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1
acinar cell carcinoma of pancreas 2005:2010[pubdate] *count=100
164 results
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acinar cell carcinoma of pancreas
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Items 1 to 100 of about 164
1.
Chung WJ, Byun JH, Lee SS, Lee MG:
Imaging findings in a case of mixed acinar-endocrine carcinoma of the pancreas.
Korean J Radiol
; 2010 May-Jun;11(3):378-81
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[Title]
Imaging findings in a case of mixed
acinar
-endocrine
carcinoma of
the
pancreas
.
Mixed
acinar
-endocrine
carcinoma
(MAEC) of the
pancreas
is extremely uncommon.
We report here a rare case of MAEC of the
pancreas
presenting as watery diarrhea.
This is the first report in the English-language literature that describes the imaging findings of MAEC of the
pancreas
, including computed tomography (CT), magnetic resonance (MR) imaging, and MR cholangiopancreatography features.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology.
Carcinoma
,
Acinar Cell
/ radiography. Endocrine Gland Neoplasms / pathology. Endocrine Gland Neoplasms / radiography.
Pancreatic
Neoplasms / pathology.
Pancreatic
Neoplasms / radiography
[MeSH-minor]
Cholangiopancreatography, Magnetic Resonance / methods.
Diagnosis
, Differential. Diarrhea. Female. Humans. Magnetic Resonance Imaging / methods. Middle Aged.
Pancreas
/ pathology.
Pancreas
/ radiography.
Pancreas
/ surgery. Pancreatectomy. Splenectomy. Tomography, X-Ray Computed / methods
MedlinePlus Health Information.
consumer health - Pancreatic Cancer
.
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[Cites]
AJR Am J Roentgenol. 2000 Mar;174(3):671-5
[
10701607.001
]
[Cites]
Eur J Radiol. 2008 Aug;67(2):321-8
[
17766075.001
]
[Cites]
Am J Surg Pathol. 2002 Jul;26(7):893-901
[
12131156.001
]
[Cites]
Dig Dis Sci. 2002 Oct;47(10):2254-61
[
12395898.001
]
[Cites]
Pathol Annu. 1978;13 Pt 1:241-89
[
214741.001
]
[Cites]
Cancer. 1984 Nov 1;54(9):1766-70
[
6089999.001
]
[Cites]
CA Cancer J Clin. 1985 Jan-Feb;35(1):2-18
[
3917840.001
]
[Cites]
Radiol Clin North Am. 1985 Sep;23(3):489-501
[
2997833.001
]
[Cites]
Am J Surg Pathol. 1994 Aug;18(8):765-78
[
8037290.001
]
[Cites]
Radiographics. 1998 Mar-Apr;18(2):369-78
[
9536484.001
]
[Cites]
Virchows Arch. 2004 Sep;445(3):231-5
[
15517367.001
]
[Cites]
AJR Am J Roentgenol. 2005 Feb;184(2):511-9
[
15671372.001
]
[Cites]
Magn Reson Imaging Clin N Am. 2005 May;13(2):313-30
[
15935314.001
]
[Cites]
JOP. 2005 Sep;6(5):449-54
[
16186667.001
]
[Cites]
J Comput Assist Tomogr. 2006 Jul-Aug;30(4):610-7
[
16845292.001
]
[Cites]
Semin Diagn Pathol. 2000 May;17(2):104-8
[
10839610.001
]
(PMID = 20461195.001).
[ISSN]
2005-8330
[Journal-full-title]
Korean journal of radiology
[ISO-abbreviation]
Korean J Radiol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Korea (South)
[Other-IDs]
NLM/ PMC2864868
[Keywords]
NOTNLM ; Endocrine / Exocrine / Mixed acinar-endocrine carcinoma / Pancreas
2.
Adham M, Giunippero A, Hervieu V, Courbière M, Partensky C:
Central pancreatectomy: single-center experience of 50 cases.
Arch Surg
; 2008 Feb;143(2):175-80; discussion 180-1
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[Source]
The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
Indications included 18 neuroendocrine tumors (11 nonfunctioning), 10 serous and 10 mucinous cystadenomas, 5 intraductal papillary mucinous neoplasms, 3 main
pancreatic
duct strictures, 2 solid cystic papillary tumors, 1 hydatid cyst, and 1
acinar cell carcinoma
.
The proximal
pancreatic
remnant was suture ligated.
The distal
pancreatic
end was anastomosed to a Roux-en-Y jejunal loop (n = 6) or to the stomach (n = 44).
Three patients had associated procedures, 1 each for metastatic liver cytoreduction (VIPoma), hydatid liver disease, and
pancreatic
resection for multifocal mucinous cystadenoma.
The mean length of the resected
pancreas
was 45 mm (range, 20-80 mm) and the mean tumor size was 23 mm (5-60 mm).
Complications included the following: 4 patients (8%) had
pancreatic
anastomotic leak, 5 patients (10%) had acute pancreatitis, 7 patients (14%) had intra-abdominal collection, and 3 patients (6%) had bleeding.
No patients developed
de
novo diabetes.
The actuarial 5-year patient and
pancreatic
remnant survival rates were 98% and 95%, respectively.
In our series, central pancreatectomy led to effective preservation of both cephalic and distal
pancreatic
remnants without a significant increase in postoperative morbidity compared with conventional pancreatectomy.
[MeSH-major]
Neoplasm Recurrence, Local / pathology. Pancreatectomy / methods.
Pancreatic
Neoplasms / mortality.
Pancreatic
Neoplasms / surgery
[MeSH-minor]
Adolescent. Adult. Aged. Anastomosis, Surgical / methods. Biopsy, Needle. Cholangiopancreatography, Endoscopic Retrograde / methods. Cohort Studies. Female. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Postoperative Complications /
diagnosis
. Postoperative Complications / mortality. Retrospective Studies. Risk Assessment. Survival Analysis. Treatment Outcome
MedlinePlus Health Information.
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.
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(PMID = 18283143.001).
[ISSN]
1538-3644
[Journal-full-title]
Archives of surgery (Chicago, Ill. : 1960)
[ISO-abbreviation]
Arch Surg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
3.
Kebir FZ, Lahmar A, Arfa N, Manai S, El Ouaer MA, Bouraoui S, Gouttalier C, Mezabi-Regaya S:
Acinar cell carcinoma of the pancreas in a young patient with chronic pancreatitis.
Hepatobiliary Pancreat Dis Int
; 2010 Feb;9(1):103-6
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[Title]
Acinar cell carcinoma of
the
pancreas
in a young patient with chronic pancreatitis.
BACKGROUND:
Acinar cell carcinoma
(ACC) is a rare malignancy of the
pancreas
arising from
acinar
cells.
Unlike ductal
adenocarcinoma
, this tumor rarely presents with pancreatitis.
METHODS: We present a case of ACC associated with chronic calcifying pancreatitis, and a review of the literature focusing on
diagnosis
and management.
CONCLUSIONS: The clinical presentation of ACC of the
pancreas
is not specific and the tumor can be under-diagnosed when associated with chronic pancreatitis.
[MeSH-major]
Carcinoma
,
Acinar Cell
/
diagnosis
.
Pancreatic
Neoplasms /
diagnosis
. Pancreatitis, Chronic / complications
Genetic Alliance.
consumer health - Pancreatitis
.
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consumer health - Pancreatic Cancer
.
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(PMID = 20133240.001).
[ISSN]
1499-3872
[Journal-full-title]
Hepatobiliary & pancreatic diseases international : HBPD INT
[ISO-abbreviation]
HBPD INT
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
China
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4.
Radhi J, Tse F, Marcaccio M:
Papillocystic variant of acinar cell pancreatic carcinoma.
J Oncol
; 2010;2010:242016
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[Title]
Papillocystic variant
of acinar cell
pancreatic
carcinoma
.
Acinar cell
pancreatic
carcinoma
is a rare solid malignant neoplasm.
We report a large 10 cm
pancreatic
tumor with papillocystic pathology features involving
the pancreatic
head.
The growth pattern of these tumors could be mistaken for intraductal papillary mucinous tumors or other
pancreatic
cystic neoplasms.
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[Cites]
Gastroenterology. 2004 May;126(5):1330-6
[
15131794.001
]
[Cites]
Cancer Imaging. 2006;6:60-71
[
16861136.001
]
[Cites]
J Gastrointest Surg. 2009 Aug;13(8):1495-502
[
19495891.001
]
[Cites]
J Gastrointest Surg. 2008 Mar;12(3):401-4
[
17957438.001
]
[Cites]
J Gastrointest Surg. 2008 Dec;12(12):2078-86
[
18836784.001
]
[Cites]
Am J Surg Pathol. 2007 Mar;31(3):363-70
[
17325477.001
]
(PMID = 20204128.001).
[ISSN]
1687-8469
[Journal-full-title]
Journal of oncology
[ISO-abbreviation]
J Oncol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Egypt
[Other-IDs]
NLM/ PMC2831459
5.
Rodriguez S, Faigel D:
Absence of a dilated duct predicts benign disease in suspected pancreas cancer: a simple clinical rule.
Dig Dis Sci
; 2010 Apr;55(4):1161-6
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[Title]
Absence of a dilated duct predicts benign disease in suspected
pancreas
cancer
: a simple clinical rule.
BACKGROUND:
Pancreatic cancer
can be difficult to diagnose.
METHODS: Patients presenting for endoscopic ultrasound (EUS) evaluation for suspected
pancreatic
mass were prospectively enrolled.
The characteristics of patients with
cancer
were compared to the characteristics of patients without
cancer
using Chi-square testing and t-tests.
Thirty-three patients had
cancer
and 40 had benign disease.
On multivariate analysis, only vascular or organ invasion and dilation of
the pancreatic
duct (PD) were significantly associated with
cancer
.
PD dilation was examined
as a
stand-alone feature.
CONCLUSIONS: The most significant negative predictive endosonographic finding in patients with suspected
pancreatic cancer
is a non-dilated PD.
If a patient with suspected
pancreatic cancer
does not have a dilated PD and the FNA is negative for malignancy, the likelihood of
cancer
is low.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ diagnostic imaging.
Carcinoma
,
Pancreatic
Ductal / diagnostic imaging. Endosonography.
Pancreatic
Ducts / diagnostic imaging.
Pancreatic
Neoplasms / diagnostic imaging
[MeSH-minor]
Aged. Biopsy, Fine-Needle.
Diagnosis
, Differential. Dilatation, Pathologic / diagnostic imaging. Dilatation, Pathologic / pathology. Female. Humans. Male. Middle Aged. Multivariate Analysis. Neoplasm Invasiveness.
Pancreas
/ diagnostic imaging.
Pancreas
/ pathology.
Pancreatic
Diseases / diagnostic imaging.
Pancreatic
Diseases / pathology. Predictive Value of Tests. Prospective Studies
MedlinePlus Health Information.
consumer health - Pancreatic Cancer
.
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[Cites]
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]
(PMID = 19590960.001).
[ISSN]
1573-2568
[Journal-full-title]
Digestive diseases and sciences
[ISO-abbreviation]
Dig. Dis. Sci.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
6.
Kimura W:
[Pathogenesis of endocrine tumors of the pancreas].
Nihon Geka Gakkai Zasshi
; 2008 May;109(3):133-42
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[Title]
[Pathogenesis of endocrine tumors of the
pancreas
].
Precise pathohistologic and immunohistochemical investigations of the
pancreas
in elderly autopsy cases revealed that endocrine tumors are found very frequently.
Some endocrine tumors of the
pancreas
may originate from Langerhans islets, although other endocrine tumors may develop from endocrine cells or stem cells with multiple differentiation ability and occur in the duct cells or
acinar
cells.
This possibility may be supported by the evidence that ductular or tubular structures were found in or adjacent to tumors in about 60% of minute tumors and that hormone production was found in both duct cells and
acinar
cells based on immunohistochemical findings.
The occurrence of ductuloinsular tumors,
acinar
endocrine
cell
tumors, and duct-
acinar
-islet
cell
tumors may also support these observations.
Molecular biological investigations will further analyze the pathogenesis of endocrine tumors of the
pancreas
.
There are three possible origins of endocrine tumors of the
pancreas
: Langerhans islets cells, ductular cells, and
acinar
cells.
[MeSH-major]
Neuroendocrine Tumors.
Pancreatic
Neoplasms
[MeSH-minor]
Aged. Animals.
Carcinoma
,
Acinar Cell
.
Carcinoma
,
Pancreatic
Ductal. Female. Humans. Immunohistochemistry. Islets of Langerhans. Male
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(PMID = 18536316.001).
[ISSN]
0301-4894
[Journal-full-title]
Nihon Geka Gakkai zasshi
[ISO-abbreviation]
Nihon Geka Gakkai Zasshi
[Language]
jpn
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Japan
[Number-of-references]
35
7.
Stelow EB, Bardales RH, Shami VM, Woon C, Presley A, Mallery S, Lai R, Stanley MW:
Cytology of pancreatic acinar cell carcinoma.
Diagn Cytopathol
; 2006 May;34(5):367-72
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[Title]
Cytology of
pancreatic
acinar cell carcinoma
.
Acinar cell carcinoma
(ACC) of the
pancreas
is extremely uncommon and its cytologic features have rarely been described.
We describe the cytologic features of cases we have seen, review the literature regarding its cytologic features and discuss the pitfalls that may be encountered and the use of immunohistochemistry for its
diagnosis
.
We searched our databases for all cases of histologically confirmed
pancreatic
ACC which had undergone prior fine needle aspiration (FNA) of the primary
pancreatic
lesion.
Four cases of
pancreatic
ACC were found that had undergone FNA prior to histologic confirmation of the diagnoses.
All masses were in the head of the
pancreas
, 2 had apparent peri-
pancreatic
adenopathy and 1 had an apparent liver metastasis.
Original cytologic diagnoses included "
acinar cell carcinoma
," "
pancreatic
endocrine tumor," "favor neuroendocrine tumor, low-grade" and "non-diagnostic specimen."
The cytologic features included small to moderate-sized loose groups with numerous single cells, prominent
acinar
formation, little anisonucleosis and prominent nucleoli.
The cytologic features showed significant overlap with those of
pancreatic
endocrine tumors.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ secondary.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Aged. Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Female. Humans. Keratins / analysis. Liver Neoplasms / chemistry. Liver Neoplasms / secondary. Lymph Nodes / pathology. Male. Middle Aged.
Pancreas
/ chemistry.
Pancreas
/ pathology
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(PMID = 16604543.001).
[ISSN]
8755-1039
[Journal-full-title]
Diagnostic cytopathology
[ISO-abbreviation]
Diagn. Cytopathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 68238-35-7 / Keratins
8.
Habbe N, Shi G, Meguid RA, Fendrich V, Esni F, Chen H, Feldmann G, Stoffers DA, Konieczny SF, Leach SD, Maitra A:
Spontaneous induction of murine pancreatic intraepithelial neoplasia (mPanIN) by acinar cell targeting of oncogenic Kras in adult mice.
Proc Natl Acad Sci U S A
; 2008 Dec 2;105(48):18913-8
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[Title]
Spontaneous induction of murine
pancreatic
intraepithelial neoplasia (mPanIN) by
acinar cell
targeting of oncogenic Kras in adult mice.
Pancreatic
ductal
adenocarcinoma
(PDAC) is believed to arise through a multistep model comprised of putative precursor lesions known
as pancreatic
intraepithelial neoplasia (PanIN).
The most faithful genetic models activate an oncogenic Kras(G12D) knockin allele within the pdx1- or ptf1a/p48-expression domain of the entire
pancreatic
anlage during development, thus obscuring the putative
cell
(s)-of-origin from which subsequent mPanIN lesions arise.
In our study, activation of this knockin Kras(G12D) allele in the Elastase- and Mist1-expressing mature
acinar
compartment of adult mice resulted in the spontaneous induction of mPanIN lesions of all histological grades, although invasive carcinomas per se were not seen.
We observed no requirement for concomitant chronic exocrine injury in the induction of mPanIN lesions from the mature
acinar cell
compartment.
The
acinar cell
derivation of the mPanINs was established through lineage tracing in reporter mice, and by microdissection of lesional tissue demonstrating Cre-mediated recombination events.
In contrast to the uniformly penetrant mPanIN phenotype observed following developmental activation of Kras(G12D) in the Pdx1-expressing progenitor cells, the Pdx1-expressing population in the mature
pancreas
(predominantly islet beta cells) appears to be relatively resistant to the effects of oncogenic Kras.
We conclude that in the appropriate genetic context, the differentiated
acinar cell
compartment in adult mice retains its susceptibility for spontaneous transformation into mPanIN lesions, a finding with potential relevance vis-à-vis the origins of PDAC.
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Gastroenterology. 2008 Aug;135(2):621-31
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18515092.001
]
(PMID = 19028870.001).
[ISSN]
1091-6490
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK56211; United States / NIDDK NIH HHS / DK / R21 DK072532-01; United States / NCI NIH HHS / CA / R01 CA113669-02; United States / NIDDK NIH HHS / DK / R21 DK072532-02; United States / NCI NIH HHS / CA / R01 CA113669-01; United States / NCI NIH HHS / CA / CA113669-02; United States / NCI NIH HHS / CA / CA113669-04; United States / NIDDK NIH HHS / DK / DK072532-01; United States / NCI NIH HHS / CA / CA113669-03; United States / NCI NIH HHS / CA / CA113669; United States / NIDDK NIH HHS / DK / DK55489; United States / NIDDK NIH HHS / DK / DK072532; United States / NIDDK NIH HHS / DK / R01 DK055489-11A1; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586-04; United States / NCI NIH HHS / CA / R01 CA113669-05; United States / NIDDK NIH HHS / DK / DK61215; United States / NIDDK NIH HHS / DK / R21 DK072532; United States / NIDDK NIH HHS / DK / R01 DK061215; United States / NCI NIH HHS / CA / R01 CA113669-03; United States / NCI NIH HHS / CA / CA124586-04; United States / NIDDK NIH HHS / DK / T32 DK007713; United States / NCI NIH HHS / CA / R01 CA124586; United States / NIDDK NIH HHS / DK / T32DK007713; United States / NCI NIH HHS / CA / CA124586; United States / NIDDK NIH HHS / DK / DK055489-11A1; United States / NCI NIH HHS / CA / R01 CA113669; United States / NIDDK NIH HHS / DK / R01 DK056211; United States / NCI NIH HHS / CA / R01 CA113669-04; United States / NCI NIH HHS / CA / CA113669-05; United States / NIDDK NIH HHS / DK / DK072532-02; United States / NCI NIH HHS / CA / CA113669-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Receptors, Notch; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
[Other-IDs]
NLM/ PMC2596215
9.
Klimstra DS:
Nonductal neoplasms of the pancreas.
Mod Pathol
; 2007 Feb;20 Suppl 1:S94-112
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[Title]
Nonductal neoplasms of the
pancreas
.
Although the majority of
pancreatic
neoplasms are infiltrating ductal adenocarcinomas or other neoplasms with ductal differentiation, neoplasms with
acinar
, endocrine, mixed, or uncertain differentiation constitute a diverse and distinctive group.
The most common and best-characterized nonductal neoplasms are
pancreatic
endocrine neoplasm,
acinar cell carcinoma
, pancreatoblastoma, and solid pseudopapillary neoplasm.
[MeSH-major]
Adenocarcinoma
, Papillary / pathology. Adenoma, Islet
Cell
/ pathology.
Carcinoma
,
Acinar Cell
/ pathology.
Carcinoma
, Islet
Cell
/ pathology.
Pancreas
/ pathology.
Pancreatic
Neoplasms / pathology
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(PMID = 17486055.001).
[ISSN]
0893-3952
[Journal-full-title]
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
[ISO-abbreviation]
Mod. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
10.
Kuo FY, Swanson PE, Yeh MM:
Pancreatic acinar tissue in liver explants: a morphologic and immunohistochemical study.
Am J Surg Pathol
; 2009 Jan;33(1):66-71
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[Title]
Pancreatic
acinar
tissue in liver explants: a morphologic and immunohistochemical study.
BACKGROUND:
Pancreatic
acini-like tissue is occasionally seen in the liver.
To gain further insight into this issue, we performed a pathologic and immunohistochemical study in liver explants to identify
pancreatic
acinar
tissue.
Formalin-fixed, paraffin-embedded tissues were stained with hematoxylin-eosin, and immunohistochemical analyses using antibodies against CK7, CK8, and CK19 (biliary type cytokeratins), CD56 (positive in reactive bile ductules), chromogranin A (positive in reactive bile ductules and human oval-like/hepatic progenitor cells),
pancreatic
amylase, and PDX-1 were performed.
The immunohistochemical comparison group consisted of 3 gastric biopsies diagnosed as autoimmune gastritis with
pancreatic
metaplasia and 3 normal
pancreatic
tissues from pancreatectomy specimens.
RESULTS: Sixteen (4.2%) of 382 liver explants contained
pancreatic
acini-like tissue.
