluating
methods, and the relation between MVC data and metastatic potentials
remains controversial. A total of 24 pancreatic adenocarcinomas and 24
adjacent non-cancerous pancreatic parenchyma were analyzed for MVC using
anti-CD31 antibody. In addition, the MVC of 15 hypervascular tumors (10
hepatocellular carcinomas: HCC and 5 islet cell pancreatic tumors: ICT),
30 other types of adenocarcinomas (10 gastric, 10 colon and 10
intraductal papillary mucinous tumors of the pancreas: IPMT), as well as
that of non-cancerous areas, were also analyzed. The extent of hepatic
and peritoneal spread in 24 pancreatic adenocarcinoma patients was
classified and correlations with MVC were evaluated. The mean MVC of 24
pancreatic adenocarcinomas (31.6 +/- 11.1) was actually lower than that
of HCCs (91.6) or ICTs (56.4). The diversity is temperate as compared
with that of other adenocarcinomas, i.e., 42.9 in gastric carcinomas,
35.6 in colon carcinomas and 32.5 in IPMT. MVC in non-cancerous areas
were significantly higher in the pancreas (112.8) than in the stomach
(29.6) or colon (26.3). MVC ratios of the cancerous area to the
non-cancerous area were significantly lower in the pancreas (0.2818 +/-
0.100) than in the stomach (1.569 +/- 0.526, p<0.001) or the colon
(1.423 +/- 0.493, p<0.001). MVC were higher in diffuse hepatic
metastasis patients (36.0) than in limited metastasis patients (25.7).
In conclusion, MVC in pancreatic adenocarcinoma revealed vascular volume
to actually be lower than that of hypervascular tumors. We believe,
however, that this hypovascularity is due mainly to contrast with the
hyper-vascular non-cancerous pancreas, since MVC in the cancerous area
itself was at the same level as in other adenocarcinomas. In addition,
we revealed MVC to be of value for predicting the extent of liver
metastasis.
16
UI - 11836607
AU - Karanikas G; Ulrich-Pur H; Becherer A; Wiesner K; Dudczak R; Raderer M;
TI -
Kletter K
Uptake of indium-111-labeled human polyclonal immunoglobulin G in
pancreatic cancer: in vivo and in vitro studies.
SO - Oncol Rep 2002 Mar-Apr;9(2):353-7
AD - Department of Nuclear Medicine, University of Vienna, A-1090 Vienna,
Austria. georg.karanikas@akh-wien.ac.at
Radiolabeled human non-specific polyclonal immunoglobulin G (HIG), is
used for the diagnosis of inflammation/infection. Focal uptake of HIG in
malignant lesions has also been reported. We investigated the diagnostic
value of In-111-HIG in patients with known pancreatic cancer. Fourteen
consecutive patients with histologically verified pancreatic cancer were
included in this prospective study. Four of them had undergone
potentially curative surgery for their primary cancer. Eight patients
had liver metastases. Planar and SPECT images of the abdomen were
performed after administration of In-111-HIG (74-92 MBq). Scintigraphic
results were compared to conventional imaging by means of CT scanning.
In addition, In-111-HIG uptake was investigated in a panel of four
representative human pancreatic cancer cell lines. Primary pancreatic
tumors were visualized by In-111-HIG in 6 out of 10 patients
(sensitivity 60%), while 1 was false positive. In comparison, CT
scanning was true positive in 9 out of 10 patients (sensitivity 90%),
and no false positive. Visualization of liver lesions by means of
In-111-HIG was possible in 6 out of 8 patients (sensitivity 75%), while
1 was false positive. In vitro studies revealed only minimal uptake of
In-111-HIG into cells (about 3% of activity). Our data demonstrate that
In-111-HIG is able to visualize pancreatic primary cancers as well as
liver metastases. However, the minimal uptake into tumor cells, as shown
in vitro, suggests non-specific tumor related inflammatory reactions,
increased vascular permeability, release of indium from
In-111-DTPA-labeled antibody and local retention to be responsible for
visualization of the tumor site.
17
UI - 11870331
AU - Queneau PE; Sauve G; Koch S; Thibault P; Cleau D; Heyd B; Mantion G;
TI -
Carayon P
The impact on clinical practice of endoscopic ultrasonography used for
the diagnosis and staging of pancreatic adenocarcinoma.
