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Pancreatic tumors
Department of General and Transplant Surgery
Medical University of Lódź
Mucinous Tumors
Intraductal Papillary
Mucinous Tumor
Tumor of the
Most benign pancreatic
exocrine tumors are cystic,
but not all cystic tumors
Benign cystic tumors 10% 15% of pancreatic tumors
usually asymptomatic but,
when symptoms develop,
they are usually related to
pressure or obstruction of
an adjacent organ.
Serous Cystadenoma
20% to 40% of cystic
pancreatic neoplasms
Rare cases of malignant serous
cystic lesions have been
lined by a flattened
most are benign and
have no malignant
large, spherical
masses that contain a
watery fluid and have a
central, calcified
stellate scar
Resection is indicated when the
diagnosis is in doubt or when
they become symptomatic.
Mucinous Tumors
20% to 40% of cystic
could have malignant
two types:
1) contains areas of ovarian-like
stroma, almost always in women
and in the pancreatic tail.
2) lacks ovarian stroma, found
anywhere in pancreas, male-tofemale ratio 1:1
The cysts are lined by a
columnar, mucin-producing, and
sometimes papillary epithelium
Prolonged survival (i.e., >5
years) can be anticipated in
more than 50% of patients if
these tumors are resected prior
to the development of invasive
malignancy, but even after the
development of malignant
changes and invasion, long-term
survival is still better than for
ductal adenocarcinoma.
Note multiple large cystic spaces. Microscopic
examination revealed multiple areas of ovarian-like
Intraductal Papillary Mucinous
First described in Japan in the
male-to-female ratio 1:1
can be located in any or all
parts of the pancreas,
although involvement of the
head appears to be its most
common form
can involve the major ducts
(“main duct variety”), the
smaller ducts (“branch duct
variety”) or both types of
patients can experience pancreatitis
when mucus, secreted by the tumor,
transiently obstructs the orifice of the
pancreatic duct
IPMT is believed to follow an
adenoma-carcinoma sequence
minimal or no dysplasia (PanIN1), moderate dysplasia (PanIN2),
severe dysplasia/carcinoma in
situ (PanIN-3)
Resection with, at worst, PanIN-1
changes at the margin, prior to
development of invasive
malignancy, is usually curative. This
may mandate total pancreatectomy.
When resection is performed after
development of invasive
malignancy, cure rates are relatively
Management of Cystic Pancreatic
The major challenge is
distinguishing pseudocysts
and serous cystadenomas
from the other, malignant
or potentially malignant,
types of cystic pancreatic
The finding of mucin in the
cyst, mucin-secreting cells
on biopsy, a high cyst fluid
viscosity, or a high cyst
fluid carcinoembryonic
antigen (CEA) is
suggestive, but not
diagnostic, of a potentially
malignant tumor
Because of these uncertainties, all neoplastic
cysts should be resected unless the diagnosis of
a serous cystadenoma can be made with certainty
Solid-Pseudopapillary Tumor of
the Pancreas
uncommon tumor
occurs in young women
benign course but
malignant varieties have
been described.