Fifteen of these were cirrhotic livers due to cryptogenic cirrhosis (n=1), primary biliary cirrhosis (n=3), primary sclerosing cholangitis (n=1), chronic hepatitis C-related cirrhosis (n=5), and cirrhosis with hepatitis C and hepatocellular
carcinoma
(n=5).
The pancreatic
acini-like tissue appeared as small clusters of compactly packed cells that either blended imperceptibly with or were in close proximity to adjacent bile ducts or ductules.
The pancreatic
acinar
tissue was diffusely reactive for amylase, was occasionally positive for keratin 8 and chromogranin A, and was negative for CD56, keratin 7, and keratin 19.
CONCLUSIONS: Our results collectively indicate that
pancreatic
acini-like tissue in liver represent aggregates of
pancreatic
acinar
cells admixed with small intra-
acinar
terminal ductules.
Given the close spatial relationship with reactive bile ductules and the apparent transition in immunophenotype from bile ductules to
pancreatic
acinar
tissue, the latter is likely of metaplastic origin derived from a hepatic progenitor lineage.
[MeSH-major]
Cell
Transdifferentiation / physiology. Choristoma / etiology. Choristoma / pathology. Liver Diseases / pathology.
Pancreas
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(PMID = 18987542.001).
[ISSN]
1532-0979
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
11.
Qi T, Han J, Cui Y, Zong M, Liu X, Zhu B:
Comparative proteomic analysis for the detection of biomarkers in pancreatic ductal adenocarcinomas.
J Clin Pathol
; 2008 Jan;61(1):49-58
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[Title]
Comparative proteomic analysis for the detection of biomarkers in
pancreatic
ductal adenocarcinomas.
AIMS: To search for novel potential protein biomarkers for the early detection and better intervention of
pancreatic
ductal
adenocarcinoma
(PDAC).
METHODS: Eight pairs of matched PDAC and non-cancerous
pancreas
tissues were profiled with two-dimensional electrophoresis; differentially expressed proteins were identified by mass spectrometry.
Immunohistochemistry showed that TBX4 expression could be seen in both centroacinar cells and small ducts in normal
pancreas
and tumour cells in 5/5 (100%) well differentiated, 35/38 (92.1%) moderately differentiated, and 11/18 (61.1%) poorly differentiated PDAC tissues with different staining intensity.
However, in normal
acinar
cells and tumour cells in the other 3/38 (7.9%) moderately differentiated and 7/18 (38.9%) poorly differentiated PDAC tissues, there was no visible TBX4 expression.
Strong expression of HSP60 could be seen in both
acinar
cells and small ducts in normal
pancreas
tissues and tumour cells in PDAC tissues except for islets and tumour stoma; no correlation was found between HSP60 expression and differentiation of PDAC tissues.
[MeSH-major]
Biomarkers, Tumor / metabolism.
Carcinoma
,
Pancreatic
Ductal / metabolism.
Pancreatic
Neoplasms / metabolism
[MeSH-minor]
Adult. Aged.
Cell
Differentiation. Female. HSP40 Heat-Shock Proteins / metabolism. Humans. Male. Middle Aged. Neoplasm Proteins / metabolism.
Pancreas
/ metabolism. Proteomics. T-Box Domain Proteins / metabolism. Trypsin / metabolism
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(PMID = 17412869.001).
[ISSN]
1472-4146
[Journal-full-title]
Journal of clinical pathology
[ISO-abbreviation]
J. Clin. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / HSP40 Heat-Shock Proteins; 0 / Neoplasm Proteins; 0 / T-Box Domain Proteins; 0 / TBX4 protein, human; EC 3.4.21.4 / Trypsin
12.
Sabbagh C, Fuks D, Chatelain D, Flamant M, Delcenserie R, Yzet T, Regimbeau JM:
[Acinar cell carcinoma of the pancreas: a rare tumor with particular clinical and paraclinical presentation].
Rev Med Interne
; 2008 Dec;29(12):1046-9
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[Title]
[
Acinar cell carcinoma of
the
pancreas
: a rare tumor with particular clinical and paraclinical presentation].
[Transliterated title]
Carcinome
à
cellules acineuses du
pancréas : une tumeur rare avec
des
caractéristiques cliniques et paracliniques particulières.
Acinar cell carcinoma of
the
pancreas
is a rare tumour with specific clinical and paraclinical presentation.
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(PMID = 18433943.001).
[ISSN]
0248-8663
[Journal-full-title]
La Revue de medecine interne
[ISO-abbreviation]
Rev Med Interne
[Language]
FRE
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
[Chemical-registry-number]
0 / Antineoplastic Agents, Phytogenic; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin
13.
Michl J, Scharf B, Schmidt A, Huynh C, Hannan R, von Gizycki H, Friedman FK, Brandt-Rauf P, Fine RL, Pincus MR:
PNC-28, a p53-derived peptide that is cytotoxic to cancer cells, blocks pancreatic cancer cell growth in vivo.
Int J Cancer
; 2006 Oct 1;119(7):1577-85
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[Title]
PNC-28, a p53-derived peptide that is cytotoxic to
cancer
cells, blocks
pancreatic cancer
cell
growth in vivo.
PNC-28 is a p53 peptide from its mdm-2-binding domain (residues 17-26), which contains the penetratin sequence enabling
cell
penetration on its carboxyl terminal end.
We have found that this peptide induces necrosis, but not apoptosis, of a variety of human tumor
cell
lines, including several with homozygous deletion of p53, and a ras-transformed rat
acinar
pancreatic
carcinoma cell
line, BMRPA1. Tuc3.
On the other hand, PNC-28 has no effect on untransformed cells, such as rat
pancreatic
acinar
cells, BMRPA1, and human breast epithelial cells and no effect on the differentiation of human stem cells.
[MeSH-major]
Pancreatic
Neoplasms / drug therapy.
Pancreatic
Neoplasms / pathology. Peptide Fragments / toxicity. Tumor Suppressor Protein p53 / toxicity
[MeSH-minor]
Animals.
Cell
Line, Tumor.
Cell
Proliferation / drug effects. Dose-Response Relationship, Drug. Humans. Mice. Mice, Nude. Rats. Xenograft Model Antitumor Assays
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[Copyright]
Copyright 2006 Wiley-Liss, Inc.
(PMID = 16688716.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / CA42500
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / PNC-28; 0 / Peptide Fragments; 0 / Tumor Suppressor Protein p53
14.
Igarashi H, Shinozaki S, Mukada T:
A case of acinar cell carcinoma of the pancreas that formed extensive tumor thrombus of the portal vein.
Clin J Gastroenterol
; 2009 Apr;2(2):96-102
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[Title]
A case
of acinar cell carcinoma
of the
pancreas
that formed extensive tumor thrombus of the portal vein.
Abdominal ultrasonography and computed tomography revealed a large mass in the body and tail of the
pancreas
, which directly invaded the stomach and the spleen.
The specimens obtained from portal tumor thrombus were histologically compatible with
acinar cell carcinoma
.
Portal tumor thrombus is a rare condition in
pancreatic
tumors; however, it seems to be important to differentiate tumor thrombus from blood thrombus of the portal vein in order to know the true clinical stage and provide a suitable treatment.
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[ISSN]
1865-7257
[Journal-full-title]
Clinical journal of gastroenterology
[ISO-abbreviation]
Clin J Gastroenterol
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Japan
[Keywords]
NOTNLM ; Acinar cell carcinoma / Pancreas / Portal vein / Tumor thrombus
15.
Roy S, Dhingra KK, Gupta P, Khurana N, Gupta B, Meher R:
Acinic cell carcinoma with extensive neuroendocrine differentiation: a diagnostic challenge.
Head Neck Pathol
; 2009 Jun;3(2):163-8
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[Title]
Acinic
cell carcinoma
with extensive neuroendocrine differentiation: a diagnostic challenge.
Primary salivary gland
carcinoma
with neuroendocrine differentiation is of rare occurrence, especially so in the parotid gland.
Amongst the various reported primary tumors with neuroendocrine differentiation, acinic
cell carcinoma
(ACC) one such tumor.
Contrast Enhanced Computed Tomography (CECT) suggested
diagnosis
of Pleomorphic Adenoma.
Initial histopathological examination of the tumor was suggestive of neuroendocrine
carcinoma
.
Immunoexpression of S-100, Neuron specific Enolase (NSE), Chromogranin A and Synaptophysin confirmed
the diagnosis
.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology. Parotid Neoplasms / pathology
[MeSH-minor]
Adenolymphoma / pathology. Biopsy, Fine-Needle.
Diagnosis
, Differential. Female. Humans. Immunohistochemistry. Middle Aged
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Head and neck pathology
[ISO-abbreviation]
Head Neck Pathol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Keywords]
NOTNLM ; Acinic cell / Carcinoma / Chromogranin / Neuroendocrine / Parotid / Warthin’s
16.
Fu XM, Dai X, Ding J, Zhu BT:
Pancreas-specific protein disulfide isomerase has a cell type-specific expression in various mouse tissues and is absent in human pancreatic adenocarcinoma cells: implications for its functions.
J Mol Histol
; 2009 Jun;40(3):189-99
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[Title]
Pancreas
-specific protein disulfide isomerase has a
cell
type-specific expression in various mouse tissues and is absent in human
pancreatic adenocarcinoma
cells: implications for its functions.
However, the
pancreas
-specific PDI homolog was previously suggested to be exclusively expressed in the
pancreas
(thus commonly referred to as PDIp).
Notably, in the digestive organs, such as the stomach and
pancreas
, very high levels of PDIp were selectively expressed in the digestive enzyme-secreting cells (e.g., gastric chief cells and
pancreatic
acinar
cells).
This observation suggests that PDIp may function
as a
protein-folding catalyst for secretory digestive enzymes.
In addition, high levels of PDIp expression were also detected in normal human
pancreas
, but its expression was mostly absent in human
pancreatic
duct
adenocarcinoma
and
pancreatic cancer
cell
lines.
The absence of PDIp expression in
pancreatic adenocarcinoma
may serve as an additional biomarker for
pancreatic cancer
.
[MeSH-major]
Adenocarcinoma
/ enzymology.
Pancreas
/ enzymology.
Pancreatic
Neoplasms / enzymology. Protein Disulfide-Isomerases / metabolism
[MeSH-minor]
Animals. Blotting, Western. COS Cells.
Carcinoma
,
Pancreatic
Ductal / enzymology.
Carcinoma
,
Pancreatic
Ductal / pathology.
Cell
Line, Tumor. Cercopithecus aethiops. Humans. Mice. Organ Specificity. Protein Transport. Subcellular Fractions / enzymology
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[ISSN]
1567-2387
[Journal-full-title]
Journal of molecular histology
[ISO-abbreviation]
J. Mol. Histol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R01 CA097109; United States / NCI NIH HHS / CA / CA97109; United States / NCRR NIH HHS / RR / P20RR021940
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
Netherlands
[Chemical-registry-number]
EC 5.3.4.1 / Protein Disulfide-Isomerases
17.
Kayed H, Bekasi S, Keleg S, Michalski CW, Giese T, Friess H, Kleeff J:
BGLAP is expressed in pancreatic cancer cells and increases their growth and invasion.
Mol Cancer
; 2007;6:83
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[Title]
BGLAP is expressed in
pancreatic cancer
cells and increases their growth and invasion.
In this study, we analyzed the expression and role of BGLAP in the normal human
pancreas
, chronic pancreatitis (CP), and
pancreatic
ductal
adenocarcinoma
(PDAC) using quantitative RT-PCR, immunohistochemistry, immunocytochemistry and enzyme immunoassays, as well as
cell
proliferation and invasion assays.
RESULTS: Compared to the normal
pancreas
, BGLAP mRNA and protein levels were not significantly different in CP and PDAC tissues.
BGLAP was faintly present in the cytoplasm of normal
acinar
cells but was strongly expressed in the cytoplasm and nuclei of tubular complexes and PanIN lesions of CP and PDAC tissues.
Furthermore, BGLAP expression was found in
the cancer
cells in PDAC tissues as well as in 4 cultured
pancreatic cancer
cell
lines.
TNFalpha reduced BGLAP mRNA and protein expression levels in
pancreatic cancer
cell
lines.
In addition, BGLAP silencing led to reduction of both
cell
growth and invasion in those cells.
CONCLUSION: BGLAP is expressed in
pancreatic cancer
cells, where it potentially increases
pancreatic cancer
cell
growth and invasion through autocrine and/or paracrine mechanisms.
[MeSH-major]
Adenocarcinoma
/ genetics.
Carcinoma
,
Pancreatic
Ductal / genetics.
Cell
Proliferation. Gene Expression Regulation, Neoplastic / physiology. Osteocalcin / genetics.
Pancreatic
Neoplasms / genetics
[MeSH-minor]
Adult. Aged. Aged, 80 and over. Collagen / metabolism. Drug Combinations. Enzyme-Linked Immunosorbent Assay. Gene Silencing. Humans. Immunoenzyme Techniques. Laminin / metabolism. Middle Aged. Neoplasm Invasiveness.
Pancreas
/ metabolism.
Pancreas
/ pathology. Pancreatitis, Chronic / genetics. Pancreatitis, Chronic / pathology. Proteoglycans / metabolism. RNA, Messenger / metabolism. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction
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[ISSN]
1476-4598
[Journal-full-title]
Molecular cancer
[ISO-abbreviation]
Mol. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 104982-03-8 / Osteocalcin; 119978-18-6 / matrigel; 9007-34-5 / Collagen
[Other-IDs]
NLM/ PMC2245975
18.
Murtaugh LC, Leach SD:
A case of mistaken identity? Nonductal origins of pancreatic "ductal" cancers.
Cancer Cell
; 2007 Mar;11(3):211-3
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[Title]
A case of mistaken identity? Nonductal origins of
pancreatic
"ductal" cancers.
In this issue of
Cancer
Cell
, Guerra and colleagues provide important new insights regarding the ability of specific
pancreatic
cell
types to generate invasive
pancreatic cancer
.
First, they demonstrate that classical
pancreatic
"ductal" neoplasia can be induced by activation of oncogenic Kras in nonductal exocrine cells.
Second, they show that, while Kras activation in immature
acinar
and centroacinar cells is readily able to induce ductal neoplasia, Kras-mediated tumorigenesis in mature exocrine
pancreas
requires the induction of chronic epithelial injury.
The results shed new light on the "
cell of
origin" of
pancreatic
ductal
cancer
and demonstrate that chronic pancreatitis provides a permissive environment for Kras-induced
pancreatic
neoplasia.
[MeSH-major]
Carcinoma
in Situ / pathology.
Carcinoma
,
Pancreatic
Ductal / pathology. Genes, ras.
Pancreatic
Neoplasms / pathology. Pancreatitis, Chronic / pathology
[MeSH-minor]
Animals.
Cell
Lineage.
Cell
Transformation, Neoplastic. Ceruletide. Humans. Mice. Mutation. Neoplasm Invasiveness
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[CommentOn]
Cancer Cell. 2007 Mar;11(3):291-302
[
17349585.001
]
(PMID = 17349578.001).
[ISSN]
1535-6108
[Journal-full-title]
Cancer cell
[ISO-abbreviation]
Cancer Cell
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / DK56211; United States / NIDDK NIH HHS / DK / DK61215
[Publication-type]
Comment; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
888Y08971B / Ceruletide
19.
Du YC, Klimstra DS, Varmus H:
Activation of PyMT in beta cells induces irreversible hyperplasia, but oncogene-dependent acinar cell carcinomas when activated in pancreatic progenitors.
PLoS One
; 2009 Sep 07;4(9):e6932
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[Title]
Activation of PyMT in beta cells induces irreversible hyperplasia, but oncogene-dependent
acinar cell
carcinomas when activated in
pancreatic
progenitors.
It is unclear whether the cellular origin of various forms of
pancreatic cancer
involves transformation or transdifferentiation of different target cells or whether tumors arise from common precursors, with tumor types determined by the specific genetic alterations.
Previous studies suggested that
pancreatic
ductal carcinomas might be induced by polyoma middle T antigen (PyMT) expressed in non-ductal cells.
Induction of PyMT in beta cells causes beta-
cell
hyperplastic lesions that do not progress to malignant neoplasms.
When PyMT is
de
-induced, beta
cell
proliferation and growth cease; however, regression does not occur, suggesting that continued production of PyMT is not required to maintain the viable expanded beta
cell
population.
In contrast, induction of PyMT in early
pancreatic
progenitor cells under the control of Pdx1 produces
acinar cell
carcinomas and beta-
cell
hyperplasia.
The survival
of acinar
tumor cells is dependent on continued expression of PyMT.
Our findings indicate that PyMT can induce exocrine tumors from
pancreatic
progenitor cells, but cells in the beta
cell
lineage are not transdifferentiated toward exocrine
cell
types by PyMT; instead, they undergo oncogene-dependent hyperplastic growth, but do not require PyMT for survival.
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[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U01 CA105492; United States / NCI NIH HHS / CA / P30 CA08748; United States / NCI NIH HHS / CA / P01 CA94060; United States / NCI NIH HHS / CA / P30 CA008748; United States / NCI NIH HHS / CA / P30-CA 08748; United States / NCI NIH HHS / CA / P01 CA094060; United States / NCI NIH HHS / CA / R24 CA83084; United States / NCI NIH HHS / CA / 5U01CA105492; United States / NCI NIH HHS / CA / R24 CA083084
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Polyomavirus Transforming; EC 1.13.12.- / Luciferases; F8VB5M810T / Tetracycline
[Other-IDs]
NLM/ PMC2758666
20.
Perren A, Anlauf M, Henopp T, Rudolph T, Schmitt A, Raffel A, Gimm O, Weihe E, Knoefel WT, Dralle H, Heitz PU, Komminoth P, Klöppel G:
Multiple endocrine neoplasia type 1 (MEN1): loss of one MEN1 allele in tumors and monohormonal endocrine cell clusters but not in islet hyperplasia of the pancreas.
J Clin Endocrinol Metab
; 2007 Mar;92(3):1118-28
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[Title]
Multiple endocrine neoplasia type 1 (MEN1): loss of one MEN1 allele in tumors and monohormonal endocrine
cell
clusters but not in islet hyperplasia of the
pancreas
.
CONTEXT: The occurrence of multiple small
pancreatic
endocrine tumors in patients suffering from multiple endocrine neoplasia type 1 (MEN1) represents a unique possibility to study early neoplasms and their potential precursor lesions.
To date, it is unknown whether small islet-like endocrine
cell
clusters found in MEN1 patients are neoplastic or rather hyperplastic.
DESIGN: We hypothesized that monohormonal endocrine
cell
clusters observed in MEN1 patients are small neoplasms with loss of heterozygosity of the MEN1 locus.
2) monohormonal endocrine
cell
clusters;.
RESULTS: Loss of one MEN1 allele was found in all 27 microadenomas and 19 of 20 (95%) monohormonal endocrine
cell
clusters.
By contrast, it was absent in islets and ductal or
acinar
structures.
Our results indicate that monohormonal endocrine
cell
clusters represent a minute form of microadenomas.
Islet hyperplasia does not seem to be an obligatory stage in
pancreatic
MEN1-associated tumor development.
[MeSH-major]
Carcinoma
,
Pancreatic
Ductal / genetics. Loss of Heterozygosity. Multiple Endocrine Neoplasia Type 1 / genetics.
Pancreas
/ pathology.
Pancreatic
Neoplasms / genetics. Proto-Oncogene Proteins / genetics
Genetic Alliance.
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.
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.
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consumer health - Islet cell hyperplasia
.
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.
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[CommentIn]
J Clin Endocrinol Metab. 2007 Mar;92(3):811-2
[
17341576.001
]
(PMID = 17179192.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins
21.
Wisnoski NC, Townsend CM Jr, Nealon WH, Freeman JL, Riall TS:
672 patients with acinar cell carcinoma of the pancreas: a population-based comparison to pancreatic adenocarcinoma.
Surgery
; 2008 Aug;144(2):141-8
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[Title]
672 patients with
acinar cell carcinoma of
the
pancreas
: a population-based comparison to
pancreatic adenocarcinoma
.
BACKGROUND:
Acinar cell carcinoma
(ACC) is a rare
cancer
of the
pancreas
accounting for approximately 1% of nonendocrine tumors.
OBJECTIVE: Our goal was to evaluate a large population-based cohort of patients with ACC and compare their demographic factors and outcomes to those of patients with
pancreatic adenocarcinoma
(PA).
The mean age at the time of
diagnosis
was significantly lower for ACC than PA (56 years vs 70 years, P < .001).
Multivariate Cox proportional hazards regression model results suggested patients with ACC were less likely to die (hazard ratio = 0.241; 95% confidence interval, 0.22-0.27) than patients with PA after controlling for gender, race, stage, SEER region of
diagnosis
, and surgical resection status.
[MeSH-major]
Adenocarcinoma
/ pathology.
Carcinoma
,
Acinar Cell
/ pathology.
Pancreatic
Neoplasms / pathology
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(PMID = 18656619.001).