SO - JOP 2001 May;2(3):98-104
AD - Gastroenterology Unit and Digestive and Vascular Surgery Unit,
University Hospital of Besancon, Besancon Cedex, France.
pierre-edouard.queneau@huge.ch
CONTEXT: Endoscopic ultrasonography is considered a highly accurate
procedure for diagnosing small pancreatic tumors and assessing their
locoregional extension. OBJECTIVE: To evaluate the impact of endoscopic
ultrasonography on the management of pancreatic adenocarcinoma in
clinical practice. PATIENTS: Sixty-four consecutive patients (mean age
70.5 plus/minus 11.9 years) hospitalized for staging or diagnosis of
1999). SETTING: Group 1 consisted of 52 patients with pancreatic
adenocarcinoma which was discovered using computerized tomography
scanning and/or ultrasound. Endoscopic ultrasonography was utilized for
staging purposes only in patients who were considered to be operable and
the tumor to be resectable based on computerized tomography scanning
criteria. Group 2 consisted of 12 patients who were diagnosed as having
a pancreatic adenocarcinoma using endoscopic ultrasonography whereas
computerized tomography scanning and ultrasound was negative. MAIN
OUTCOME MEASURES: The impact of endoscopic ultrasonography was analyzed
on the basis of the number of patients requiring endoscopic
ultrasonography as a staging procedure (Group 1) and by evaluating the
performance of endoscopic ultrasonography in determining resectability
(Groups 1 and 2) based on the surgical and anatomopathological results.
RESULTS: Endoscopic ultrasonography was performed in 20 out of 64
patients (31.3%): 8/52 in Group 1 (15.4%) and all 12 patients of Group
2. Endoscopic ultrasonography correctly assessed an absolute
contraindication to resection in 11 cases. Resection was confirmed in 8
of the 9 cases selected by endoscopic ultrasonography. The positive
predictive value, negative predictive value and overall accuracy of
endoscopic ultrasonography for determining resection were 89%, 100%, and
95%, respectively. CONCLUSIONS: The impact of endoscopic ultrasonography
seems especially relevant for the detection of pancreatic tumors after
negative computerized tomography scanning, and for the prevention of
unnecessary laparotomies as complementary staging after ultrasonography
and computerized tomography scanning.
18
UI - 11959716
AU - Oshikawa O; Tanaka S; Ioka T; Nakaizumi A; Hamada Y; Mitani T
TI -
Dynamic sonography of pancreatic tumors: comparison with dynamic CT.
SO - AJR Am J Roentgenol 2002 May;178(5):1133-7
AD - Division of Digestive Organs, Department of Cancer Survey, Osaka Medical
Center for Cancer and Cardiovascular Diseases, 1-3-3, Nakamichi,
Higashinari, Osaka, 537-8511, Japan.
OBJECTIVE: The aim of this study was to examine the usefulness of
dynamic sonography in the characterization of pancreatic tumors.
MATERIALS AND METHODS: IV contrast-enhanced pancreatic sonography
(dynamic sonography) with Levovist was performed in 43 patients with
pancreatic mass lesions (32 with pancreatic adenocarcinomas, four with
inflammatory pancreatic masses, three with islet cell tumors, two with
serous cystadenomas, one with a solid and cystic tumor, and one with
metastatic pancreatic cancer). We calculated a contrast index using a
time-intensity curve: contrast index equals elevation of intensity in
the tumor divided by elevation of intensity in the pancreatic
parenchyma. We classified the tumors into three groups according to the
contrast index: a slightly enhanced group (contrast index < 0.5), a
moderately enhanced group (contrast index = 0.5-1.5), and a
well-enhanced group (contrast index > 1.5), and we compared these
results with those from dynamic CT. RESULTS: The contrast indexes of 32
adenocarcinomas, four inflammatory pancreatic masses, three islet cell
tumors, two serous cystadenomas, one solid and cystic tumor, and one
metastatic tumor were, respectively, 0.12 +/- 0.095 (mean +/- SD), 0.54
+/- 0.420, 1.74 +/- 0.555, 1.09 +/- 1.380, 1.67, and 2.07. Thirty-five
tumors, including all 32 adenocarcinomas, were classified in the
slightly enhanced group, three were classified in the moderately
enhanced group, and five were classified in the well-enhanced group. In
93% (40/43) of tumors, the grade of enhancement on dynamic sonography
was closely correlated with the grade of enhancement on dynamic CT.
CONCLUSION: Dynamic sonography can assist in the characterization of
pancreatic tumors.
19
UI - 11993688
AU - Wick MR; Graeme-Cook FM
TI -
Pancreatic neuroendocrine neoplasms: a current summary of diagnostic,
prognostic, and differential diagnostic information.