local resection is usually
usually large, round, and welldemarcated masses that can
occur in any part of the
histologically, the tumor is
mostly solid and consists of
monomorphous eosinophilic or
clear cells that demonstrate a
pseudopapillary architecture. In
suitable operative candidates,
solid-pseudopapillary tumors of
the pancreas should be
Pancreatic cancer
affects 25,000 to 30,000
people in the United States
4th or 5th leading cause of
cancer-related death
ductal adenocarcinoma
and its variants account for
80% to 90%
80% of cases occur
between 60 and 80 years of
Only 2 % in patients <40
years of age
risk factors:
- a history
of hereditary or
chronic pancreatitis,
- cigarette smoking
- occupational exposure to
Genetic abnormalities in pancreatic cancer
activation of growthpromoting oncogenes,
mutations that result in the
inactivation of tumor
suppressor genes,
excessive expression of
growth factors and/or their
codon 12 mutations of the K-ras
oncogene (95%)
mutation of the p53 tumor
suppressor gene (75%)
mutations of the tumor
suppressor genes, including
p16, SMAD-4, DPC, and DCC
EGF receptor abnormalities
HER2, HER3, and HER4
receptors abnormalities
pancreas cancer evolves in a progressive,
step-wise fashion, much like that observed for
colon cancer
Hereditary Pancreatic Cancer Syndromes
hereditary nonpolyposis colon cancer
familial breast cancer (associatedwith
the BRCA2 mutation)
Peutz-Jeghers syndrome
those with ataxia-telangiectasia
familial atypical multiple mole
melanoma (FAMMM)syndrome
patients with hereditary pancreatitis are
also at increased risk of developing
pancreatic cancer. This is particularly
true in those with a paternal pattern of
inheritance who may have a 75% risk
of developing pancreatic cancer
Even in the absence of one
of these familial cancer
syndromes or hereditary
pancreatitis,individuals with a
family history of pancreatic
cancer, especially those with
two or more pancreatic
cancer–affected first-degree
relatives, have an increased
risk of developing pancreatic
Symptoms and Signs
Symptoms and Signs
Blood Tests
CA 19–9 > 37 U/mL
sensitivity of 86% and a
specificity of 87%
elevation of bilirubin
elevation of alkaline
phosphatase level
Imaging Studies
US scan
helical contrast-enhanced
Positron emission
tomography (PET)
helical contrast-enhanced
hypodense mass with
poorly demarcated
It may have a more
hypodense center,
indicating either
central necrosis or
cystic change, and
the pancreatic duct to
the left of the lesion
may be dilated
(A) Slight enlargement of pancreatic head and without circumscribed tumor on helical CT in arterial
phase; suspicion of liver lesions. (B) Marked tracer uptake on 18F-FDG PET in middle abdomen
without definite anatomic identification; SUV > 3.5 leads to diagnosis of malignant lesion;
additional liver metastases. (C) On image fusion, tracer accumulations are projected on pancreatic
body and right liver lobe, proving the presence of hepatic metastases of pancreatic carcinoma.
(A) Clear enlargement of pancreatic head on arterial helical CT. (B) Increased tracer uptake on
18F-FDG PET located on retroperitoneal space; SUV of 2.4 leads to diagnosis of inflammatory
process (arrow). (C) Image fusion enables definite localization of focal uptake onto pancreatic
(A) Helical CT demonstrates circumscribed thickening of pancreatic body and atrophy of
pancreatic tail commonly seen as indirect sign for malignancy of pancreas. (B) 18F-FDG PET
verifies pancreatic carcinoma with SUV of 5.8 and demonstrates additional lesion posterior to first
lesion. (C) Image fusion allocates second tumor to unsuspected lymph node on CT representing
lymph node metastases.
(A) Detection of large pancreatic head carcinoma on retrospective image fusion of helical CT
and 18F-FDG PET. (B) Detection of additional pancreatic lesion not evident before image
Glucose uptake was quantified by the standard uptake value (SUV), with an SUV of
>3.5 considered as indicative of malignancy
American Joint Committee on Cancer:
TNM System for Staging of Pancreatic Cancer
High-resolution helical CT, with phased imaging for
visualization of the pancreas and major peripancreatic
vessels, is the most widely used method of evaluating tumor
Circumferential encasement, invasion, or occlusion of the
portal vein/superior mesenteric vein and/or the superior
mesenteric artery is generally considered to be a sign of
Adenocarcinoma of the pancreatic head in a 71-year-old woman who did not undergo surgery. (a)
Transverse CT image shows tumor (straight arrows) abutting the portal vein (curved arrow) near
confluence. (b) Thin-slab MIP image shows contour irregularity (arrow) of the inferior surface of
the portal confluence.
(a) Transverse CT image obtained at the level of the superior mesenteric vein just caudal to the
confluence, in which vascular invasion by tumor (arrow) is difficult to appreciate. (b) Shaded
surface display of the portal phase shows indentation (arrows) at the confluence of the superior
mesenteric and portal veins. Surgical finding confirmed tumor invasion.
Palliative double bypass for
unresectable pancreatic cancer.
An end-to-side
is performed, followed by a
side-to side
jejunojejunostomy between the
afferent loop leading to the
biliary anastomosis and the
loop leading from it. An
opening is made in the lesser
omentum, and a chemical
splanchnicectomy is performed
by injecting alcohol into the
celiac plexus.