[ISSN]
1532-7361
[Journal-full-title]
Surgery
[ISO-abbreviation]
Surgery
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
22.
Mataki Y, Shinchi H, Kurahara H, Maemura K, Minami K, Setoyama T, Ueno S, Sakoda M, Yamamoto T, Takao S, Natsugoe S:
[A case of acinar cell carcinoma diagnosed by endoscopic ultrasound-guided fine-needle aspiration prior to surgical treatment].
Nihon Shokakibyo Gakkai Zasshi
; 2010 Aug;107(8):1328-34
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[Title]
[A case
of acinar cell carcinoma
diagnosed by endoscopic ultrasound-guided fine-needle aspiration prior to surgical treatment].
She was given
a diagnosis
of acute pancreatitis and treated with intravenous infusion.
After recovering, abdominal enhanced-CT showed a low density area in the head of the
pancreas
, measuring 2 cm in maximum dimension.
Endoscopic ultrasound guided fine-needle aspiration (EUS-FNA) revealed
acinar cell carcinoma
(ACC).
The definitive
diagnosis
, based on the histopathological examinations including immunohistochemical staining, was ACC.
ACC of the
pancreas
is extremely rare, occurring in approximately 1% of all cases of
pancreatic
neoplasm.
[MeSH-major]
Biopsy, Fine-Needle / methods.
Carcinoma
,
Acinar Cell
/ pathology. Endosonography.
Pancreatic
Neoplasms / pathology
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(PMID = 20693758.001).
[ISSN]
0446-6586
[Journal-full-title]
Nihon Shokakibyo Gakkai zasshi = The Japanese journal of gastro-enterology
[ISO-abbreviation]
Nihon Shokakibyo Gakkai Zasshi
[Language]
jpn
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Japan
[Number-of-references]
26
23.
Huang Y, Cao YF, Lin JL, Gao F, Li F:
Acinar cell cystadenocarcinoma of the pancreas in a 4-year-old child.
Pancreas
; 2006 Oct;33(3):311-2
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[Title]
Acinar cell
cystadenocarcinoma of the
pancreas
in a 4-year-old child.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ surgery. Cystadenocarcinoma / surgery.
Pancreatic
Neoplasms / surgery
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(PMID = 17003655.001).
[ISSN]
1536-4828
[Journal-full-title]
Pancreas
[ISO-abbreviation]
Pancreas
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
24.
Gerloff A, Singer MV, Feick P:
Beer and its non-alcoholic compounds: role in pancreatic exocrine secretion, alcoholic pancreatitis and pancreatic carcinoma.
Int J Environ Res Public Health
; 2010 03;7(3):1093-104
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[Title]
Beer and its non-alcoholic compounds: role in
pancreatic
exocrine secretion, alcoholic pancreatitis and
pancreatic
carcinoma
.
In this article we provide an overview of the newest data concerning the effect of non-alcoholic constituents of alcoholic beverages, especially of beer, on
pancreatic
secretion, and their possible role in alcoholic pancreatitis and
pancreatic
carcinoma
.
The data indicate that non-alcoholic constituents of beer stimulate
pancreatic
enzyme secretion in humans and rats, at least in part, by direct action on
pancreatic
acinar
cells.
Some non-alcoholic compounds of beer, such as quercetin, resveratrol, ellagic acid or catechins, have been shown to be protective against experimentally induced pancreatitis by inhibiting
pancreatic
secretion, stellate
cell
activation or by reducing oxidative stress.
Their relevance in beer-induced functional alterations of
pancreatic
cells leading to pancreatitis and
pancreatic cancer
in humans needs to be further evaluated.
[MeSH-major]
Beer. Catechin / pharmacology. Ellagic Acid / pharmacology.
Pancreas
/ secretion.
Pancreatic
Neoplasms / physiopathology. Pancreatitis, Alcoholic / physiopathology. Quercetin / pharmacology. Stilbenes / pharmacology
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QUERCETIN
.
Hazardous Substances Data Bank.
ELLAGIC ACID
.
Hazardous Substances Data Bank.
RESVERATROL
.
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(PMID = 20617020.001).
[ISSN]
1660-4601
[Journal-full-title]
International journal of environmental research and public health
[ISO-abbreviation]
Int J Environ Res Public Health
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Stilbenes; 19YRN3ZS9P / Ellagic Acid; 8R1V1STN48 / Catechin; 9IKM0I5T1E / Quercetin; Q369O8926L / resveratrol
[Other-IDs]
NLM/ PMC2872306
[Keywords]
NOTNLM ; beer (major topic) / non-alcoholic constituents (major topic) / pancreatic carcinoma (major topic) / pancreatitis (major topic)
25.
Frankel WL:
Update on pancreatic endocrine tumors.
Arch Pathol Lab Med
; 2006 Jul;130(7):963-6
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[Title]
Update on
pancreatic
endocrine tumors.
Endocrine tumors of the
pancreas
represent 1% to 2% of all
pancreatic
neoplasms.
The morphologic spectrum of these tumors can be variable, and the differential
diagnosis
includes chronic pancreatitis with neuroendocrine hyperplasia, ductal
adenocarcinoma
, solid pseudopapillary tumor,
acinar cell carcinoma
, and pancreatoblastoma.
It is important to be aware that unusual morphologic variants of
pancreatic
endocrine tumors are common, and immunohistochemical stains can help avoid misdiagnosis.
[MeSH-major]
Adenoma, Islet
Cell
/ pathology.
Carcinoma
, Islet
Cell
/ pathology.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Carcinoma
,
Acinar Cell
/
diagnosis
.
Carcinoma
,
Pancreatic
Ductal /
diagnosis
.
Carcinoma
, Papillary /
diagnosis
.
Diagnosis
, Differential. Humans. Islets of Langerhans / pathology. Neoplasms, Germ
Cell
and Embryonal /
diagnosis
. Pancreatitis, Chronic /
diagnosis
. Prognosis
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(PMID = 16831051.001).
[ISSN]
1543-2165
[Journal-full-title]
Archives of pathology & laboratory medicine
[ISO-abbreviation]
Arch. Pathol. Lab. Med.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Number-of-references]
26
26.
Tapia B, Ahrens W, Kenney B, Touloukian R, Reyes-Múgica M:
Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature.
Pediatr Dev Pathol
; 2008 Sep-Oct;11(5):384-90
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[Title]
Acinar cell carcinoma
versus solid pseudopapillary tumor of the
pancreas
in children: a comparison of two rare and overlapping entities with review of the literature.
Primary epithelial tumors of the
pancreas
are extremely uncommon in children, and among these,
acinar cell carcinoma
(ACC) is the most rare.
The histologic
diagnosis
of ACC was supported by both immunohistochemistry and electron microscopy.
Despite its rarity, ACC should be kept in the differential
diagnosis
of pediatric
pancreatic
exocrine tumors.
We also provide a comparison with an example of solid pseudopapillary tumor, another relatively infrequent epithelial tumor of the
pancreas
in the young.
We review the relevant literature addressing the clinical and pathologic features of ACC and its distinction from other
pancreatic
neoplasms.
[MeSH-major]
Carcinoma
,
Acinar Cell
/
diagnosis
.
Carcinoma
,
Acinar Cell
/ pathology.
Pancreatic
Cyst / pathology.
Pancreatic
Neoplasms /
diagnosis
.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Child.
Diagnosis
, Differential. Humans. Immunohistochemistry. Male. Pancreatectomy. Treatment Outcome. alpha 1-Antitrypsin / metabolism
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(PMID = 19006424.001).
[ISSN]
1093-5266
[Journal-full-title]
Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
[ISO-abbreviation]
Pediatr. Dev. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Comparative Study; Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
[Number-of-references]
37
27.
Minakawa K, Oka K, Nihei T, Sando N, Oikawa H, Toda J, Hosokawa Y, Matsumoto T, Yanagisawa A:
Pancreatic endocrine tumor with partial acinar cell differentiation.
APMIS
; 2006 Oct;114(10):720-5
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[Title]
Pancreatic
endocrine tumor with partial
acinar cell
differentiation.
We examined a 70-year-old woman in whom
a pancreatic
endocrine tumor with partial
acinar cell
differentiation had been diagnosed.
The tumor was located in
the pancreatic
tail and measured 12.5 x 9.5 x 8 cm.
The cells had proliferated in islet-like solid medullary, trabecular,
acinar
, and papillary patterns.
[MeSH-major]
Carcinoma
,
Acinar Cell
/
diagnosis
.
Carcinoma
, Islet
Cell
/
diagnosis
. Neoplasms, Multiple Primary /
diagnosis
.
Pancreas
/ pathology.
Pancreatic
Neoplasms /
diagnosis
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(PMID = 17004975.001).
[ISSN]
0903-4641
[Journal-full-title]
APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
[ISO-abbreviation]
APMIS
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Denmark
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Synaptophysin; 0 / alpha 1-Antitrypsin
28.
Hervieu V, Lombard-Bohas C, Dumortier J, Boillot O, Scoazec JY:
Primary acinar cell carcinoma of the liver.
Virchows Arch
; 2008 Mar;452(3):337-41
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[Title]
Primary
acinar cell carcinoma of
the liver.
We report a case
of acinar cell carcinoma
primary to the liver.
In well-differentiated areas, tumor cells formed
acinar
structures, had a pyramidal shape and a highly eosinophilic, granular cytoplasm, PAS diastase resistant.
The final
diagnosis
, based on histological, immunohistochemical, and ultrastructural arguments, was extra-
pancreatic
acinar cell carcinoma
, primary to the liver.
This unusual lesion is likely to be the result of an abnormal differentiation pathway involving a transformed multipotential progenitor
cell
.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology. Liver / pathology. Liver Neoplasms / pathology
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[Cites]
Development. 2001 Mar;128(6):871-81
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Appl Immunohistochem Mol Morphol. 2000 Sep;8(3):203-9
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12775714.001
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Hum Pathol. 2002 Apr;33(4):449-51
[
12055683.001
]
(PMID = 18193278.001).
[ISSN]
0945-6317
[Journal-full-title]
Virchows Archiv : an international journal of pathology
[ISO-abbreviation]
Virchows Arch.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / alpha 1-Antitrypsin; 0 / alpha-Fetoproteins
29.
Martínez-Romero C, Rooman I, Skoudy A, Guerra C, Molero X, González A, Iglesias M, Lobato T, Bosch A, Barbacid M, Real FX, Hernández-Muñoz I:
The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and pancreatic ductal adenocarcinoma.
J Pathol
; 2009 Oct;219(2):205-13
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[Title]
The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and
pancreatic
ductal
adenocarcinoma
.
Chronic pancreatitis and
pancreatic
ductal
adenocarcinoma
(PDAC) are associated with major changes in
cell
differentiation.
Polycomb proteins are epigenetic silencers expressed in adult stem cells; up-regulation of Polycomb proteins has been reported to occur in a variety of solid tumours such as colon and breast
cancer
.
We hypothesized that Polycomb might play a role in preneoplastic states in the
pancreas
and in tumour development/progression.
To test these ideas, we determined the expression of PRC1 complex proteins (Bmi1 and Ring1b) during
pancreatic
development and in
pancreatic
tissue from mouse models of disease: acute and chronic
pancreatic
injury, duct ligation, and in K-Ras(G12V) conditional knock-in and caerulein-treated K-Ras(G12V) mice.
The study was extended to human
pancreatic
tissue samples.
To obtain mechanistic insights, Bmi1 expression in cells undergoing in vitro exocrine
cell
metaplasia and the effects of Bmi1 depletion in an
acinar
cancer
cell
line were studied.
We found that Bmi1 and Ring1B are expressed in
pancreatic
exocrine precursor cells during early development and in ductal and islet cells-but not
acinar
cells-in the adult
pancreas
.
Bmi1 expression was induced in
acinar
cells during acute injury, in
acinar
-ductal metaplastic lesions, as well as in
pancreatic
intraepithelial neoplasia (PanIN) and PDAC.
Bmi1 knockdown in cultured
acinar
tumour cells led to changes in the expression of various digestive enzymes.
Our results suggest that Bmi1 and Ring1B are modulated in
pancreatic
diseases and could contribute differently to tumour development.
[MeSH-major]
Carcinoma
,
Pancreatic
Ductal / metabolism. Nuclear Proteins / metabolism.
Pancreatic
Neoplasms / metabolism. Pancreatitis, Chronic / metabolism. Proto-Oncogene Proteins / metabolism. Repressor Proteins / metabolism
[MeSH-minor]
Acute Disease. Animals. Cells, Cultured. Disease Models, Animal. Humans. Male. Metaplasia / metabolism. Mice. Mice, Inbred C57BL.
Pancreas
/ metabolism.
Pancreas
, Exocrine / metabolism.
Pancreas
, Exocrine / pathology. Pancreatitis / metabolism. Polycomb Repressive Complex 1. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Rats. Rats, Wistar. Transcription Factors / metabolism
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[Copyright]
2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
(PMID = 19585519.001).
[ISSN]
1096-9896
[Journal-full-title]
The Journal of pathology
[ISO-abbreviation]
J. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / BMI1 protein, human; 0 / Bmi1 protein, mouse; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / transcription factor PTF1; EC 6.3.2.19 / Polycomb Repressive Complex 1
30.
Valentich MA, Eynard AR, Barotto NN, Díaz MP, Bongiovanni GA:
Effect of the co-administration of phenobarbital, quercetin and mancozeb on nitrosomethylurea-induced pancreatic tumors in rats.
Food Chem Toxicol
; 2006 Dec;44(12):2101-5
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[Title]
Effect of the co-administration of phenobarbital, quercetin and mancozeb on nitrosomethylurea-induced
pancreatic
tumors in rats.
We have previously shown that a single i.p. injection of nitrosomethylurea (NMU) in 3-day-old rats orally treated with the pesticide mancozeb (MZ), the flavonoid quercetin (Q) or in combination (MZ-Q) induces hyperplasia, atypical
acinar cell
proliferation and
carcinoma
in situ (CIS) in the
pancreas
.
This work studies the effect of oral administration of phenobarbital (PB) on this model of
pancreatic
carcinogenesis.
Acinar cell
hyperplasia was found in all groups of NMU-treated rats.
[MeSH-major]
Carcinogens / pharmacology.
Carcinoma
in Situ / chemically induced. Fungicides, Industrial / toxicity. Maneb / toxicity.
Pancreatic
Neoplasms / chemically induced. Phenobarbital / pharmacology. Quercetin / pharmacology. Zineb / toxicity
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Hazardous Substances Data Bank.
QUERCETIN
.
Hazardous Substances Data Bank.
Zineb
.
Hazardous Substances Data Bank.
Maneb
.
Hazardous Substances Data Bank.
Phenobarbital
.
Hazardous Substances Data Bank.
N-NITROSO-N-METHYLUREA
.
Hazardous Substances Data Bank.
Mancozeb
.
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(PMID = 16965848.001).
[ISSN]
0278-6915
[Journal-full-title]
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
[ISO-abbreviation]
Food Chem. Toxicol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Alkylating Agents; 0 / Carcinogens; 0 / Fungicides, Industrial; 12427-38-2 / Maneb; 684-93-5 / Methylnitrosourea; 9IKM0I5T1E / Quercetin; R0HY55EB9E / mancozeb; X1FSB1OZPT / Zineb; YQE403BP4D / Phenobarbital
31.
Saif MW:
Pancreatoblastoma.
JOP
; 2007;8(1):55-63
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Pancreatoblastoma (PB), or infantile
pancreatic
carcinoma
, is an extremely rare
pancreatic
tumor in childhood, comprising 0.5% of
pancreatic
non-endocrine tumors.
Mechanical obstruction of the upper duodenum and gastric outlet by tumor in the head of the
pancreas
may be associated with vomiting, jaundice and gastrointestinal bleeding.
Histologically, PB is characterized with distinct
acinar
and squamoid
cell
differentiation.
The majority of these tumors arise in the head of the
pancreas
.
Ultrasound and CT scan may be useful but preoperative
diagnosis
is often quite difficult.
On the whole, PB is regarded to be a curable tumor; hence the clinical
diagnosis
should be made early.
Awareness of this rare tumor
of pancreas
is essential for early detection and proper management.
The author review the clinical presentation, etiology,
diagnosis
, treatment and prognosis of PB in this presentation.
[MeSH-major]
Carcinoma
/
diagnosis
.
Pancreatic
Neoplasms /
diagnosis
[MeSH-minor]
Adolescent. Adult. Aged. Child. Child, Preschool. Female. Humans. Infant. Male. Middle Aged.
Pancreas
/ pathology
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(PMID = 17228135.001).
[ISSN]
1590-8577
[Journal-full-title]
JOP : Journal of the pancreas
[ISO-abbreviation]
JOP
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
32.
Ambrosini-Spaltro A, Potì O, De Palma M, Filotico M:
Pancreatic-type acinar cell carcinoma of the stomach beneath a focus of pancreatic metaplasia of the gastric mucosa.
Hum Pathol
; 2009 May;40(5):746-9
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[Title]
Pancreatic
-type
acinar cell carcinoma of
the stomach beneath a focus of
pancreatic
metaplasia of the gastric mucosa.
Acinar cell carcinoma
is an uncommon type
of carcinoma
of the
pancreas
that can exceptionally arise in ectopic
pancreatic
tissue.
Herein, we report a case of a 52-year-old man with
pancreatic
-type
acinar cell carcinoma of
the stomach and concomitant
pancreatic
metaplasia of the adjacent nonneoplastic gastric mucosa.
There was neither clinical nor radiographic evidence of a tumor in the
pancreas
itself.
The neoplastic cells and those of the adjacent metaplastic mucosa were both strongly immunoreactive for alpha-1-antitrypsin, consistent with
pancreatic
acinar cell
differentiation.
Ectopic
pancreatic
-type
acinar cell carcinoma
is an extremely rare condition, having been previously reported only in 5 occasions, none of them in association with
pancreatic
acinar cell
metaplasia of the gastric mucosa.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology. Gastric Mucosa / pathology.
Pancreas
/ pathology. Stomach Neoplasms / pathology
[MeSH-minor]
Cell
Differentiation. Humans. Male. Metaplasia / pathology. Middle Aged. alpha 1-Antitrypsin / biosynthesis
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(PMID = 19144387.001).
[ISSN]
1532-8392
[Journal-full-title]
Human pathology
[ISO-abbreviation]
Hum. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / SERPINA1 protein, human; 0 / alpha 1-Antitrypsin
33.
Stanger BZ, Stiles B, Lauwers GY, Bardeesy N, Mendoza M, Wang Y, Greenwood A, Cheng KH, McLaughlin M, Brown D, Depinho RA, Wu H, Melton DA, Dor Y:
Pten constrains centroacinar cell expansion and malignant transformation in the pancreas.
Cancer Cell
; 2005 Sep;8(3):185-95
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[Title]
Pten constrains centroacinar
cell
expansion and malignant transformation in the
pancreas
.
To determine the role of the phosphatidylinositol 3-kinase (PI3-K) pathway in
pancreas
development, we generated a
pancreas
-specific knockout of Pten, a negative regulator of PI3-K signaling.
Knockout mice display progressive replacement of the
acinar pancreas
with highly proliferative ductal structures that contain abundant mucins and express Pdx1 and Hes1, two markers of
pancreatic
progenitor cells.
We provide evidence that ductal metaplasia results from the expansion of centroacinar cells rather than transdifferentiation
of acinar
cells.
These results indicate that Pten actively maintains the balance between different
cell
types in the adult
pancreas
and that misregulation of the PI3-K pathway in centroacinar cells may contribute to the initiation of
pancreatic
carcinoma
in vivo.
[MeSH-major]
Pancreatic
Neoplasms / pathology. Protein Tyrosine Phosphatases / metabolism. Tumor Suppressor Proteins / metabolism
[MeSH-minor]
Animals.
Cell
Differentiation.
Cell
Transformation, Neoplastic. Metaplasia / pathology. Mice. PTEN Phosphohydrolase.
Pancreas
/ pathology.
Pancreas
/ physiopathology.
Pancreas
/ ultrastructure
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(PMID = 16169464.001).
[ISSN]
1535-6108
[Journal-full-title]
Cancer cell
[ISO-abbreviation]
Cancer Cell
[Language]
eng
[Grant]
United States / NIDDK NIH HHS / DK / K08 DK064136
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Tumor Suppressor Proteins; EC 3.1.3.48 / Protein Tyrosine Phosphatases; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
34.
Sawey ET, Johnson JA, Crawford HC:
Matrix metalloproteinase 7 controls pancreatic acinar cell transdifferentiation by activating the Notch signaling pathway.
Proc Natl Acad Sci U S A
; 2007 Dec 4;104(49):19327-32
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[Title]
Matrix metalloproteinase 7 controls
pancreatic
acinar cell
transdifferentiation by activating the Notch signaling pathway.
Acinar
-to-ductal metaplasia in the
pancreas
is associated with an increased risk for tumorigenesis.