SO - Am J Clin Pathol 2001 Jun;115 Suppl():S28-45
AD - Department of Pathology, University of Virginia Health System,
Charlottesville 22908-0214, USA.
Pancreatic endocrine tumors (PETs) continue to be challenging diagnostic
and prognostic lesions in surgical pathology and clinical medicine.
These neoplasms can be graded into 1 of 3 tiers, based on histologic
characteristics in likeness to epithelial neuroendocrine tumors in other
anatomic sites. However, grade 1 tumors are by far the most common and
are the most difficult to prognosticate. The most helpful features by
which to gauge the behavior of such lesions include size (3 cm or
larger); mitotic activity (2 or more mitoses per 10 high-power [x400]
microscopic fields); marked nuclear atypia, especially with atypical
mitoticfigures; predominant tumor synthesis of gastrin, vasoactive
intestinal polypeptide, somatostatin, glucagon, calcitonin, or
adrenocorticotropic hormone; complete nonfunctionality of the tumor at
an immunohistochemical level; or invasion of blood vessels, nerves, or
adjacent organs by the neoplasm. Differential diagnosis of PETs includes
lesions such as solid-pseudopapillary neoplasms, acinar carcinomas,
metastatic neuroendocrine tumors, and plasmacytomas.
20
UI - 11753234
AU - Camera L; Bresciani M; Soscia E; Percopo V; Mainenti PP; Salvatore M
TI -
[Morphological imaging of gastroenteropancreatic neuroendocrine tumours]
SO - Minerva Endocrinol 2001 Sep;26(3):123-8
AD - Consiglio Nazionale delle Ricerche, Dipartimento di Scienze
Bio-morfologiche, Universita degli Studi Federico II, Naples, Italy.
Biologically active neuroendocrine tumours produce early symptoms and
are often difficult to diagnose owing to their small dimensions (<1 cm),
whereas biologically inactive forms are often coarse and sometimes found
by chance. As well as identifying the lesion, locoregional staging is
also particularly important for therapeutic planning. Morphological
imaging plays an important role in the identification of
gastroenteropancreatic neuroendocrine tumours, providing an anatomic
substrate for receptorial imaging which usually precede it in the
diagnostic work-up, whereas it plays a primary role in the locoregional
staging of these neoplasms for which surgery is the first and essential
therapeutic approach. In the case of endocrine tumours of the pancreas
alone, the most accurate method of diagnosis is currently echo-endoscopy
using high-frequency probes. Two-phase spiral CT and dynamic MR have
proved equally effective means of identifying endocrine tumours of the
pancreas with slightly higher sensitivity for MR, both playing a role in
the locoregional staging of biologically active and inactive tumours.
Traditional radiology also plays a role in the identification of
intestinal carcinoids.
21
UI - 11995268
AU - Magee CJ; Shekouh A; Ghaneh P; Neoptolemos JP
TI -
Update on pancreatic cancer.
SO - Hosp Med 2002 Apr;63(4):200-6
AD - University of Liverpool, Department of Surgery, Royal Liverpool,
University Hospital, Liverpool L69 3GA.
Pancreatic cancer is one of the commonest causes of cancer death
worldwide. Patients with pancreatic cancer benefit from resectional
surgery (improved quality of life) and adjuvant treatment (enhanced
survival). This review covers advances in the understanding of the
development of pancreatic cancer, state-of-the-art clinical management
and, finally, novel treatment and screening techniques.
22
UI - 11942011
AU - Alberti A; Dattola P; Littori F; Dattola A; Maccarone P; Basile M
TI -
[Intraoperative ultrasonography in the staging of pancreatic head
neoplasms]
SO - Chir Ital 2002 Jan-Feb;54(1):59-64
AD - Istituto di Chirurgia Generale, 1a Clinica Chirurgica Generale e Terapia
Chirurgica, Via Consolare Valeria, Gazzi, 98100 Messina.
Tumours of the head of the pancreas constitute the fourth most common
cause of cancer deaths. These tumours are characterised by low survival
rates (5% at 5 years) and low surgical resectability rates (20-25%).
Liver metastases, lymph-node and vascular involvement, and peritoneal
metastases are, in our opinion, exclusion criteria for curative surgical
resection. The aim of the study was to evaluate the impact of
intraoperative ultrasonography on the staging of such tumours. Over the
period from 1990 to 2000 we introduced intraoperative ultrasonography in
the staging of pancreatic cancer. We evaluated 51 patients who at
preoperative staging had been regarded as candidates for surgical
therapy consisting in a pancreaticoduodenectomy. All patients had been
staged by preoperative abdominal ultrasound, ERCP, CT and MRI.