Molecular dissection of this process in vitro has shown that primary
acinar
cells, in response to EGF receptor ligands, can transdifferentiate into duct-like epithelia, passing through a nestin-positive intermediate, in a Notch pathway-dependent manner.
Here, we show that in vitro
acinar
transdifferentiation depends on matrix metalloproteinase 7 (MMP-7), a proteinase expressed in most metaplastic epithelia in vivo.
MMP-7 was found to be required for Notch activation, which leads to dedifferentiation
of acinar
cells to the nestin-positive transitional
cell
.
Besides being necessary for
acinar
transdifferentiation, it was found that MMP-7 activity was sufficient to induce the process, indicating that molecular signals capable of initiating MMP-7 expression also have the potential to induce formation of metaplastic epithelia in the
pancreas
.
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]
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[ISSN]
1091-6490
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R01 CA100126; United States / NCI NIH HHS / CA / R01CA100126
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Intermediate Filament Proteins; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Receptors, Notch; EC 3.4.24.23 / Matrix Metalloproteinase 7
[Other-IDs]
NLM/ PMC2148289
35.
Seth AK, Argani P, Campbell KA, Cameron JL, Pawlik TM, Schulick RD, Choti MA, Wolfgang CL:
Acinar cell carcinoma of the pancreas: an institutional series of resected patients and review of the current literature.
J Gastrointest Surg
; 2008 Jun;12(6):1061-7
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[Title]
Acinar cell carcinoma of
the
pancreas
: an institutional series of resected patients and review of the current literature.
INTRODUCTION:
Acinar cell carcinoma
(ACC) is a rare, malignant neoplasm with a generally poor prognosis.
MATERIALS AND METHODS: The Johns Hopkins pathology prospective database was reviewed from 1988 to 2006 to identify patients with
pancreatic
neoplasms possessing features
of acinar cell
differentiation.
Overall median survival and disease-free survival were 33 and 25 months, respectively, as compared to a median survival of 18 months for
pancreatic adenocarcinoma
.
CONCLUSION:
Acinar cell
carcinomas are rare, aggressive neoplasms that are difficult to diagnose and treat.
These lesions have a better prognosis than the more common
pancreatic
adenocarcinomas.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology. Pancreatectomy / methods.
Pancreatic
Neoplasms / pathology. Pancreaticoduodenectomy / methods
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[ISSN]
1091-255X
[Journal-full-title]
Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
[ISO-abbreviation]
J. Gastrointest. Surg.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
36.
Stelow EB, Woon C, Pambuccian SE, Thrall M, Stanley MW, Lai R, Mallery S, Gulbahce HE:
Fine-needle aspiration cytology of pancreatic somatostatinoma: the importance of immunohistochemistry for the cytologic diagnosis of pancreatic endocrine neoplasms.
Diagn Cytopathol
; 2005 Aug;33(2):100-5
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[Title]
Fine-needle aspiration cytology of
pancreatic
somatostatinoma: the importance of immunohistochemistry for the cytologic
diagnosis
of
pancreatic
endocrine neoplasms.
Pancreatic
somatostatinoma is a rare
pancreatic
endocrine neoplasm representing as little as 1% of
pancreatic
endocrine neoplasms (PENs).
The histologic features of this tumor are like those of other PENs, except that it commonly forms
acinar
structures and often has cells with abundant, granular cytoplasm.
We discuss the cytologic and immunohistochemical findings of these two cases and the cytologic similarities these neoplasms share with
pancreatic
acinar
-
cell carcinoma
(PACC).
We review the cytologic features of PEN and PACC and discuss the importance
of cell
block immunohistochemistry in
the diagnosis
of
pancreatic
neoplasia sampled by EUS-guided FNA.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology.
Pancreatic
Neoplasms / pathology
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[Copyright]
Copyright 2005 Wiley-Liss, Inc.
(PMID = 16007666.001).
[ISSN]
8755-1039
[Journal-full-title]
Diagnostic cytopathology
[ISO-abbreviation]
Diagn. Cytopathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
37.
Hashimoto M, Miki K, Beck Y, Kokudo N, Makuuchi M, Tanaka H:
Femoral neck fracture as a complication of lipase-secreting pancreatic acinar cell carcinoma.
Surgery
; 2007 Nov;142(5):779-80
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[Title]
Femoral neck fracture
as a
complication of lipase-secreting
pancreatic
acinar cell carcinoma
.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ complications. Femoral Neck Fractures / etiology.
Pancreatic
Neoplasms / complications
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(PMID = 17981202.001).
[ISSN]
0039-6060
[Journal-full-title]
Surgery
[ISO-abbreviation]
Surgery
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
[Chemical-registry-number]
EC 3.1.1.3 / Lipase
38.
Matos JM, Schmidt CM, Turrini O, Agaram NP, Niedergethmann M, Saeger HD, Merchant N, Johnson CS, Lillemoe KD, Grützmann R:
Pancreatic acinar cell carcinoma: a multi-institutional study.
J Gastrointest Surg
; 2009 Aug;13(8):1495-502
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[Title]
Pancreatic
acinar cell carcinoma
: a multi-institutional study.
INTRODUCTION: The presentation and outcome of patients with
acinar cell carcinoma
(ACC) of the
pancreas
compared to the more common ductal
cell
adenocarcinoma
(DCA) may be distinct.
American Joint Commission on
Cancer
tumor stages were stage I (two), stage II (eight), stage III (four), and stage IV (three).
This is in contrast to 1,608 patients with ductal
cell
adenocarcinoma
who underwent resection identified from recent literature reports where the average median survival was only 24 months.
CONCLUSION:
Acinar cell carcinoma of
the
pancreas
is rare and appears to have a presentation and outcome distinct from the more common
pancreatic
DCA.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Aged. Antineoplastic Agents / therapeutic use. Biopsy. Cholangiopancreatography, Endoscopic Retrograde.
Diagnosis
, Differential. Follow-Up Studies. Germany / epidemiology. Humans. Incidence. Middle Aged. Neoplasm Recurrence, Local. Neoplasm Staging. Pancreatectomy / methods. Prognosis. Prospective Studies. Survival Rate. United States / epidemiology
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[ISSN]
1873-4626
[Journal-full-title]
Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
[ISO-abbreviation]
J. Gastrointest. Surg.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Multicenter Study
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents
39.
Flores LG, Bertolini S, Yeh HH, Young D, Mukhopadhyay U, Pal A, Ying Y, Volgin A, Shavrin A, Soghomonyan S, Tong W, Bornmann W, Alauddin MM, Logsdon C, Gelovani JG:
Detection of pancreatic carcinomas by imaging lactose-binding protein expression in peritumoral pancreas using [18F]fluoroethyl-deoxylactose PET/CT.
PLoS One
; 2009 Nov 24;4(11):e7977
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[Title]
Detection of
pancreatic
carcinomas by imaging lactose-binding protein expression in peritumoral
pancreas
using [18F]fluoroethyl-deoxylactose PET/CT.
BACKGROUND: Early
diagnosis
of
pancreatic
carcinoma
with highly sensitive diagnostic imaging methods could save lives of many thousands of patients, because early detection increases resectability and survival rates.
Current non-invasive diagnostic imaging techniques have inadequate resolution and sensitivity for detection of small size ( approximately 2-3 mm) early
pancreatic
carcinoma
lesions.
Therefore, we have assessed the efficacy of positron emission tomography and computer tomography (PET/CT) imaging with beta-O-D-galactopyranosyl-(1,4')-2'-deoxy-2'-[(18)F]fluoroethyl-D-glucopyranose ([(18)F]FEDL) for detection of less than 3 mm orthotopic xenografts of L3.6pl
pancreatic
carcinomas in mice.
[(18)F]FEDL is a novel radioligand of hepatocarcinoma-intestine-
pancreas
/pancreatitis-associated protein (HIP/PAP), which is overexpressed in peritumoral
pancreatic
acinar
cells.
METHODOLOGY/PRINCIPAL FINDINGS: Dynamic PET/CT imaging demonstrated rapid accumulation of [(18)F]FEDL in peritumoral
pancreatic
tissue (4.04+/-2.06%ID/g), bi-exponential blood clearance with half-lives of 1.65+/-0.50 min and 14.14+/-3.60 min, and rapid elimination from other organs and tissues, predominantly by renal clearance.
Using model-independent graphical analysis of dynamic PET data, the average distribution volume ratio (DVR) for [(18)F]FEDL in peritumoral
pancreatic
tissue was estimated as 3.57+/-0.60 and 0.94+/-0.72 in sham-operated control
pancreas
.
The in situ analysis demonstrated that at least a 2-4 fold apparent lesion size amplification was achieved for submillimeter tumors and to nearly half a murine
pancreas
for tumors larger than 3 mm.
CONCLUSION/SIGNIFICANCE: We have demonstrated the feasibility of detection of early
pancreatic
tumors by non-invasive imaging with [(18)F]FEDL PET/CT of tumor biomarker HIP/PAP over-expressed in peritumoral
pancreatic
tissue.
Non-invasive non-invasive detection of early
pancreatic
carcinomas with [(18)F]FEDL PET/CT imaging should aid the guidance of biopsies and additional imaging procedures, facilitate the resectability and improve the overall prognosis.
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]
(PMID = 19956730.001).
[ISSN]
1932-6203
[Journal-full-title]
PloS one
[ISO-abbreviation]
PLoS ONE
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / U24 CA126577; United States / NCI NIH HHS / CA / U24 CA126577-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Fluorine Radioisotopes; 0 / Lectins, C-Type; 0 / Ligands; 0 / O-galactopyranosyl-(1-4')-2'-deoxy-2'-fluoroethylglucopyranose; 0 / Radiopharmaceuticals; 0 / pancreatitis-associated protein; J2B2A4N98G / Lactose
[Other-IDs]
NLM/ PMC2776527
40.
Khalili M, Wax BN, Reed WP, Schuss A, Drexler S, Weston SR, Katz DS:
Radiology-pathology conference. Acinar cell carcinoma of the pancreas.
Clin Imaging
; 2006 Sep-Oct;30(5):343-6
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[Title]
Radiology-pathology conference.
Acinar cell carcinoma of
the
pancreas
.
Acinar cell carcinoma
(ACC) is a rare tumor that constitutes 1% of
pancreatic
neoplasms.
ACC is defined
as a
carcinoma
exhibiting
pancreatic
enzyme production by neoplastic cells.
In this Radiology-Pathology Conference, the clinical presentation and imaging findings of a patient with ACC of the
pancreas
, along with the differential
diagnosis
, are reviewed.
[MeSH-major]
Carcinoma
,
Acinar Cell
/
diagnosis
. Intestinal Obstruction /
diagnosis
.
Pancreatic
Neoplasms /
diagnosis
. Retroperitoneal Neoplasms /
diagnosis
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.
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.
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(PMID = 16919557.001).
[ISSN]
0899-7071
[Journal-full-title]
Clinical imaging
[ISO-abbreviation]
Clin Imaging
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
41.
Sanlioglu AD, Dirice E, Elpek O, Korcum AF, Ozdogan M, Suleymanlar I, Balci MK, Griffith TS, Sanlioglu S:
High TRAIL death receptor 4 and decoy receptor 2 expression correlates with significant cell death in pancreatic ductal adenocarcinoma patients.
Pancreas
; 2009 Mar;38(2):154-60
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[Title]
High TRAIL death receptor 4 and decoy receptor 2 expression correlates with significant
cell
death in
pancreatic
ductal
adenocarcinoma
patients.
OBJECTIVES: The importance of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and TRAIL receptor expression in
pancreatic
carcinoma
development is not known.
To reveal the putative connection of TRAIL and TRAIL receptor expression profile to this process, we analyzed and compared the expression profile of TRAIL and its receptors in
pancreatic
tissues of both noncancer patients and patients with
pancreatic
ductal
adenocarcinoma
(PDAC).
Annexin V binding revealed the apoptotic index in
pancreas
.
In addition,
acinar
cells from PDAC patients had higher DcR2 expression but lower death receptor 4 expression.
CONCLUSIONS: Differential alteration of TRAIL and TRAIL receptor expression profiles in PDAC patients suggest that the TRAIL/TRAIL receptor system may play a pivotal role during
pancreatic
carcinoma
development.
[MeSH-major]
Adenocarcinoma
/ pathology. Apoptosis.
Carcinoma
,
Pancreatic
Ductal / pathology.
Pancreatic
Neoplasms / pathology. Receptors, Tumor Necrosis Factor / physiology. Tumor Necrosis Factor Decoy Receptors / physiology
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(PMID = 18981952.001).
[ISSN]
1536-4828
[Journal-full-title]
Pancreas
[ISO-abbreviation]
Pancreas
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF10A protein, human; 0 / TNFRSF10D protein, human; 0 / Tumor Necrosis Factor Decoy Receptors
42.
Distler M, Rückert F, Dittert DD, Stroszczynski C, Dobrowolski F, Kersting S, Grützmann R:
Curative resection of a primarily unresectable acinar cell carcinoma of the pancreas after chemotherapy.
World J Surg Oncol
; 2009;7:22
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[Title]
Curative resection of a primarily unresectable
acinar cell carcinoma of
the
pancreas
after chemotherapy.
BACKGROUND:
Acinar cell carcinoma
(ACC) represents only 1-2% of
pancreatic
cancers and is a very rare malignancy.
At the time of
diagnosis
only 50% of the tumors appear to be resectable.
MRI-imaging showed a tumor within the head of the
pancreas
concomitant with Serum-Lipase and CA19-9.
Endosonographic fine needle biopsy confirmed an
acinar cell carcinoma
.
[MeSH-major]
Antimetabolites, Antineoplastic / therapeutic use.
Carcinoma
,
Acinar Cell
/ drug therapy.
Carcinoma
,
Acinar Cell
/ surgery. Fluorouracil / therapeutic use.
Pancreatic
Neoplasms / drug therapy.
Pancreatic
Neoplasms / surgery
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.
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FLUOROURACIL
.
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[Cites]
J Hepatobiliary Pancreat Surg. 2000;7(2):222-5
[
10982618.001
]
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Pancreas. 2003 Jul;27(1):e18-22
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]
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Hum Pathol. 2000 Aug;31(8):938-44
[
10987254.001
]
(PMID = 19239719.001).
[ISSN]
1477-7819
[Journal-full-title]
World journal of surgical oncology
[ISO-abbreviation]
World J Surg Oncol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; U3P01618RT / Fluorouracil
[Other-IDs]
NLM/ PMC2657786
43.
Fujii M, Sato H, Ogasawara T, Ando T, Tsujii S, Nagahori J, Komatsu Y, Matsuoka A:
[A case of liver metastasis of pancreatic acinar cell carcinoma treated with S-1 and intra-arterial CDDP combination therapy].
Gan To Kagaku Ryoho
; 2010 Oct;37(10):1987-90
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[Title]
[A case of liver metastasis of
pancreatic
acinar cell carcinoma
treated with S-1 and intra-arterial CDDP combination therapy].
A 55-year-old man underwent a pylorus-preserving pancreatoduodenectomy in August 2006 because
of acinar cell carcinoma
of the head of the
pancreas
.
We suggest that combination chemotherapy with oral S-1 and intra-arterial CDDP can be effective treatments for
pancreatic
acinar cell carcinoma
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Carcinoma
,
Acinar Cell
/ drug therapy. Cisplatin / therapeutic use. Liver Neoplasms / drug therapy. Oxonic Acid / therapeutic use.
Pancreatic
Neoplasms / drug therapy. Tegafur / therapeutic use
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.
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.
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CIS-DIAMINEDICHLOROPLATINUM
.
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(PMID = 20948270.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Drug Combinations; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
44.
Bockman DE:
Transition to pancreatic cancer in response to carcinogen.
Langenbecks Arch Surg
; 2008 Jul;393(4):557-60
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[Title]
Transition to
pancreatic cancer
in response to carcinogen.
BACKGROUND: It has become obvious that the traditional assumptions about the transition from normal
pancreas
to
pancreatic cancer
are incomplete.
Experimental studies reveal that the earliest changes during transition to
pancreatic adenocarcinoma
involve premalignant lesions that are derived from
acinar
, islet, and ductal cells.
As part of redifferentiation and transformation to
adenocarcinoma
, cells regain the characteristics of developing
pancreas
.
Elements significant in identifying precursor
cell
types include Pdx1, hedgehog signaling, notch signaling, and nestin, an intermediate filament expressed by precursor
cell
types.
CONCLUSIONS: Thus
pancreatic
carcinogenesis is not simply a matter of transition of ductal cells to
cancer
cells months after insult by the carcinogen; ductal cells are not the sole source transitioning to
cancer
, and PanINs are not the sole route to
adenocarcinoma
.
Tubular complexes, derived from multiple
cell
sources, are included in routes to
pancreatic cancer
.
Markers characteristic of developing
pancreas
are consistent with this transition.
[MeSH-major]
Carcinogens.
Cell
Transformation, Neoplastic / chemically induced.
Pancreatic
Neoplasms / chemically induced. Precancerous Conditions / chemically induced
[MeSH-minor]
Animals.
Carcinoma
,
Pancreatic
Ductal / genetics.
Carcinoma
,
Pancreatic
Ductal / pathology. Gene Expression Regulation, Neoplastic / genetics. Hedgehog Proteins / genetics. Homeodomain Proteins / genetics. Humans. Intermediate Filament Proteins / genetics. Nerve Tissue Proteins / genetics. Nestin. Receptors, Notch / genetics. Signal Transduction / drug effects. Signal Transduction / genetics. Smoking / adverse effects. Stem Cells / drug effects. Stem Cells / pathology. Trans-Activators / genetics
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.
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[ISSN]
1435-2451
[Journal-full-title]
Langenbeck's archives of surgery
[ISO-abbreviation]
Langenbecks Arch Surg
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Germany
[Chemical-registry-number]
0 / Carcinogens; 0 / Hedgehog Proteins; 0 / Homeodomain Proteins; 0 / Intermediate Filament Proteins; 0 / NES protein, human; 0 / Nerve Tissue Proteins; 0 / Nestin; 0 / Receptors, Notch; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein
[Number-of-references]
35
45.
Volkan Adsay N:
Cystic lesions of the pancreas.
Mod Pathol
; 2007 Feb;20 Suppl 1:S71-93
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[Title]
Cystic lesions of the
pancreas
.
Although cystic tumors of the
pancreas
are relatively rare, they constitute an increasingly important category.
Advances in imaging and interventional techniques and the sharp drop in the mortality rate of
pancreatic
surgery have rendered
pancreatic
biopsies and resections commonplace specimens.
Consensus criteria for the distinction of these from the ordinary precursors of
adenocarcinoma
,
the pancreatic
intraepithelial neoplasia, were established.
The definition of mucinous cystic neoplasms was refined; ovarian-like stroma has now become almost a requirement for
the diagnosis
of mucinous cystic neoplasia, and defined as such, the propensity of these tumors to occur in perimenopausal women became even more striking.
The validity and clinical value of classifying
the pancreatic
cysts of mucinous type as adenoma, borderline, CIS and invasive have been established.
Greater accessibility of the
pancreas
afforded by improved invasive as well as noninvasive modalities has also increased the detection of otherwise clinically silent cystic tumors, which has led to the recognition of more innocuous entities such as
acinar cell
cystadenoma and squamoid cyst of
pancreatic
ducts.
Thus, significant developments have taken place in the classification and our understanding of
pancreatic
cystic tumors in the past few years, and experience with these lesions is likely to grow exponentially in the coming years.
[MeSH-major]
Cystadenocarcinoma, Mucinous / pathology. Cystadenocarcinoma, Papillary / pathology.
Pancreas
/ pathology.
Pancreatic
Neoplasms / pathology.
Pancreatic
Pseudocyst / pathology
[MeSH-minor]
Adenoma / pathology.
Carcinoma
in Situ / pathology. Humans.
Pancreatic
Ducts / pathology. Precancerous Conditions
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(PMID = 17486054.001).
[ISSN]
0893-3952
[Journal-full-title]
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
[ISO-abbreviation]
Mod. Pathol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
46.
National Toxicology Program:
Toxicology and carcinogenesis studies of 2,3',4,4',5-pentachlorobiphenyl (PCB 118) (CAS No. 31508-00-6) in female harlan Sprague-Dawley rats (gavage studies).
Natl Toxicol Program Tech Rep Ser
; 2010 Nov;(559):1-174
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Since human exposure to DLCs always occurs
as a
complex mixture, the toxic equivalency factor (TEF) methodology has been developed
as a
mathematical tool to assess the health risk posed by complex mixtures of these compounds.
The toxic equivalency of DLCs was nominated for evaluation because of the widespread human exposure to DLCs and the lack of data on the adequacy of the TEF methodology for predicting relative potency for
cancer
risk.
There were increases in hepatic
cell
proliferation in the 4,600 g/kg group at 14, 31, and 53 weeks.
At 2 years, a significant dose-related increase in hepatic toxicity was observed and was characterized by increased incidences of numerous lesions including hepatocyte hypertrophy, inflammation, oval
cell
hyperplasia, pigmentation, multinucleated hepatocyte, eosinophilic and mixed
cell
foci, diffuse fatty change, toxic hepatopathy, nodular hyperplasia, necrosis, bile duct hyperplasia and cyst, and cholangiofibrosis.
The incidence
of carcinoma
of the uterus in the 4,600 g/kg stop-exposure group was significantly greater than those in the vehicle control and 4,600 g/kg core study groups at 2 years.
A marginal increase in squamous
cell carcinoma
occurred in the 220 g/kg group.
At 2 years, there were marginally increased incidences of exocrine
pancreatic
adenoma or
carcinoma
in the 460, 1,000, and 4,600 g/kg core study groups.
Numerous nonneoplastic effects were seen in other organs including: adrenal cortical atrophy and cytoplasmic vacuolization,
pancreatic
acinar cell
cytoplasmic vacuolization and arterial chronic active inflammation, follicular
cell
hypertrophy of the thyroid gland, inflammation and respiratory epithelial hyperplasia of the nose, and kidney pigmentation.
Occurrences
of carcinoma
in the uterus were considered to be related to the administration of PCB 118.
Occurrences of squamous
cell carcinoma
of the uterus and
acinar
neoplasms of the
pancreas
may have been related to administration of PCB 118.
Administration of PCB 118 caused increased incidences of nonneoplastic lesions in the liver, lung, adrenal cortex,
pancreas
, thyroid gland, nose, and kidney.
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(PMID = 21383778.001).
[ISSN]
0888-8051
[Journal-full-title]
National Toxicology Program technical report series
[ISO-abbreviation]
Natl Toxicol Program Tech Rep Ser
[Language]
eng
[Publication-type]
Journal Article; Technical Report
[Publication-country]
United States
[Chemical-registry-number]
31508-00-6 / 2,3',4,4',5-pentachlorobiphenyl; DFC2HB4I0K / Polychlorinated Biphenyls; DO80M48B6O / Tetrachlorodibenzodioxin
47.
Kaifi JT, Heidtmann S, Schurr PG, Reichelt U, Mann O, Yekebas EF, Wachowiak R, Strate T, Schachner M, Izbicki JR:
Absence of L1 in pancreatic masses distinguishes adenocarcinomas from poorly differentiated neuroendocrine carcinomas.
Anticancer Res
; 2006 Mar-Apr;26(2A):1167-70
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[Title]
Absence of L1 in
pancreatic
masses distinguishes adenocarcinomas from poorly differentiated neuroendocrine carcinomas.
BACKGROUND:
Pancreatic adenocarcinoma
is a tumor with fatal outcome.
Cell
adhesion molecules, such as L1 (CD171), have an essential function in tumor progression.
L1 has been shown to be specifically expressed in poorly differentiated neuroendocrine carcinomas of the
pancreas
.
The aim of this study was to determine the expression of L1 in
pancreatic
adenocarcinomas to evaluate whether L1 might differentiate between
pancreatic
carcinomas of neuroendocrine and ductal origin.
MATERIALS AND METHODS: L1 expression was retrospectively analyzed in 111 cases of
pancreatic
adenocarcinomas by immunohistochemistry on paraffin sections of primary tumors.
RESULTS: The focal expression of L1 was detected in 2 (2%) out of 111
pancreatic
carcinomas only, the remaining 109 (98%) being L1-negative.
No expression was found in
acinar
or ductal cells of normal
pancreatic
tissue.
CONCLUSION: Our data suggest that L1 is expressed in few cases of
pancreatic
ductal
adenocarcinoma
.
Since L1 was previously found to be expressed specifically in neuroendocrine
pancreatic
carcinomas, its absence in unclear
pancreatic
masses might hint at a ductal origin for a malignant
pancreatic
tumor.
[MeSH-major]
Adenocarcinoma
/ immunology.
Adenocarcinoma
/ pathology.
Carcinoma
, Neuroendocrine / immunology.
Carcinoma
, Neuroendocrine / pathology. Leukocyte L1 Antigen Complex / biosynthesis.
Pancreatic
Neoplasms / immunology.
Pancreatic
Neoplasms / pathology
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(PMID = 16619519.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Greece
[Chemical-registry-number]
0 / Leukocyte L1 Antigen Complex
48.
Wu X, Tao R, Lei R, Han B, Cheng D, Shen B, Peng C:
Distal pancreatectomy combined with celiac axis resection in treatment of carcinoma of the body/tail of the pancreas: a single-center experience.
Ann Surg Oncol
; 2010 May;17(5):1359-66
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[Title]
Distal pancreatectomy combined with celiac axis resection in treatment
of carcinoma
of the body/tail of the
pancreas
: a single-center experience.
The aim of this study was to assess the safety and efficacy of this extended procedure in treatment of advanced
carcinoma of
the body/tail of the
pancreas
.
METHODS: This was a retrospective analysis of 206 patients with
carcinoma of
the body/tail of the
pancreas
from January 2003 through June 2008.
Group A had longer mean operative time than group B (323 versus 225 min, P = 0.000); there was no difference in mean estimated blood loss, percentage of
pancreatic
fistula or median survival time (14 versus 15 months, P = 0.197).
CONCLUSIONS: DP combined with CA resection can be safely performed in certain patients with
carcinoma of
body/tail of the
pancreas
and significantly improves patient survival and quality of life.
[MeSH-major]
Celiac Artery / surgery. Pancreatectomy.
Pancreatic
Neoplasms / surgery
[MeSH-minor]
Adenocarcinoma
.
Adenocarcinoma
, Clear
Cell
.
Adenocarcinoma
, Mucinous. Adult. Aged.
Carcinoma
,
Acinar Cell
. Female. Humans. Liver Neoplasms / secondary. Liver Neoplasms / surgery. Male. Middle Aged. Neoplasm Invasiveness. Postoperative Complications /
diagnosis
. Retrospective Studies. Survival Rate. Tomography, X-Ray Computed. Treatment Outcome
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[CommentIn]
Ann Surg Oncol. 2011 Dec;18 Suppl 3:S244; author reply S245
[
20967503.001
]
(PMID = 20198445.001).
[ISSN]
1534-4681
[Journal-full-title]
Annals of surgical oncology
[ISO-abbreviation]
Ann. Surg. Oncol.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
United States
49.
Colby JK, Klein RD, McArthur MJ, Conti CJ, Kiguchi K, Kawamoto T, Riggs PK, Pavone AI, Sawicki J, Fischer SM:
Progressive metaplastic and dysplastic changes in mouse pancreas induced by cyclooxygenase-2 overexpression.
Neoplasia
; 2008 Aug;10(8):782-96
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[Title]
Progressive metaplastic and dysplastic changes in mouse
pancreas
induced by cyclooxygenase-2 overexpression.
We generated transgenic mice (BK5.COX-2) in which elevation of COX-2 and its effectors trigger a metaplasia-dysplasia sequence in exocrine
pancreas
.
Histologic evaluation revealed a chronic pancreatitis-like state characterized by
acinar
-to-ductal metaplasia and a well-vascularized fibroinflammatory stroma that develops by 3 months.
By 6 to 8 months, strongly dysplastic features suggestive of
pancreatic
ductal
adenocarcinoma
emerge in the metaplastic ducts.
Increased proliferation, cellular atypia, and loss of normal
cell
/tissue organization are typical features in transgenic pancreata.
Alterations in biomarkers associated with human inflammatory and neoplastic
pancreatic
disease were detected using immunohistochemistry.
The abnormal
pancreatic
phenotype can be completely prevented by maintaining mice on a diet containing celecoxib, a well-characterized COX-2 inhibitor.
However,
cell
lines derived from spontaneous lesions are aggressively tumorigenic when injected into syngeneic or nude mice.
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[ISSN]
1476-5586
[Journal-full-title]
Neoplasia (New York, N.Y.)
[ISO-abbreviation]
Neoplasia
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA122815; United States / NCI NIH HHS / CA / R25 CA057730; United States / NIEHS NIH HHS / ES / T32 ES07247; United States / NCI NIH HHS / CA / R21 CA122815; United States / NIEHS NIH HHS / ES / P30 ES007784; United States / NIEHS NIH HHS / ES / ES07784; United States / NIEHS NIH HHS / ES / T32 ES007247; United States / NCI NIH HHS / CA / R25CA57730; United States / NCI NIH HHS / CA / CA105345; United States / NCI NIH HHS / CA / U01 CA105345
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Pyrazoles; 0 / Sulfonamides; 63231-63-0 / RNA; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone
[Other-IDs]
NLM/ PMC2481568
50.
Yamaue H:
[Clinical characteristics of invasive ductal carcinomas of the pancreas according to the histological differentiation].
Nihon Rinsho
; 2006 Jan;64 Suppl 1:48-51
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[Title]
[Clinical characteristics of invasive ductal carcinomas of the
pancreas
according to the histological differentiation].
[MeSH-major]
Carcinoma
,
Pancreatic
Ductal / pathology.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Carcinoma
/ epidemiology.
Carcinoma
/ pathology.
Carcinoma
,
Acinar Cell
/ epidemiology.
Carcinoma
,
Acinar Cell
/ pathology. Humans. Neoplasm Invasiveness / pathology. Prognosis. Survival Rate. Time Factors
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(PMID = 16457220.001).
[ISSN]
0047-1852
[Journal-full-title]
Nihon rinsho. Japanese journal of clinical medicine
[ISO-abbreviation]
Nippon Rinsho
[Language]
jpn
[Publication-type]
Journal Article; Review
[Publication-country]
Japan
[Number-of-references]
14
51.
Jang SH, Choi SY, Min JH, Kim TW, Lee JA, Byun SJ, Lee JW:
[A case of acinar cell carcinoma of pancreas, manifested by subcutaneous nodule as initial clinical symptom].
Korean J Gastroenterol
; 2010 Feb;55(2):139-43
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[Title]
[A case
of acinar cell carcinoma of pancreas
, manifested by subcutaneous nodule as initial clinical symptom].
Pancreas acinar cell carcinoma
(ACC) accounts for only 1-2% of
pancreatic
exocrine malignant tumor.
[MeSH-major]
Carcinoma
,
Acinar Cell
/
diagnosis
.
Pancreatic
Neoplasms /
diagnosis
. Subcutaneous Fat / pathology
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(PMID = 20168061.001).
[ISSN]
2233-6869
[Journal-full-title]
The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
[ISO-abbreviation]
Korean J Gastroenterol
[Language]
kor
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Synaptophysin; 68238-35-7 / Keratins
52.
Dall'igna P, Cecchetto G, Bisogno G, Conte M, Chiesa PL, D'Angelo P, De Leonardis F, De Salvo G, Favini F, Ferrari A, TREP Group:
Pancreatic tumors in children and adolescents: the Italian TREP project experience.
Pediatr Blood Cancer
; 2010 May;54(5):675-80
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[Title]
Pancreatic
tumors in children and adolescents: the Italian TREP project experience.
INTRODUCTION: Malignant
pancreatic
tumors are exceedingly rare in pediatric age and their clinical features and treatment usually go unappreciated by most pediatric oncologists and surgeons.
METHODS: From January 2000 to July 2009, 21 patients <18 years old with
pancreatic
tumors were prospectively registered in the Italian cooperative TREP project dedicated to very rare pediatric tumors.
RESULTS: Tumor types were 4 pancreatoblastomas, 2
pancreatic
carcinomas, 3 neoplasms of the endocrine
pancreas
, and 12 solid pseudopapillary tumors.
Three of the four patients with pancreatoblastoma had advanced disease at
diagnosis
and were given chemotherapy; at the time of this report, three patients were alive in first remission, while one died due to treatment toxicity.
Both the cases of
pancreatic
carcinoma
had the
acinar cell
subtype and successfully underwent pancreaticoduodenectomy with complete tumor resection, remaining without evidence of disease at the time of this analysis.
The histological diagnoses of the three endocrine tumors were a malignant islet
cell
tumor, a gastrinoma, and a well-differentiated tumor.
All 12 patients with solid pseudopapillary tumors underwent complete tumor resection and were given no adjuvant treatment; 11 were alive in first remission, while one experienced a local and distant relapse 5 years after
diagnosis
.
CONCLUSIONS: Surgery remains the keystone of treatment for
pancreatic
tumors in pediatric age as in adults.
The TREP project shows that prospective cooperative studies are feasible even for such very rare tumors as these and may serve
as a
model for developing international cooperative schemes.
[MeSH-major]
Pancreatic
Neoplasms / epidemiology. Rare Diseases / epidemiology
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[CommentIn]
Pediatr Blood Cancer. 2010 May;54(5):659-60
[
20063425.001
]
(PMID = 19998473.001).
[ISSN]
1545-5017
[Journal-full-title]
Pediatric blood & cancer
[ISO-abbreviation]
Pediatr Blood Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
53.
Mizgireuv IV, Revskoy SY:
Transplantable tumor lines generated in clonal zebrafish.
Cancer Res
; 2006 Mar 15;66(6):3120-5
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Transplantable zebrafish tumors are a novel and very promising model in
cancer
research.
The histologic analysis of these tumors revealed different types of hepatocellular carcinomas, hepatoblastomas, hepatoma, cholangiocarcinoma, and
pancreatic
carcinoma
.
Four spontaneous
acinar cell
carcinomas
of pancreas
were also found in 10- to 18-month-old CB1 fish.
Small pieces of tissue or
cell
suspensions of either DEN-induced or spontaneous tumors were serially transplanted into the peritoneal cavity of syngeneic fish at different stages of development from 5-day-old larvae to adult fish.
[MeSH-minor]
Animals.
Cell
Line, Tumor. Diethylnitrosamine. Diploidy. Disease Models, Animal. Homozygote. Humans. Male. Neoplasm Transplantation
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(PMID = 16540662.001).
[ISSN]
0008-5472
[Journal-full-title]
Cancer research
[ISO-abbreviation]
Cancer Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
3IQ78TTX1A / Diethylnitrosamine
54.
Chen Y, Yu G, Ma D, Ni C, Zhu M:
Microadenocarcinoma of the pancreas.
Eur J Gastroenterol Hepatol
; 2009 Dec;21(12):1373-8
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[Title]
Microadenocarcinoma of the
pancreas
.
BACKGROUND: Microadenocarcinoma (MA) of the
pancreas
is a rare kind of neoplasm, whose status as an independent tumor entity is still a matter of controversy.
Cells of MA were morphologically uniform and were less pleomorphic than those of the ductal
adenocarcinoma
.
Immunohistochemistry revealed that MA, though with a certain extent of epithelial differentiation, possesses a different immunological phenotype from those of ductal
carcinoma
,
acinar cell carcinoma
, and endocrine tumors.
Genetic analysis showed no abnormality of p53, K-ras, and beta-catenin, which were usually mutated in
pancreatic
ductal
adenocarcinoma
.
CONCLUSION: Therefore, we suggest that MA should be taken as an independent tumor entity rather than a kind of growth pattern, but a final decision should be reached after cautious differential
diagnosis
of other kinds of
pancreatic
neoplasms.
[MeSH-major]
Adenocarcinoma
/ pathology.
Pancreatic
Neoplasms / pathology
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(PMID = 19916245.001).
[ISSN]
1473-5687
[Journal-full-title]
European journal of gastroenterology & hepatology
[ISO-abbreviation]
Eur J Gastroenterol Hepatol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
England
55.
Imamura M, Kimura Y, Ito H, Nobuoka T, Koito K, Sasaki A, Hirata K:
Acinar cell carcinoma of the pancreas with intraductal growth: report of a case.
Surg Today
; 2009;39(11):1006-9
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[Title]
Acinar cell carcinoma of
the
pancreas
with intraductal growth: report of a case.
Acinar cell
carcinomas (ACCs) of the
pancreas
are rare neoplasms, accounting for approximately 1% of all exocrine
pancreatic
tumors.
This type of tumor is known to be aggressive, although the survival rates are somewhat better than they are for ductal
carcinoma
.
This report presents a case of ACC of the
pancreas
with intraductal papillary growth and lymph node metastasis.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ surgery. Neoplasm Invasiveness. Pancreatectomy / methods.
Pancreatic
Ducts / pathology.
Pancreatic
Neoplasms / surgery
[MeSH-minor]
Aged. Cholangiopancreatography, Endoscopic Retrograde.
Diagnosis
, Differential. Endosonography. Female. Humans
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[ISO-abbreviation]
Surg. Today
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
56.
Hosoda W, Takagi T, Mizuno N, Shimizu Y, Sano T, Yamao K, Yatabe Y:
Diagnostic approach to pancreatic tumors with the specimens of endoscopic ultrasound-guided fine needle aspiration.
Pathol Int
; 2010 May;60(5):358-64
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[Title]
Diagnostic approach to
pancreatic
tumors with the specimens of endoscopic ultrasound-guided fine needle aspiration.
Endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA) has enabled clinicians to histologically diagnose
pancreatic
tumors.
Using immunostaining of CK7, CDX2, neuroendocrine markers and KRAS mutation analysis, we examined 57 FNA
cell
block sections and 61 surgically-resected specimens (25 invasive ductal carcinomas, 25 endocrine tumors, and 11
acinar cell
tumors).
In the majority of the matched pairs, the diagnoses between EUS-FNA and surgical specimens were concordant using the following criteria: neuroendocrine markers negative, CK7 positive, and mutated KRAS gene for invasive ductal carcinomas; neuroendocrine markers diffusely positive, CK7 and CDX2 negative, and wild-type KRAS gene for well-differentiated endocrine tumors; and neuroendocrine markers no more than focal positive, CK7 and CDX2 with various staining patterns, and wild-type KRAS gene for
acinar cell
carcinomas.
The usefulness of these markers was confirmed using 13 additional
pancreatic
tumors, prospectively.
Although minimal in selection, these markers are helpful in making
diagnosis
from EUS-FNA specimens of the major
pancreatic
tumors.
[MeSH-major]
Carcinoma
,
Acinar Cell
/
diagnosis
.
Carcinoma
, Islet
Cell
/
diagnosis
.
Carcinoma
,
Pancreatic
Ductal /
diagnosis
. Endosonography / methods.
Pancreatic
Neoplasms /
diagnosis
[MeSH-minor]
Biomarkers, Tumor / genetics. Biomarkers, Tumor / metabolism. Biopsy, Fine-Needle. DNA Mutational Analysis. DNA, Neoplasm / analysis. Homeodomain Proteins / metabolism. Humans. Keratin-7 / metabolism.
Pancreas
/ metabolism.
Pancreas
/ pathology. Pancreatectomy. Prognosis. Prospective Studies. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. ras Proteins / genetics. ras Proteins / metabolism
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(PMID = 20518885.001).
[ISSN]
1440-1827
[Journal-full-title]
Pathology international
[ISO-abbreviation]
Pathol. Int.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
[Publication-country]
Australia
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / CDX2 protein, human; 0 / DNA, Neoplasm; 0 / Homeodomain Proteins; 0 / KRAS protein, human; 0 / Keratin-7; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
57.
Awadallah NS, Shroyer KR, Langer DA, Torkko KC, Chen YK, Bentz JS, Papkoff J, Liu W, Nash SR, Shah RJ:
Detection of B7-H4 and p53 in pancreatic cancer: potential role as a cytological diagnostic adjunct.
Pancreas
; 2008 Mar;36(2):200-6
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[Title]
Detection of B7-H4 and p53 in
pancreatic cancer
: potential role
as a
cytological diagnostic adjunct.
OBJECTIVES: This study compared p53 expression with B7-H4, a novel
cancer
biomarker, in
pancreatic
ductal
adenocarcinoma
(PDA) resection specimens and in a pilot series of endoscopic ultrasound-guided fine-needle aspirations (EUS-FNAs).
Some benign tissue components (intercalated cells/ducts, main
pancreatic
ducts, and
acinar
cells) were also positive for B7-H4 and/or p53.
Overall expression of B7-H4 in benign tissues, however, was relatively low compared with that seen in most
carcinoma
cases.
[MeSH-major]
Antigens, CD80 / analysis. Biomarkers, Tumor / analysis.
Carcinoma
,
Pancreatic
Ductal / chemistry.
Pancreatic
Neoplasms / chemistry. Tumor Suppressor Protein p53 / analysis
[MeSH-minor]
Adult. Aged. Biopsy, Fine-Needle / methods. Endosonography. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Staging.
Pancreas
/ chemistry. Pilot Projects. Predictive Value of Tests. Reproducibility of Results. Tissue Fixation. V-Set Domain-Containing T-
Cell
Activation Inhibitor 1
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(PMID = 18376314.001).
[ISSN]
1536-4828
[Journal-full-title]
Pancreas
[ISO-abbreviation]
Pancreas
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antigens, CD80; 0 / Biomarkers, Tumor; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / V-Set Domain-Containing T-Cell Activation Inhibitor 1; 0 / VTCN1 protein, human
58.
Chang SC, Liao JW, Lin YC, Liu CI, Wong ML:
Pancreatic acinar cell carcinoma with intracranial metastasis in a dog.