Intraoperative ultrasound and colour-Doppler imaging (from 1997 on)
revealed involvement of (i) the liver, (ii) the splenomesenteric vessels
and (iii) the portal vein. Intraoperative ultrasonography yielded a
diagnosis of occult liver metastases in 10 cases and signs of vascular
involvement (absence of cleavage, partial and total thrombosis) in 12.
One false-negative was registered. Intraoperative ultrasonography in our
experience showed 98% sensitivity and specificity in the detection of
vascular and lymph-node involvement. Its sensitivity in the detection of
liver metastases was 100%. Intraoperative ultrasound is a procedure with
a very high sensitivity in the operative staging of cancer of the head
of the pancreas.
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 - 11978580
AU - Stolzenberg-Solomon RZ; Pietinen P; Taylor PR; Virtamo J; Albanes D
TI -
Prospective study of diet and pancreatic cancer in male smokers.
SO - Am J Epidemiol 2002 May 1;155(9):783-92
AD - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and
Genetics, National Cancer Institute, Bethesda, MD 20892-7232, USA.
rs221z@nih.gov
There have been few prospective studies relating diet to pancreatic
cancer, with most having fewer than 100 cases and only one examining
dietary nutrients. The authors prospectively examined dietary factors
hypothesized to be associated with exocrine pancreatic cancer in the
Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort in
Finland. Of the 27,111 male smokers aged 50-69 years with complete
dietary information, as ascertained from a self-administered dietary
history questionnaire given at baseline (1985-1988), 163 developed
hazards models were used to estimate smoking- and age-adjusted hazard
ratios and 95% confidence intervals. Energy-adjusted butter consumption
and saturated fat intake were positively associated with pancreatic
cancer (highest quintile vs. lowest: hazard ratio (HR) = 1.40, 95%
confidence interval (CI): 0.87, 2.25 (p trend = 0.04), and HR = 1.60,
95% CI: 0.96, 2.64 (p trend = 0.02), respectively). Energy intake and
energy-adjusted carbohydrate intake were inversely associated with the
disease (highest quintile vs. lowest: HR = 0.62, 95% CI: 0.36, 1.07 (p
trend = 0.05), and HR = 0.62, 95% CI: 0.37, 1.03 (p trend = 0.02),
respectively). These results support the hypothesis that a high intake
of saturated fat may increase the risk of pancreatic cancer in smokers,
while greater intakes of energy and carbohydrate may reduce the risk.
25
UI - 11978581
AU - Potter JD
TI -
Pancreas cancer--we know about smoking, but do we know anything else?
SO - Am J Epidemiol 2002 May 1;155(9):793-5; discussion 796-7
AD - Cancer Prevention Research Program, Fred Hutchinson Cancer Research
Center, Seattle, WA 98109-1024, USA. jpotter@fhcrc.org
26
UI - 12004989
AU - Baron TH; Fleischer DE
TI -
Past, present, and future of endoscopic retrograde
cholangiopancreatography: perspectives on the National Institutes of
Health consensus conference.
SO - Mayo Clin Proc 2002 May;77(5):407-12
27
UI - 11839686
AU - Hindle KS; Kirkpatrick K; Mokbel K
TI -
Correspondence re: Seki et al., Diagnosis of pancreatic adenocarcinoma
by detection of human telomerase reverse transcriptase messenger RNA in
pancreatic juice with sample qualification. Clin. Cancer Res., 7:
1976-1981, 2001.
SO - Clin Cancer Res 2002 Feb;8(2):628-9
28
UI - 11920735
AU - Pizzi S; D'Adda T; Azzoni C; Rindi G; Grigolato P; Pasquali C; Corleto
TI -
VD; Delle Fave G; Bordi C
Malignancy-associated allelic losses on the X-chromosome in foregut but
not in midgut endocrine tumours.
SO - J Pathol 2002 Apr;196(4):401-7
AD - Department of Pathology and Laboratory Medicine, Section of Pathological
Anatomy, University of Parma, Parma, Italy.
Information on genetic changes involved in the progression of
gastroenteropancreatic (GEP) endocrine tumours is scanty. On the other
hand, the identification of molecular markers of malignancy could be
crucial for the prognostic evaluation of these neoplasms, which is
hardly predictable on the basis of conventional histological criteria.