J Vet Med Sci
; 2007 Jan;69(1):91-3
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[Title]
Pancreatic
acinar cell carcinoma
with intracranial metastasis in a dog.
This report concerns a case of
pancreatic
carcinoma
with widespread metastases to many organs including intracranial metastasis.
Based on gross and microscopic examination, the primary tumor cells were located in the left lobe of the
pancreas
and widespread metastasis was found into various organs, including the brain, lungs, liver, kidneys, tonsils, serosal surface of the esophagus, and submandibular, pulmonary hilar, mediastinal, and mesenteric lymph nodes.
This case indicates that
pancreatic adenocarcinoma
should be included in the differential
diagnosis
list when cervical neck masses are detected.
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(PMID = 17283409.001).
[ISSN]
0916-7250
[Journal-full-title]
The Journal of veterinary medical science
[ISO-abbreviation]
J. Vet. Med. Sci.
[Language]
ENG
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
59.
Kitagami H, Kondo S, Hirano S, Kawakami H, Egawa S, Tanaka M:
Acinar cell carcinoma of the pancreas: clinical analysis of 115 patients from Pancreatic Cancer Registry of Japan Pancreas Society.
Pancreas
; 2007 Jul;35(1):42-6
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[Title]
Acinar cell carcinoma of
the
pancreas
: clinical analysis of 115 patients from
Pancreatic Cancer
Registry of Japan
Pancreas
Society.
OBJECTIVES:
Acinar cell carcinoma
(ACC) of the
pancreas
is a rare tumor, and many aspects remain unclear because no large-scale clinical studies have been conducted.
METHODS: The present study investigated the clinical characteristics, treatment, and therapeutic outcomes of 115 patients registered in
the Pancreatic Cancer
Registry of the Japan
Pancreas
Society, and therapeutic plans were reviewed.
CONCLUSIONS: Confirming
the diagnosis
of ACC preoperatively is difficult, but this
diagnosis
should be kept in mind while planning surgery for ordinary
pancreatic cancer
.
Once
the diagnosis
has been confirmed, a possibility of surgical resection should be pursued to achieve better prognosis.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ mortality.
Pancreatic
Neoplasms / mortality. Registries / statistics & numerical data
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(PMID = 17575544.001).
[ISSN]
1536-4828
[Journal-full-title]
Pancreas
[ISO-abbreviation]
Pancreas
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
60.
Esposito I, Seiler C, Bergmann F, Kleeff J, Friess H, Schirmacher P:
Hypothetical progression model of pancreatic cancer with origin in the centroacinar-acinar compartment.
Pancreas
; 2007 Oct;35(3):212-7
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[Title]
Hypothetical progression model of
pancreatic cancer
with origin in the centroacinar-
acinar
compartment.
OBJECTIVES: Based mainly on animal models, 2 lesions have been suggested as possible precursors of
pancreatic
ductal
adenocarcinoma
(PDAC):
pancreatic
intraepithelial neoplasia (PanIN) and tubular complexes (TCs).
The aim of the study was to find support for either of the 2 models through the analysis of a large panel of human
pancreatic
tissues.
In 50% to 70% of the cases with TC and associated PanIN, a transitional zone
of acinar
-ductular transformation with mucinous differentiation of the ductular epithelium was identified.
Expression
of acinar
and centroacinar markers was detected in TC, in the ductular structures of the transitional zones, as well as within the epithelium of mature PanINs.
A progression model that originates in the centroacinar-
acinar
compartment and ends with the development of PanIN lesions is suggested.
[MeSH-major]
Carcinoma
,
Pancreatic
Ductal / pathology.
Pancreatic
Diseases / pathology.
Pancreatic
Neoplasms / pathology. Precancerous Conditions / pathology
[MeSH-minor]
Animals.
Carcinoma
in Situ / pathology.
Cell
Differentiation.
Cell
Transformation, Neoplastic. Cystadenoma, Serous / pathology. Disease Progression. Humans. Mice. Mice, Transgenic. Models, Animal. Models, Biological. Pancreatitis, Chronic / pathology. Rats. Species Specificity
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(PMID = 17895840.001).
[ISSN]
1536-4828
[Journal-full-title]
Pancreas
[ISO-abbreviation]
Pancreas
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
United States
61.
Seki Y, Okusaka T, Ikeda M, Morizane C, Ueno H:
Four cases of pancreatic acinar cell carcinoma treated with gemcitabine or S-1 as a single agent.
Jpn J Clin Oncol
; 2009 Nov;39(11):751-5
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[Title]
Four cases of
pancreatic
acinar cell carcinoma
treated with gemcitabine or S-1
as a
single agent.
Pancreatic
acinar cell carcinoma
(ACC) is a comparatively rare tumor and account for approximately 1% of all cases of
pancreatic cancer
.
There are no established treatments for unresectable
pancreatic
ACC.
Prospective clinical trials are necessary to confirm the effectiveness of fluoropyrimidine for the treatment of
pancreatic
ACC.
[MeSH-major]
Antimetabolites, Antineoplastic / therapeutic use.
Carcinoma
,
Acinar Cell
/ drug therapy. Deoxycytidine / analogs & derivatives. Oxonic Acid / therapeutic use.
Pancreatic
Neoplasms / drug therapy. Tegafur / therapeutic use
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(PMID = 19666905.001).
[ISSN]
1465-3621
[Journal-full-title]
Japanese journal of clinical oncology
[ISO-abbreviation]
Jpn. J. Clin. Oncol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0W860991D6 / Deoxycytidine; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; B76N6SBZ8R / gemcitabine
62.
Logsdon CD, Ji B:
Ras activity in acinar cells links chronic pancreatitis and pancreatic cancer.
Clin Gastroenterol Hepatol
; 2009 Nov;7(11 Suppl):S40-3
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[Title]
Ras activity in
acinar
cells links chronic pancreatitis and
pancreatic cancer
.
The relationship between chronic pancreatitis (CP) and
pancreatic
ductal
adenocarcinoma
(PDAC) is unclear.
However, we have recently found that excessive activity within the Ras signaling pathway can lead to
acinar cell
death or metaplasia and is associated with the development of fibrosis resembling CP and the development of PDAC from
acinar
cells through the full complement of preneoplastic (
pancreatic
intraepithelial neoplasia) lesions.
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(PMID = 19896097.001).
[ISSN]
1542-7714
[Journal-full-title]
Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association
[ISO-abbreviation]
Clin. Gastroenterol. Hepatol.
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / DK052067-11; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIDDK NIH HHS / DK / R21 DK068414; United States / NCI NIH HHS / CA / CA16672; United States / NIDDK NIH HHS / DK / R01 DK052067; United States / NIDDK NIH HHS / DK / R01 DK052067-11; United States / NIDDK NIH HHS / DK / 5R21DK068414; United States / NCI NIH HHS / CA / P20 CA101936; United States / NIAAA NIH HHS / AA / R01 AA020822; United States / NIDDK NIH HHS / DK / DK052067
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
46
[Other-IDs]
NLM/ NIHMS268542; NLM/ PMC3050544
63.
Martin SK, Agarwal G, Lynch GR:
Subcutaneous fat necrosis as the presenting feature of a pancreatic carcinoma: the challenge of differentiating endocrine and acinar pancreatic neoplasms.
Pancreas
; 2009 Mar;38(2):219-22
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[Title]
Subcutaneous fat necrosis as the presenting feature of
a pancreatic
carcinoma
: the challenge of differentiating endocrine and
acinar
pancreatic
neoplasms.
The association between
pancreatic
panniculitis and
pancreatic
disease is well described, but differentiation among the neoplastic causes of the syndrome remains difficult due to substantial overlap in histological and immunohistochemical features.
We report a case of subcutaneous fat necrosis as the presenting feature in a 61-year-old man with metastatic
carcinoma of
pancreatic
origin.
Previous pathological evaluation of the patient's liver biopsy led to an initial
diagnosis
of
adenocarcinoma
of unknown primary site.
One month later, the patient presented with
pancreatic
panniculitis, prompting further investigation.
Immunohistochemistry was consistent with neuroendocrine differentiation, but the patient rapidly decompensated and died before the evaluation was complete, leaving the definitive
diagnosis
in question.
In our review of the published reports of tumor types associated with
pancreatic
panniculitis, we found that immunohistochemical staining and electron microscopy can and should be used in conjunction with clinical correlation to accurately differentiate neuroendocrine tumors from carcinomas with
acinar cell
features.
Accurate
diagnosis
of these tumors is necessary to determine prognosis and define appropriate therapy.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology. Fat Necrosis / pathology. Neuroendocrine Tumors / pathology.
Pancreatic
Neoplasms / pathology. Panniculitis / pathology. Skin / pathology
[MeSH-minor]
Diagnosis
, Differential. Humans. Immunohistochemistry. Male. Middle Aged
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(PMID = 19238022.001).
[ISSN]
1536-4828
[Journal-full-title]
Pancreas
[ISO-abbreviation]
Pancreas
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
64.
Roldo C, Missiaglia E, Hagan JP, Falconi M, Capelli P, Bersani S, Calin GA, Volinia S, Liu CG, Scarpa A, Croce CM:
MicroRNA expression abnormalities in pancreatic endocrine and acinar tumors are associated with distinctive pathologic features and clinical behavior.
J Clin Oncol
; 2006 Oct 10;24(29):4677-84
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[Title]
MicroRNA expression abnormalities in
pancreatic
endocrine and
acinar
tumors are associated with distinctive pathologic features and clinical behavior.
PURPOSE: We investigated the global microRNA expression patterns in normal
pancreas
,
pancreatic
endocrine tumors and
acinar
carcinomas to evaluate their involvement in transformation and malignant progression of these tumor types.
MATERIALS AND METHODS: Using a custom microarray, we studied the global microRNA expression in 12 nontumor
pancreas
and 44
pancreatic
primary tumors, including 12 insulinomas, 28 nonfunctioning endocrine tumors, and four
acinar
carcinomas.
RESULTS: Our data showed that a common pattern of microRNA expression distinguishes any tumor type from normal
pancreas
, suggesting that this set of microRNAs might be involved in
pancreatic
tumorigenesis; the expression of miR-103 and miR-107, associated with lack of expression of miR-155, discriminates tumors from normal; a set of 10 microRNAs distinguishes endocrine from
acinar
tumors and is possibly associated with either normal endocrine differentiation or endocrine tumorigenesis; miR-204 is primarily expressed in insulinomas and correlates with immunohistochemical expression of insulin; and the overexpression of miR-21 is strongly associated with both a high Ki67 proliferation index and presence of liver metastasis.
CONCLUSION: These results suggest that alteration in microRNA expression is related to endocrine and
acinar
neoplastic transformation and progression of malignancy, and might prove useful in distinguishing tumors with different clinical behavior.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ genetics.
Carcinoma
,
Acinar Cell
/ pathology. Insulinoma / genetics. Insulinoma / pathology. MicroRNAs / metabolism.
Pancreatic
Neoplasms / genetics.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Cell
Transformation, Neoplastic. Gene Expression Profiling. Humans. Liver Neoplasms / secondary.
Pancreas
/ metabolism. Prognosis. Survival
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(PMID = 16966691.001).
[ISSN]
1527-7755
[Journal-full-title]
Journal of clinical oncology : official journal of the American Society of Clinical Oncology
[ISO-abbreviation]
J. Clin. Oncol.
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / P01CA76259; United States / NCI NIH HHS / CA / P01CA81534
[Publication-type]
Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MicroRNAs
65.
Sipos B, Klöppel G:
[Acinar cell carcinomas and pancreatoblastomas: related but not the same].
Pathologe
; 2005 Feb;26(1):37-40
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[Title]
[
Acinar cell
carcinomas and pancreatoblastomas: related but not the same].
Acinar cell
carcinomas and pancreatoblastomas are malignant tumors of the
pancreas
, showing predominantly
acinar
differentiation characterized by the immunohistochemical expression of
pancreatic
enzymes.
Histologically, they usually display
acinar
and/or solid patterns, but may occasionally also exhibit cystic structures.
Acinar cell
carcinomas predominantly occur in adults, pancreatoblastomas in children.
Pancreatoblastomas, in contrast to
acinar cell
carcinomas, are potentially curable.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Cell
Differentiation.
Diagnosis
, Differential. Female. Humans. Male. Prognosis. Sex Characteristics
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[Cites]
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]
(PMID = 15614488.001).
[ISSN]
0172-8113
[Journal-full-title]
Der Pathologe
[ISO-abbreviation]
Pathologe
[Language]
ger
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Germany
66.
Schmidt CM, Matos JM, Bentrem DJ, Talamonti MS, Lillemoe KD, Bilimoria KY:
Acinar cell carcinoma of the pancreas in the United States: prognostic factors and comparison to ductal adenocarcinoma.
J Gastrointest Surg
; 2008 Dec;12(12):2078-86
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[Title]
Acinar cell carcinoma of
the
pancreas
in the United States: prognostic factors and comparison to ductal
adenocarcinoma
.
INTRODUCTION:
Pancreatic
acinar cell carcinoma
(ACC) is a rare tumor with poorly defined prognosis.
OBJECTIVE: Our objective was to compare a large population of patients with ACC to
pancreatic
ductal
cell
adenocarcinoma
(DCC) in order to determine distinguishing characteristics and to assess survival.
METHODS: Patients were identified from the National
Cancer
Database.
Patients with ACC were more likely to be male, white, and have larger tumor size, no nodal involvement, or
pancreatic
tail tumors.
Aggressive surgical resection with negative margins is associated with long-term survival in these more favorable
pancreatic
cancers.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ epidemiology.
Carcinoma
,
Acinar Cell
/ surgery.
Pancreatic
Neoplasms / epidemiology.
Pancreatic
Neoplasms / surgery
[MeSH-minor]
Aged.
Carcinoma
,
Pancreatic
Ductal / epidemiology.
Carcinoma
,
Pancreatic
Ductal / pathology.
Carcinoma
,
Pancreatic
Ductal / surgery. Chi-Square Distribution. Female. Humans. Lymphatic Metastasis. Male. Middle Aged. Pancreatectomy. Prognosis. ROC Curve. Regression Analysis. Statistics, Nonparametric. Survival Rate. Treatment Outcome. United States / epidemiology
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[Cites]
Br Med J. 1970 Jun 20;2(5711):708-9
[
5429656.001
]
[Cites]
J Comput Assist Tomogr. 2004 Mar-Apr;28(2):180-6
[
15091120.001
]
[Cites]
Ann Surg Oncol. 2008 Mar;15(3):683-90
[
18183467.001
]
[Cites]
J Clin Oncol. 2002 Dec 15;20(24):4673-8
[
12488412.001
]
[Cites]
J Gastrointest Surg. 2008 Jun;12(6):1061-7
[
17957440.001
]
[Cites]
Cancer. 2007 Aug 15;110(4):738-44
[
17580363.001
]
[Cites]
Pancreas. 2007 Jul;35(1):42-6
[
17575544.001
]
[Cites]
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[
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]
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]
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[
19495891.001
]
[Cites]
Am J Surg Pathol. 1992 Sep;16(9):815-37
[
1384374.001
]
(PMID = 18836784.001).
[ISSN]
1873-4626
[Journal-full-title]
Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
[ISO-abbreviation]
J. Gastrointest. Surg.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
67.
Scoazec JY:
[Case 8: Liver metastasis of pancreatic acinar cell carcinoma].
Ann Pathol
; 2007 Apr;27(2):120-7
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[Title]
[Case 8: Liver metastasis of
pancreatic
acinar cell carcinoma
].
[MeSH-major]
Carcinoma
,
Acinar Cell
/ secondary. Liver Neoplasms / secondary.
Pancreatic
Neoplasms / pathology
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.
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(PMID = 17909469.001).
[ISSN]
0242-6498
[Journal-full-title]
Annales de pathologie
[ISO-abbreviation]
Ann Pathol
[Language]
fre
[Publication-type]
Case Reports; Journal Article
[Publication-country]
France
68.
Shah S, Mortele KJ:
Uncommon solid pancreatic neoplasms: ultrasound, computed tomography, and magnetic resonance imaging features.
Semin Ultrasound CT MR
; 2007 Oct;28(5):357-70
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[Title]
Uncommon solid
pancreatic
neoplasms: ultrasound, computed tomography, and magnetic resonance imaging features.
This article reviews the ultrasound, computed tomography, and magnetic resonance imaging features of rare solid tumors of the
pancreas
with attention to distinctive imaging appearances, which can help radiologists to discriminate between the different entities.
Various uncommon solid
pancreatic
neoplasms, including exocrine and endocrine epithelial tumors, mesenchymal tumors, and metastases, are reviewed, with emphasis on key differential points, including morphologic features and patterns of contrast enhancement.
[MeSH-major]
Pancreatic
Neoplasms /
diagnosis
[MeSH-minor]
Carcinoma
,
Acinar Cell
/
diagnosis
.
Carcinoma
,
Acinar Cell
/ pathology.
Carcinoma
, Giant
Cell
/
diagnosis
.
Carcinoma
, Giant
Cell
/ pathology. Contrast Media.
Diagnosis
, Differential. Endocrine Gland Neoplasms /
diagnosis
. Endocrine Gland Neoplasms / pathology. Humans. Lymphoma /
diagnosis
. Lymphoma / pathology. Magnetic Resonance Imaging. Neoplasm Metastasis. Neoplasm Staging. Neoplasms, Complex and Mixed /
diagnosis
. Neoplasms, Complex and Mixed / pathology. Tomography, X-Ray Computed
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(PMID = 17970552.001).
[ISSN]
0887-2171
[Journal-full-title]
Seminars in ultrasound, CT, and MR
[ISO-abbreviation]
Semin. Ultrasound CT MR
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Contrast Media
[Number-of-references]
41
69.
Salla C, Chatzipantelis P, Konstantinou P, Karoumpalis I, Pantazopoulou A, Dappola V:
Endoscopic ultrasound-guided fine-needle aspiration cytology diagnosis of solid pseudopapillary tumor of the pancreas: a case report and literature review.
World J Gastroenterol
; 2007 Oct 14;13(38):5158-63
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[Title]
Endoscopic ultrasound-guided fine-needle aspiration cytology
diagnosis
of solid pseudopapillary tumor of the
pancreas
: a case report and literature review.
We describe the clinical, imaging and cytopathological features of solid pseudopapillary tumor of the
pancreas
(SPTP) diagnosed by endoscopic ultrasound-guided (EUS-guided) fine-needle aspiration (FNA).
Computed tomography (CT) analysis revealed a mass of
the pancreatic
tail with solid and cystic consistency.
EUS confirmed the mass, both in body and tail of the
pancreas
, with distinct borders, which caused dilation of the peripheral part of
the pancreatic
duct (major diameter 3.7 mm).
Biopsy confirmed the above cytologic
diagnosis
.
EUS-guided FNA
diagnosis
of SPTP is accurate.
EUS findings, cytomorphologic features and immunostains
of cell
block help distinguish SPTP from
pancreatic
endocrine tumors,
acinar cell carcinoma
and papillary mucinous
carcinoma
.
[MeSH-major]
Carcinoma
, Papillary /
diagnosis
.
Carcinoma
, Papillary / pathology.
Pancreatic
Neoplasms /
diagnosis
.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Adenocarcinoma
, Mucinous /
diagnosis
.
Adenocarcinoma
, Mucinous / pathology. Adolescent. Biopsy, Fine-Needle / methods.
Carcinoma
,
Acinar Cell
/
diagnosis
.
Carcinoma
,
Acinar Cell
/ pathology.
Diagnosis
, Differential. Endosonography / methods. Female. Humans.
Pancreas
/ pathology.
Pancreas
/ ultrasonography
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(PMID = 17876886.001).
[ISSN]
1007-9327
[Journal-full-title]
World journal of gastroenterology
[ISO-abbreviation]
World J. Gastroenterol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
China
[Number-of-references]
59
[Other-IDs]
NLM/ PMC4434650
70.
Vakiani E, Young RH, Carcangiu ML, Klimstra DS:
Acinar cell carcinoma of the pancreas metastatic to the ovary: a report of 4 cases.
Am J Surg Pathol
; 2008 Oct;32(10):1540-5
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[Title]
Acinar cell carcinoma of
the
pancreas
metastatic to the ovary: a report of 4 cases.
We report 4 cases
of acinar cell carcinoma
of the
pancreas
, 3 presenting as metastases in the ovary, the first report of this circumstance, which may pose a broad differential
diagnosis
and caused significant diagnostic difficulty in all the cases.
In 3 cases, the ovarian tumors were detected before
the pancreatic
tumor; in 1 case, a large abdominal mass and ovarian tumors were discovered synchronously.
Two cases had a predominant
acinar
growth pattern of cells with brightly eosinophilic, granular cytoplasm.
The main differential diagnostic consideration was well-differentiated neuroendocrine neoplasm (carcinoid tumor); positive immunostaining with antibodies against chymotrypsin and trypsin and negative immunostaining with antibodies against synaptophysin and chromogranin helped exclude this
diagnosis
.