An association of X-chromosome deletions with malignancy has already
been found in gastric endocrine tumours. To investigate this further, a
comparative loss of heterozygosity (LOH) analysis was performed on 17
pancreatic endocrine tumours (PETs) and 17 intestinal (ten ileal, six
appendiceal, and one rectal) carcinoids from female patients. The
relationship of X-chromosome LOH with the ploidy status of the neoplasms
was also investigated. LOH was found in six of eight malignant PETs (60%
of the informative markers), but was infrequent in the nine benign ones
(4.5%). In contrast, although retention of heterozygosity was
consistently observed in benign midgut tumours, LOH was infrequent in
malignant carcinoids (15%). No correlation was found between LOH and the
ploidy status. These results indicate an association between
X-chromosome LOH and malignancy in foregut endocrine tumours. The lack
of such an association in midgut carcinoids suggests that different
molecular mechanisms are involved in the progression of these two
categories of endocrine neoplasms, which are otherwise considered to be
closely related. These findings emphasize the need for further molecular
studies on GEP endocrine tumours, carefully subdivided according to
their anatomical site of origin. Copyright 2002 John Wiley & Sons, Ltd.
29
UI - 11935313
AU - Maacke H; Hundertmark C; Miska S; Voss M; Kalthoff H; Sturzbecher HW
TI -
Autoantibodies in sera of pancreatic cancer patients identify
recombination factor Rad51 as a tumour-associated antigen.
SO - J Cancer Res Clin Oncol 2002 Apr;128(4):219-22
AD - Present address: Clinic for Internal Medicine II, Friedrich-Schiller
University Jena, Erlanger Allee 101, 07743 Jena, Germany.
PURPOSE: The recombination factor Rad51 is highly expressed in human
pancreatic adenocarcinoma. In this study we asked whether high-level
expression of Rad51 antigen stimulates a B-cell response leading to
Rad51-specific autoantibodies in human pancreatic cancer patients.
METHODS: Sera of patients suffering from pancreatic cancer (57) as well
as sera of healthy donors (86) were screened for Rad51 autoantibodies by
Western-blot analysis. Rad51 over-expressing cell lines were used as
antigen source. RESULTS: Four out of 57 (7%) sera tested were found
positive for Rad51 autoantibodies of IgG subclass, while all 86 control
sera were negative. CONCLUSION: This observation identifies Rad51 as a
tumour-associated antigen in pancreatic adenocarcinoma. Since high-level
expression of Rad51 is restricted to tumour cells, Rad51 is also a
tumour-specific antigen. Further analyses should reveal whether Rad51
might also function as a tumour-specific transplantation antigen (TSTA)
and whether it might serve as a target for new immunotherapeutical
approaches.
30
UI - 11990650
AU - Horton KM
TI -
How we do it: pancreatic cancer staging.
SO - Crit Rev Comput Tomogr 2002;43(1):1-4
AD - Johns Hopkins Medical Institutions, USA.
31
UI - 11972546
AU - Yachida S; Fukushima N; Sakamoto M; Matsuno Y; Kosuge T; Hirohashi S
TI -
Implications of peritoneal washing cytology in patients with potentially
resectable pancreatic cancer.
SO - Br J Surg 2002 May;89(5):573-8
AD - Clinical Laboratory Division and Hepatobiliary and Pancreatic Surgery
Division, National Cancer Center Hospital and Pathology Division,
National Cancer Center Research Institute, Tokyo, Japan.
BACKGROUND: The aim of this study was to assess the implications of
positive peritoneal washing cytology for management of patients with
potentially resectable pancreatic cancer.METHODS: Cytological
examination of peritoneal washings was performed in 134 patients who
underwent surgical resection for pancreatic adenocarcinoma. The
clinicopathological findings and the relationship between cytology
results (including cytomorphology) and survival were
investigated.RESULTS: One hundred and fourteen patients (85 per cent)
had negative cytology results (group 1). Excluding one patient with
atypical cells, positive cytology results were obtained in 19 patients
(14 per cent): 16 patients without macroscopic peritoneal metastases
(group 2) and three patients with minimal macroscopic peritoneal
metastases (group 3). The patients in group 2 had significantly larger
(P < 0.001) and more advanced (P = 0.022) tumours than those in group 1.
However, there were no significant differences in postoperative
cumulative survival rates between groups 1 and 2 (P = 0.347). Two
patients in group 2 are long-term survivors (40 and 58 months). In
cytomorphological analyses, the presence of clusters with ragged edges
and isolated carcinoma cells can be considered to indicate a high risk
of peritoneal recurrence.CONCLUSION: Positive cytology does not directly
predict
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