We observed focal alpha-inhibin immunostaining in 2 cases, which may represent a potential diagnostic pitfall,
as a
Sertoli
cell
tumor or unusual granulosa
cell
tumor may also enter the differential
diagnosis
.
Inclusion of antibodies against
the pancreatic
enzymes chymotrypsin and trypsin in the immunohistochemical panel is critical in establishing the correct
diagnosis
and should be considered when evaluating ovarian tumors with architectural (mainly
acinar
) and cytologic (granular eosinophilic cytoplasm) characteristics that should bring a metastatic
acinar cell carcinoma
into consideration.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ secondary. Ovarian Neoplasms / secondary.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Adult. Aged. Aged, 80 and over.
Diagnosis
, Differential. Female. Humans. Middle Aged
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(PMID = 18724247.001).
[ISSN]
1532-0979
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
71.
Díaz Sánchez A, Ponferrada Díaz A, Senosiain Labiano M, Huerta Madrigal A:
[Upper digestive hemorrhage as the first manifestation of acinar cell carcinoma of the pancreas].
Gastroenterol Hepatol
; 2006 Jun-Jul;29(6):380
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[Title]
[Upper digestive hemorrhage as the first manifestation
of acinar cell carcinoma
of the
pancreas
].
[Transliterated title]
Hemorragia digestiva alta como presentación
de
un
carcinoma acinar
pancreático.
[MeSH-major]
Carcinoma
,
Acinar Cell
/
diagnosis
. Gastrointestinal Hemorrhage / etiology.
Pancreatic
Neoplasms /
diagnosis
[MeSH-minor]
Aged. Duodenal Neoplasms /
diagnosis
. Female. Humans. Neoplasm Invasiveness
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.
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(PMID = 16790192.001).
[ISSN]
0210-5705
[Journal-full-title]
Gastroenterología y hepatología
[ISO-abbreviation]
Gastroenterol Hepatol
[Language]
spa
[Publication-type]
Case Reports; Letter
[Publication-country]
Spain
72.
Svrcek M, Lesurtel M, Lewin M, Afchain P, Fabre M, Scoazec JY, Parc R, Fléjou JF:
[Acinar cell carcinoma of the pancreas with predominant intraductal growth: report of a case].
Gastroenterol Clin Biol
; 2007 May;31(5):543-6
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[Title]
[
Acinar cell carcinoma of
the
pancreas
with predominant intraductal growth: report of a case].
[Transliterated title]
Carcinome
à
cellules acineuses du
pancréas,
de
développement essentiellement intracanalaire: à propos d'un cas.
Acinar cell carcinoma
(ACC) of the
pancreas
accounts for approximately 1% of all exocrine
pancreatic
tumours.
Abdominal computed tomography showed a hypodense, well-demarcated, heterogeneous lesion, in the head of the
pancreas
, measuring 4.2 cm in diameter.
There was a marked dilatation of the main
pancreatic
duct upstream, with tumour spreading within this duct.
The diagnosis
of ACC was made on the fine needle aspiration cytology performed during endoscopic ultrasound examination.
On the pancreaticoduodenectomy specimen, the dilated main
pancreatic
duct (2.5 cm in diameter) was filled by an exophytic tumour.
Histological examination showed an ACC, with predominant intraductal growth (main and accessory
pancreatic
ducts), with
pancreatic
parenchymal and duodenal invasion.
[MeSH-major]
Carcinoma
,
Acinar Cell
/
diagnosis
.
Pancreatic
Ducts / pathology.
Pancreatic
Neoplasms /
diagnosis
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(PMID = 17541347.001).
[ISSN]
0399-8320
[Journal-full-title]
Gastroentérologie clinique et biologique
[ISO-abbreviation]
Gastroenterol. Clin. Biol.
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
73.
Machado MC, Machado MA, Perini MV, Herman P, Jukemura J, Leite KR, Bacchella T:
Acinar cell carcinoma of the pancreas: is the absence of neuroendocrine component related to a more malignant behavior?
Hepatogastroenterology
; 2008 Mar-Apr;55(82-83):708-10
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[Title]
Acinar cell carcinoma of
the
pancreas
: is the absence of neuroendocrine component related to a more malignant behavior?
BACKGROUND/AIMS:
Acinar cell
carcinomas are uncommon malignant tumors of the
pancreas
, accounting for 1-2% of all the cases of exocrine
pancreatic
tumor.
Some authors have estimated
acinar cell
tumors to be as aggressive as ductal
adenocarcinoma
of the
pancreas
whereas other series showed
acinar cell
tumors to have a favorable clinical outcome.
METHODOLOGY: With the aim to evaluate the possible relationship between the presence of neuroendocrine differentiation and behavior of these tumors, the authors reviewed all patients presenting
acinar cell carcinoma of
the
pancreas
in the last 5 years with emphasis in the immunohistochemical evaluation.
This data suggests that this tumor is less aggressive than ductal
adenocarcinoma
and even with nodal involvement, long-term survival after complete resection can be achieved.
Due to the rarity of this
pancreatic
tumor, this relationship remains to be confirmed with a multicentric study including a larger number of patients.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology.
Pancreatic
Neoplasms / pathology
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(PMID = 18613439.001).
[ISSN]
0172-6390
[Journal-full-title]
Hepato-gastroenterology
[ISO-abbreviation]
Hepatogastroenterology
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
74.
Yoshida T, Shiraki N, Baba H, Goto M, Fujiwara S, Kume K, Kume S:
Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreas.
Genes Cells
; 2008 Jul;13(7):667-78
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[Title]
Expression patterns of epiplakin1 in
pancreas
,
pancreatic cancer
and regenerating
pancreas
.
Here we analyzed the expression patterns of Eppk1 in the developing and adult
pancreas
in the mice.
In the embryonic
pancreas
, Eppk1+/Pdx1+ and Eppk1+/Sox9+
pancreatic
progenitor cells were observed in early
pancreatic
epithelium.
In the adult
pancreas
, Eppk1 is expressed in centroacinar cells (CACs) and in duct cells.
Eppk1 is observed in
pancreatic
intraepithelial neoplasia (PanIN), previously identified
as pancreatic
ductal
adenocarcinoma
(PDAC) precursor lesions.
In addition, the expansion of Eppk1-positive cells occurs in a caerulein-induced acute pancreatitis, an
acinar cell
regeneration model.
These results suggest that Eppk1 serves
as a
useful marker for detecting
pancreatic
progenitor cells in developing and regenerating
pancreas
.
[MeSH-major]
Autoantigens / biosynthesis. Autoantigens / genetics. Gene Expression Regulation / physiology.
Pancreas
/ metabolism.
Pancreatic
Neoplasms / metabolism. Regeneration / physiology
[MeSH-minor]
Animals. Biomarkers / metabolism.
Carcinoma
,
Pancreatic
Ductal / metabolism.
Carcinoma
,
Pancreatic
Ductal / pathology. Gene Expression Regulation, Neoplastic / physiology. Mice. Mice, Knockout. Mice, Transgenic. Stem Cells / cytology. Stem Cells / metabolism
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.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
SciCrunch.
The Antibody Registry: Reagent: Antibodies
.
The Lens.
Cited by Patents in
.
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(PMID = 18498355.001).
[ISSN]
1365-2443
[Journal-full-title]
Genes to cells : devoted to molecular & cellular mechanisms
[ISO-abbreviation]
Genes Cells
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Autoantigens; 0 / Biomarkers; 0 / epiplakin
75.
Treiber M, Schulz HU, Landt O, Drenth JP, Castellani C, Real FX, Akar N, Ammann RW, Bargetzi M, Bhatia E, Demaine AG, Battagia C, Kingsnorth A, O'Reilly D, Truninger K, Koudova M, Spicak J, Cerny M, Menzel HJ, Moral P, Pignatti PF, Romanelli MG, Rickards O, De Stefano GF, Zarnescu NO, Choudhuri G, Sikora SS, Jansen JB, Weiss FU, Pietschmann M, Teich N, Gress TM, Ockenga J, Schmidt H, Kage A, Halangk J, Rosendahl J, Groneberg DA, Nickel R, Witt H:
Keratin 8 sequence variants in patients with pancreatitis and pancreatic cancer.
J Mol Med (Berl)
; 2006 Dec;84(12):1015-22
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[Title]
Keratin 8 sequence variants in patients with pancreatitis and
pancreatic cancer
.
Transgenic mice over-expressing human KRT8 display
pancreatic
mononuclear infiltration, interstitial fibrosis and dysplasia
of acinar
cells resulting in exocrine
pancreatic
insufficiency.
This prompted us to investigate KRT8 polymorphisms in patients with
pancreatic
disorders.
The KRT8 Y54H and G62C polymorphisms were assessed in a cohort of patients with acute and chronic pancreatitis of various aetiologies or
pancreatic cancer
originating from Austria (n=16), the Czech Republic (n=90), Germany (n=1698), Great Britain (n=36), India (n=60), Italy (n=143), the Netherlands (n=128), Romania (n=3), Spain (n=133), and Switzerland (n=129).
The frequency of G62C did not differ between patients with acute or chronic pancreatitis,
pancreatic adenocarcinoma
and control individuals.
Our data suggest that the KRT8 alterations, Y54H and G62C, do not predispose patients to the development of pancreatitis or
pancreatic cancer
.
[MeSH-major]
Genetic Variation. Keratin-8 / genetics.
Pancreatic
Neoplasms / genetics. Pancreatitis / genetics. Pancreatitis, Alcoholic / genetics
[MeSH-minor]
Acute Disease.
Adenocarcinoma
/ genetics.
Adenocarcinoma
/ pathology. Adult. African Continental Ancestry Group / genetics. Aged. Alleles. Asian Continental Ancestry Group / genetics.
Carcinoma
,
Pancreatic
Ductal / genetics.
Carcinoma
,
Pancreatic
Ductal / pathology. Case-Control Studies. Chronic Disease. Cohort Studies. European Continental Ancestry Group / genetics. Female. Gene Frequency. Geography. Heterozygote. Humans. Male. Middle Aged. Polymorphism, Genetic. Retrospective Studies
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[Cites]
Am J Physiol Gastrointest Liver Physiol. 2000 Dec;279(6):G1343-54
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]
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N Engl J Med. 1998 Sep 3;339(10):645-52
[
9725921.001
]
(PMID = 17039343.001).
[ISSN]
0946-2716
[Journal-full-title]
Journal of molecular medicine (Berlin, Germany)
[ISO-abbreviation]
J. Mol. Med.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Germany
[Chemical-registry-number]
0 / KRT8 protein, human; 0 / Keratin-8
76.
National Toxicology Program:
NTP technical report on the toxicology and carcinogenesis studies of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (CAS No. 1746-01-6) in female Harlan Sprague-Dawley rats (Gavage Studies).
Natl Toxicol Program Tech Rep Ser
; 2006 Apr;(521):4-232
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Since human exposure to DLCs always involves a complex mixture, the toxic equivalency factor (TEF) methodology has been developed
as a
mathematical tool to assess the health risk posed by complex mixtures of these compounds.
The toxic equivalency of DLCs was nominated for evaluation because of the widespread human exposure to DLCs and the lack of data on the adequacy of the TEF methodology for predicting relative potency for
cancer
risk.
TCDD (dioxin) was selected for study by the National Toxicology Program
as a
part of the dioxin TEF evaluation to assess
the cancer
risk posed by complex mixtures of polychlorinated dibenzodioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and PCBs.
HEPATIC
CELL
PROLIFERATION DATA: To evaluate hepatocyte replication, analysis of labeling of replicating hepatocytes with 5-bromo-2'-deoxyuridine was conducted at the 14-, 31-, and 53-week interim evaluations.
At 2 years, there was a significant increase in toxic hepatopathy characterized by increased incidences of numerous nonneoplastic liver lesions including hepatocyte hypertrophy, multinucleated hepatocytes, altered hepatocellular foci, inflammation, pigmentation, diffuse fatty change, necrosis, portal fibrosis, oval
cell
hyperplasia, bile duct hyperplasia, bile duct cysts, cholangiofibrosis, and nodular hyperplasia At 2 years, the incidence of hepatocellular adenoma was significantly increased in the 100 ng/kg core study group.
The incidence of gingival squamous
cell carcinoma
of the oral mucosa was significantly increased in the 100 ng/kg core study group at 2 years and was accompanied by an increased incidence of gingival squamous hyperplasia.
At 2 years, the incidence of squamous
cell carcinoma
of the uterus in the 46 ng/kg group was significantly increased, and there were two squamous
cell
carcinomas in the 100 ng/kg stop-exposure group.
At 2 years, one
acinar
adenoma and two
acinar cell
carcinomas of the
pancreas
were seen in the 100 ng/kg core study group; one
acinar carcinoma
was seen in the 100 ng/kg stop-exposure group.
The incidences
of acinar cell
adenoma or
carcinoma
(combined) exceeded the historical vehicle control range.
Nonneoplastic effects in the lung included
acinar
cytoplasmic vacuolization, chronic active inflammation,
acinar
atrophy, and arterial chronic active inflammation. (ABSTRACT TRUNCATED)
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(PMID = 16835633.001).
[ISSN]
0888-8051
[Journal-full-title]
National Toxicology Program technical report series
[ISO-abbreviation]
Natl Toxicol Program Tech Rep Ser
[Language]
eng
[Publication-type]
Journal Article; Technical Report
[Publication-country]
United States
[Chemical-registry-number]
0 / Carcinogens; DO80M48B6O / Tetrachlorodibenzodioxin
77.
Zhang N, Lyons S, Lim E, Lassota P:
A spontaneous acinar cell carcinoma model for monitoring progression of pancreatic lesions and response to treatment through noninvasive bioluminescence imaging.
Clin Cancer Res
; 2009 Aug 1;15(15):4915-24
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[Title]
A spontaneous
acinar cell carcinoma
model for monitoring progression of
pancreatic
lesions and response to treatment through noninvasive bioluminescence imaging.
PURPOSE: We have generated an EL1-luc/TAg transgenic mouse model that develops spontaneous and bioluminescent
acinar cell
carcinomas.
RESULTS: EL1-luc/TAg transgenic mice showed
pancreas
-specific bioluminescence signal before tumor progression and produced increasing light emission from the onset of
the pancreatic
acinar cell
carcinomas.
Progression of the primary
acinar cell carcinoma
was accompanied by emergence of metastatic lesions in the abdominal organs, including liver and gastrointestinal fat tissues.
CONCLUSIONS: The EL1-luc/TAg mouse provides a noninvasive approach for monitoring spontaneous
acinar cell carcinoma
development and comprises a convenient tool for the evaluation of novel therapeutics against
pancreatic
cancers.
[MeSH-major]
Antibiotics, Antineoplastic / metabolism.
Carcinoma
,
Acinar Cell
/ metabolism. Drug Monitoring.
Pancreas
/ pathology.
Pancreatic
Neoplasms / pathology
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gene/protein/disease-specific - KOMP Repository
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Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
SciCrunch.
Marmoset Gene list: Data: Gene Annotation
.
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(PMID = 19622581.001).
[ISSN]
1078-0432
[Journal-full-title]
Clinical cancer research : an official journal of the American Association for Cancer Research
[ISO-abbreviation]
Clin. Cancer Res.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Antibiotics, Antineoplastic; W36ZG6FT64 / Sirolimus
78.
Hashimoto M, Miki K, Kokudo N, Beck Y, Makuuchi M:
A long-term survivor of metastatic acinar cell carcinoma.
Pancreas
; 2007 Mar;34(2):271-2
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[Title]
A long-term survivor of metastatic
acinar cell carcinoma
.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ secondary. Liver Neoplasms / secondary.
Pancreatic
Neoplasms / pathology
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(PMID = 17312470.001).
[ISSN]
1536-4828
[Journal-full-title]
Pancreas
[ISO-abbreviation]
Pancreas
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
United States
79.
Kawakami H, Kuwatani M, Hirano S, Kondo S, Nakanishi Y, Itoh T, Asaka M:
Pancreatic endocrine tumors with intraductal growth into the main pancreatic duct and tumor thrombus within the portal vein: a case report and review of the literature.
Intern Med
; 2007;46(6):273-7
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[Title]
Pancreatic
endocrine tumors with intraductal growth into the main
pancreatic
duct and tumor thrombus within the portal vein: a case report and review of the literature.
Pancreatic
endocrine tumors are rare tumors classified into "functioning" and "nonfunctioning" tumors.
Various imaging studies demonstrated a mass in the head of the
pancreas
with intraductal growth into the main
pancreatic
duct and an intraportal mass.
Histopathological examination revealed that it was nonfunctioning endocrine
carcinoma of
the
pancreas
.
This is the first reported case of
a pancreatic
endocrine tumor with intraductal growth into the main
pancreatic
duct and tumor thrombus within the portal vein.
[MeSH-major]
Pancreatic
Neoplasms / complications.
Pancreatic
Neoplasms /
diagnosis
. Portal Vein. Venous Thrombosis / etiology
[MeSH-minor]
Adult. Aged. Biomarkers, Tumor / blood.
Carcinoma
,
Acinar Cell
/
diagnosis
.
Carcinoma
,
Pancreatic
Ductal /
diagnosis
.
Diagnosis
, Differential. Endosonography. Fatal Outcome. Female. Humans. Male. Middle Aged. Pancreaticoduodenectomy
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(PMID = 17379993.001).
[ISSN]
1349-7235
[Journal-full-title]
Internal medicine (Tokyo, Japan)
[ISO-abbreviation]
Intern. Med.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Biomarkers, Tumor
[Number-of-references]
15
80.
Peng HQ, Darwin P, Papadimitriou JC, Drachenberg CB:
Liver metastases of pancreatic acinar cell carcinoma with marked nuclear atypia and pleomorphism diagnosed by EUS FNA cytology: a case report with emphasis on FNA cytological findings.
Cytojournal
; 2006;3:29
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[Title]
Liver metastases of
pancreatic
acinar cell carcinoma
with marked nuclear atypia and pleomorphism diagnosed by EUS FNA cytology: a case report with emphasis on FNA cytological findings.
BACKGROUND:
Acinar cell carcinoma of
the
pancreas
is a rare neoplasm.
Unlike ductal adenocarcinomas, endocrine tumors, and solid pseudopapillary tumors of the
pancreas
with their characteristic FNA cytological features,
acinar cell
carcinomas pose a particular diagnostic challenge by sharing many cytomorphologic features with endocrine tumors of the
pancreas
.
Computed tomography revealed a 7.8 x 7.3 cm irregular, partially cystic mass in the body and tail of the
pancreas
, and two lesions in the liver compatible with metastases.
FNA cytology revealed abundant, loosely cohesive clusters of malignant epithelial cells with vaguely
acinar
and trabecular formations.
A pancreatic
endocrine tumor was suspected initially, but
acinar cell carcinoma of
the
pancreas
was confirmed by immunohistochemistry, cytochemical and ultrastructural studies.
CONCLUSION: We describe a case of
pancreatic
acinar cell carcinoma
with unusual cytomorphologic features mimicking an endocrine tumor
of pancreas
, encountered in endoscopic ultrasound-guided fine needle aspiration of a metastatic liver mass and discuss the diagnostic approach for this unusual
pancreatic
tumor in fine needle aspiration cytology.
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[Cites]
Diagn Cytopathol. 2005 Aug;33(2):100-5
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[ISSN]
1742-6413
[Journal-full-title]
CytoJournal
[ISO-abbreviation]
Cytojournal
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Other-IDs]
NLM/ PMC1779360
81.
De La O JP, Emerson LL, Goodman JL, Froebe SC, Illum BE, Curtis AB, Murtaugh LC:
Notch and Kras reprogram pancreatic acinar cells to ductal intraepithelial neoplasia.
Proc Natl Acad Sci U S A
; 2008 Dec 2;105(48):18907-12
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[Title]
Notch and Kras reprogram
pancreatic
acinar
cells to ductal intraepithelial neoplasia.
Efforts to model
pancreatic cancer
in mice have focused on mimicking genetic changes found in the human disease, particularly the activating KRAS mutations that occur in
pancreatic
tumors and their putative precursors,
pancreatic
intraepithelial neoplasia (PanIN).
The basis for this selective response is unknown, and it is similarly unknown what
cell
types in the mature
pancreas
actually contribute to PanINs.
One clue comes from the fact that PanINs, unlike most cells in the adult
pancreas
, exhibit active Notch signaling.
We hypothesize that Notch, which inhibits differentiation in the embryonic
pancreas
, contributes to PanIN formation by abrogating the normal differentiation program of tumor-initiating cells.
Through conditional expression in the mouse
pancreas
, we find dramatic synergy between activated Notch and Kras in inducing PanIN formation.
Furthermore, we find that Kras activation in mature
acinar
cells induces PanIN lesions identical to those seen upon ubiquitous Kras activation, and that Notch promotes both initiation and dysplastic progression of these
acinar
-derived PanINs, albeit short of invasive
adenocarcinoma
.
At the cellular level, Notch/Kras coactivation promotes rapid reprogramming
of acinar
cells to a duct-like phenotype, providing an explanation for how a characteristically ductal tumor can arise from nonductal
acinar
cells.
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[Cites]
Genes Dev. 2001 Dec 15;15(24):3243-8
[
11751630.001
]
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Annu Rev Pathol. 2008;3:157-88
[
18039136.001
]
(PMID = 19028876.001).
[ISSN]
1091-6490
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R21-CA123066; United States / NCI NIH HHS / CA / P30-CA042014; United States / NICHD NIH HHS / HD / 5T32-HD07491; United States / NCI NIH HHS / CA / CA123066-02; United States / NCI NIH HHS / CA / R21 CA123066; United States / NCI NIH HHS / CA / R21 CA123066-02; United States / NICHD NIH HHS / HD / T32 HD007491; United States / NCI NIH HHS / CA / P30 CA042014
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Estrogen Antagonists; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Notch; 094ZI81Y45 / Tamoxifen; EC 3.6.5.2 / ras Proteins
82.
Khanna AK, Yadav SK, Dixit VK, Kumar M:
AgNOR count and subjective AgNOR pattern assessment (SAPA) score in carcinoma of the pancreatic head including periampullary tumors.
JOP
; 2005 Nov;6(6):575-80
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[Title]
AgNOR count and subjective AgNOR pattern assessment (SAPA) score in
carcinoma of
the pancreatic
head including periampullary tumors.
CONTEXT: Only a few studies are available in the literature regarding the AgNOR (argyrophilic nucleolar organizer region) count in
pancreatic adenocarcinoma
but studies on the SAPA (subjective AgNOR pattern assessment) score are completely lacking.
OBJECTIVE: We attempted to estimate the AgNOR count and the SAPA score in
carcinoma of
the pancreatic
head including periampullary tumors and to correlate them with other various clinico-histological parameters.
SETTING: Patients undergoing
pancreatic
resection at the University Hospital, Banaras Hindu University, Varanasi, India.
PATIENTS: Twenty-four cases
of carcinoma
of
the pancreatic
head including periampullary tumors.
In addition, on the resected specimen of the
pancreas
, the area which was normal was chosen and, in that normal tissue, the AgNOR was also studied.
RESULTS: The values of the AgNOR count and the SAPA score were significantly higher in cases of
pancreatic cancer
than in the healthy
pancreas
.
The AgNOR count was 1.6+/-0.1 in the healthy
pancreas
while it was 2.8+/-0.5 in cases of
pancreatic
carcinoma
(P<0.001).
The SAPA score was 5.6+/-0.2 in the healthy
pancreas
while it was 8.0+/-1.4 in
pancreatic
carcinoma
(P<0.001).
Periampullary tumors had a significantly lower (P<0.001) AgNOR count (2.7+/-0.06) and SAPA score (7.8+/-0.2) as compared to
carcinoma of
the head of the
pancreas
(AgNOR count 3.3+/-0.03 and SAPA score 9.2+/-0.7).
Well-differentiated carcinomas had significantly lower AgNOR counts as compared to other tumors except
acinar cell
carcinomas since
acinar cell
carcinomas are also well-differentiated tumors.
The SAPA score was also higher in moderately-differentiated tumors and the difference between moderately-differentiated tumor and other types of tumors was significant although there was no significant difference between cystadenocarcinomas and unclassified tumors, and between
acinar cell
carcinomas and well-differentiated tumors on SAPA scoring.
[MeSH-major]
Antigens, Nuclear. Nuclear Proteins.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Adult. Aged.
Cell
Count. Female. Humans. Male. Middle Aged. Pancreatectomy
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(PMID = 16286708.001).
[ISSN]
1590-8577
[Journal-full-title]
JOP : Journal of the pancreas
[ISO-abbreviation]
JOP
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Antigens, Nuclear; 0 / Nuclear Proteins; 0 / nucleolar organizer region associated proteins
83.
Chiaravalli AM, Finzi G, Bertolini V, La Rosa S, Capella C:
Colonic carcinoma with a pancreatic acinar cell differentiation. A case report.
Virchows Arch
; 2009 Dec;455(6):527-31
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[Title]
Colonic
carcinoma
with
a pancreatic
acinar cell
differentiation. A case report.
A case of a colonic
carcinoma
showing
a pancreatic
acinar cell
differentiation is described for the first time.
Histologically, tumour cells were organized in
acinar
structures resembling
pancreatic
acini and in solid nests and ribbons or diffusely infiltrated as poorly cohesive cells.
Immunohistochemically, both
acinar
and diffuse patterns of growth showed an intense staining for trypsin, chymotrypsin and BCL10 and a weaker immunoreactivity for lipase and carboxyl ester hydrolase.
No immunoreactivity was observed for cytokeratin 7, MUC1, MUC5AC,
pancreatic
amylase or PDX1.
There was no evidence of
a pancreatic
acinar cell carcinoma
or of heterotopic
pancreatic
tissue.
A colonic origin ought to be suspected when a metastatic
carcinoma of
unknown primary shows an
acinar
differentiation.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ pathology. Colonic Neoplasms / pathology.
Pancreatic
Neoplasms / pathology
[MeSH-minor]
Aged. CDX2 Transcription Factor.
Cell
Differentiation. Fatal Outcome. Female. Homeodomain Proteins / metabolism. Humans. Immunohistochemistry. Keratin-20 / metabolism. Lymphatic Metastasis. Tumor Suppressor Protein p53 / metabolism
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[Cites]
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[
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]
(PMID = 19908063.001).
[ISSN]
1432-2307
[Journal-full-title]
Virchows Archiv : an international journal of pathology
[ISO-abbreviation]
Virchows Arch.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / CDX2 Transcription Factor; 0 / CDX2 protein, human; 0 / Homeodomain Proteins; 0 / Keratin-20; 0 / Tumor Suppressor Protein p53
84.
Sanchez D, Mueller CM, Zenilman ME:
Pancreatic regenerating gene I and acinar cell differentiation: influence on cellular lineage.
Pancreas
; 2009 Jul;38(5):572-7
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[Title]
Pancreatic
regenerating gene I and
acinar cell
differentiation: influence on cellular lineage.
OBJECTIVES:
Pancreatic
regenerating gene I (reg I) has been implicated in cellular differentiation.
Acinar
cells can transdifferentiate into other
pancreatic
-derived cells, and we postulated that changes in intracellular levels of reg I would affect the state of differentiation.
Specifically, amylase mRNA and protein levels increased in SS cells, whereas AS cells showed increased
pancreatic
and duodenal homeobox 1 (Pdx1) and insulin mRNAs and cytokeratin protein.
CONCLUSIONS: These data demonstrate that in
acinar
cells, reg I overexpression is linked to
acinar cell
differentiation, whereas inhibition of reg I leads to beta
cell
and possibly ductal phenotype.
Reg I expression in
acinar
cells is important in maintaining
pancreatic
cell
lineage, and when decreased, cells can dedifferentiate and move toward becoming other
pancreatic
cells.
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10720454.001
]
(PMID = 19557902.001).
[ISSN]
1536-4828
[Journal-full-title]
Pancreas
[ISO-abbreviation]
Pancreas
[Language]
ENG
[Grant]
United States / NIDDK NIH HHS / DK / R01 DK054511; United States / NIDDK NIH HHS / DK / DK054511-03; United States / NIDDK NIH HHS / DK / R01 DK054511-04; United States / NIDDK NIH HHS / DK / DK054511-04; United States / NIDDK NIH HHS / DK / R01 DK054511-03; United States / NIDDK NIH HHS / DK / Z01 DK054511
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / DNA, Complementary; 0 / Homeodomain Proteins; 0 / Insulin; 0 / Lithostathine; 0 / RNA, Messenger; 0 / Reg1 protein, rat; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; EC 3.2.1.- / Amylases
[Other-IDs]
NLM/ NIHMS100566; NLM/ PMC2702698
85.
Mueller SB, Micke O, Herbst H, Schaefer U, Willich N:
Alpha-fetoprotein-positive carcinoma of the pancreas: a case report.
Anticancer Res
; 2005 May-Jun;25(3A):1671-4
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[Title]
Alpha-fetoprotein-positive
carcinoma of
the
pancreas
: a case report.
We report on the case of a 19-year-old male with an alpha-fetoprotein (AFP)-producing
acinar cell carcinoma of
the
pancreas
.
Originally, AFP was thought to be specific to hepatocellular
carcinoma
and germ
cell
tumours.
Rare cases
of acinar cell
carcinomas of the
pancreas
were found to express AFP.
When present, AFP expression is useful for
diagnosis
and
as a
marker for monitoring therapeutic response and recurrence of the disease.
[MeSH-major]
Pancreatic
Neoplasms / metabolism. alpha-Fetoproteins / metabolism
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(PMID = 16033080.001).
[ISSN]
0250-7005
[Journal-full-title]
Anticancer research
[ISO-abbreviation]
Anticancer Res.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / alpha-Fetoproteins
86.
De La O JP, Murtaugh LC:
Notch and Kras in pancreatic cancer: at the crossroads of mutation, differentiation and signaling.
Cell Cycle
; 2009 Jun 15;8(12):1860-4
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[Title]
Notch and Kras in
pancreatic cancer
: at the crossroads of mutation, differentiation and signaling.
Activating mutations in the KRAS proto-oncogene occur almost ubiquitously in
pancreatic
ductal
adenocarcinoma
(PDAC) and in its putative precursor lesions,
pancreatic
intraepithelial neoplasia (PanIN).
Conditional expression of an activated Kras allele in the mouse
pancreas
produces a model that faithfully recapitulates PanIN formation and progression to PDAC.
Importantly, although nearly every
cell
in the pancreata of these mice express activated Kras, only a very small minority of cells give rise to PanINs.
How the transforming activity of Kras is constrained in the
pancreas
remains unknown, and the
cell
types from which PanINs and PDAC arise are similarly unknown.
Here, we describe our recent results demonstrating that
acinar
cells are competent to form Kras-induced PanINs, and that active Notch signaling can synergize with Kras in PanIN initiation and progression.
Further efforts to understand how Notch and Kras synergize, as well as experiments to determine how other
pancreatic
cell
types contribute to PDAC development, should aid in the development of new therapies and early detection techniques that are desperately needed for this
cancer
.
[MeSH-major]
Carcinoma
,
Pancreatic
Ductal / metabolism.
Pancreatic
Neoplasms / metabolism. Proto-Oncogene Proteins p21(ras) / metabolism. Receptors, Notch / metabolism
[MeSH-minor]
Animals.
Cell
Differentiation. Disease Models, Animal. Humans. Mice. Mice, Transgenic. Mutation / genetics. Mutation / physiology. Signal Transduction / physiology
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(PMID = 19440048.001).
[ISSN]
1551-4005
[Journal-full-title]
Cell cycle (Georgetown, Tex.)
[ISO-abbreviation]
Cell Cycle
[Language]
eng
[Grant]
United States / NCI NIH HHS / CA / R21-CA123066; United States / NCI NIH HHS / CA / R21 CA123066-02; United States / NICHD NIH HHS / HD / 5T32-HD07491; United States / NCI NIH HHS / CA / R21 CA123066; United States / NICHD NIH HHS / HD / T32 HD007491
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural
[Publication-country]
United States
[Chemical-registry-number]
0 / Receptors, Notch; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
[Other-IDs]
NLM/ NIHMS118588; NLM/ PMC2719432
87.
Klipin M, Sparaco A, Omoshoro-Jones J, Smith MD:
Acinar cell carcinoma--a rare tumour of the pancreas.
S Afr J Surg
; 2008 Aug;46(3):88
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[Title]
Acinar cell carcinoma
--a rare tumour of the
pancreas
.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ therapy.
Pancreatic
Neoplasms / therapy
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(PMID = 18807305.001).
[ISSN]
0038-2361
[Journal-full-title]
South African journal of surgery. Suid-Afrikaanse tydskrif vir chirurgie
[ISO-abbreviation]
S Afr J Surg
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
South Africa
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
88.
Ikezoe M, Nishihara T, Yanagawa K, Kohro T, Yamai T, Ikezoe S, Yasunaga Y, Inui Y, Nishikawa M:
A case of pancreatic acinar cell carcinoma metastatic to skin.
Rare Tumors
; 2010;2(4):e62
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[Title]
A case of
pancreatic
acinar cell carcinoma
metastatic to skin.
We report a rare case of
pancreatic
acinar cell carcinoma
with widespread metastases in a 68-year-old woman who presented with subcutaneous nodules as the initial symptom.
Computed tomography showed
a pancreatic
mass with hepatic tumors and enlarged lymph nodes besides ring-enhanced subcutaneous nodules.
Histological analysis of a colonic polypoid lesion revealed
carcinoma
with endocrine and
acinar
differentiation compatible with
pancreatic
origin.
Regrettably, she died of a cerebral infarction without any treatment, and autopsy findings confirmed our
diagnosis
.
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(PMID = 21234254.001).
[ISSN]
2036-3613
[Journal-full-title]
Rare tumors
[ISO-abbreviation]
Rare Tumors
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Other-IDs]
NLM/ PMC3019597
[Keywords]
NOTNLM ; magnetic resonance diffusion-weighted imaging. / pancreatic acinar cell carcinoma / subcutaneous nodules / widespread metastases
89.
Lee JH, Lee KG, Park HK, Lee KS:
[Acinar cell carcinoma of the pancreas in Korea--clinicopathologic analysis of 27 patients from korean literature and 2 cases from our hospital--].
Korean J Gastroenterol
; 2010 Apr;55(4):245-51
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[Title]
[
Acinar cell carcinoma of
the
pancreas
in Korea--clinicopathologic analysis of 27 patients from korean literature and 2 cases from our hospital--].
BACKGROUND/AIMS:
Acinar cell carcinoma
(ACC) of the
pancreas
is a rare malignancy.
ACC has been considered
a cancer
with poor prognosis due to frequent metastasis, a high recurrence rate, and low resectability.
RESULTS: ACC was more common in male, and age at
diagnosis
ranged from 25 to 68 years (median 54).
Liver was most common organ of metastasis at
diagnosis
and recurrence after operation.
[MeSH-major]
Carcinoma
,
Acinar Cell
/
diagnosis
.
Pancreatic
Neoplasms /
diagnosis
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(PMID = 20389178.001).
[ISSN]
1598-9992
[Journal-full-title]
The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
[ISO-abbreviation]
Korean J Gastroenterol
[Language]
kor
[Publication-type]
Case Reports; English Abstract; Journal Article; Review
[Publication-country]
Korea (South)
[Chemical-registry-number]
0 / Biomarkers, Tumor
[Number-of-references]
22
90.
Borka K:
[Claudin expression in different pancreatic cancers and its significance in differential diagnostics].
Magy Onkol
; 2009 Sep;53(3):273-8
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[Title]
[Claudin expression in different
pancreatic
cancers and its significance in differential diagnostics].
The aim of our studies was to compare the different CLDN expression patterns in normal
pancreas
cells,
pancreatic
endocrine tumors, adenocarcinomas, mucinous cystic tumors and
acinar cell
carcinomas.
) In addition to the well-known CLDN-1 and -4 expression CLDN-2, -3 and -7 proteins were demonstrated in ductal cells, while CLDN-3 and -7 proteins showed expression in
acinar
cells.
4.) This is a first review on childhood
acinar cell carcinoma
causing Cushing syndrome.
The adenocarcinomas and cystic mucinous tumors of exocrine origin denoted CLDN-1, -2, -4 and -7 positivity, whereas
acinar cell
carcinomas expressed only CLDN-1 and -2.
Considering the CLDN expression observed in normal
pancreas
cells, it can be established that CLDN-1, -2 and -4 proteins are definitely markers of ductal differentiation, CLDN-1 protein
of acinar
and CLDN-3 of endocrine differentiation. 2).
The claudin expression pattern
of pancreas
tumors may be employed in the differential
diagnosis
of these tumors and may be of help in deciding dignity.
[MeSH-major]
Biomarkers, Tumor / metabolism. Claudins / metabolism.
Pancreatic
Neoplasms /
diagnosis
.
Pancreatic
Neoplasms / metabolism
[MeSH-minor]
Carcinoma
,
Pancreatic
Ductal /
diagnosis
.
Carcinoma
,
Pancreatic
Ductal / metabolism. Claudin-1. Claudin-3. Claudin-4. Cystadenocarcinoma, Mucinous /
diagnosis
. Cystadenocarcinoma, Mucinous / metabolism.
Diagnosis
, Differential. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Luminescence. Membrane Proteins / metabolism. Microscopy, Electron. Reverse Transcriptase Polymerase Chain Reaction
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(PMID = 19793693.001).
[ISSN]
0025-0244
[Journal-full-title]
Magyar onkologia
[ISO-abbreviation]
Magy Onkol
[Language]
hun
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Hungary
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / CLDN1 protein, human; 0 / CLDN2 protein, human; 0 / CLDN3 protein, human; 0 / CLDN4 protein, human; 0 / CLDN7 protein, human; 0 / Claudin-1; 0 / Claudin-3; 0 / Claudin-4; 0 / Claudins; 0 / Membrane Proteins
91.
Kolb-van Harten P, Rosien U, Klöppel G, Layer P:
Pancreatic acinar cell carcinoma with excessive alpha-fetoprotein expression.
Pancreatology
; 2007;7(4):370-2
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[Title]
Pancreatic
acinar cell carcinoma
with excessive alpha-fetoprotein expression.
We report a case
of acinar cell carcinoma
of the
pancreas
associated with excessively elevated levels of serum alpha-fetoprotein (>32,000 ng/ml).
Abdominal computed tomography scan revealed a large
pancreatic
mass with infiltration of the splenic artery.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ metabolism.
Pancreatic
Neoplasms / metabolism. alpha-Fetoproteins / metabolism
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MITOMYCIN C
.
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[Copyright]
2007 S. Karger AG, Basel and IAP
(PMID = 17703084.001).
[ISSN]
1424-3911
[Journal-full-title]
Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
[ISO-abbreviation]
Pancreatology
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / alpha-Fetoproteins; 0W860991D6 / Deoxycytidine; 50SG953SK6 / Mitomycin; B76N6SBZ8R / gemcitabine
92.
Mathieu A, Clerc P, Portolan G, Bierkamp C, Lulka H, Pradayrol L, Seva C, Fourmy D, Dufresne M:
Transgenic expression of CCK2 receptors sensitizes murine pancreatic acinar cells to carcinogen-induced preneoplastic lesions formation.
Int J Cancer
; 2005 May 20;115(1):46-54
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[Title]
Transgenic expression of CCK2 receptors sensitizes murine
pancreatic
acinar
cells to carcinogen-induced preneoplastic lesions formation.
In humans, initial events of
pancreatic
carcinogenesis remain unknown, and the question of whether this
cancer
, which has a ductal phenotype, exclusively arises from duct cells has been raised.
Previous studies have demonstrated that transgenic expression of the CCK2 receptor in
acinar
cells of ElasCCK2 mice plays a role in the development of
pancreatic
neoplasia.
Transition
of acinar
cells into duct-like cells expressing Pdx1 and gastrin, as well as proliferation
of acinar
cells, were transiently observed in both transgenic and control mice.
Importantly, expression of the CCK2 receptor increased the susceptibility
of pancreas
to azaserine.
Indeed, treated ElasCCK2 mice exhibited larger areas of
pancreatic
acinar
-ductal transition, increased cellular proliferation as well as larger adenomas areas vs. control mice.
[MeSH-major]
Carcinoma
,
Acinar Cell
/ etiology.
Carcinoma
,
Acinar Cell
/ genetics.
Pancreatic
Neoplasms / etiology.
Pancreatic
Neoplasms / genetics. Receptor, Cholecystokinin B / genetics. Receptor, Cholecystokinin B / physiology. Transgenes
[MeSH-minor]
Adenoma / metabolism. Animals. Antimetabolites, Antineoplastic / pharmacology. Azaserine / chemistry. Azaserine / pharmacology. Bromodeoxyuridine / pharmacology. Carcinogens.
Cell
Proliferation. Coloring Agents / pharmacology. Homeodomain Proteins / metabolism. Homozygote. Immunohistochemistry. Inflammation. Lymphocytes / metabolism. Mice. Mice, Transgenic. Phenotype. Precancerous Conditions / metabolism. Receptors, G-Protein-Coupled / metabolism. Risk. Time Factors. Trans-Activators / metabolism
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AZASERINE
.
Hazardous Substances Data Bank.
BROMODEOXYURIDINE
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
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[Copyright]
(c) 2005 Wiley-Liss, Inc.
(PMID = 15688412.001).
[ISSN]
0020-7136
[Journal-full-title]
International journal of cancer
[ISO-abbreviation]
Int. J. Cancer
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antimetabolites, Antineoplastic; 0 / Carcinogens; 0 / Coloring Agents; 0 / Homeodomain Proteins; 0 / Receptor, Cholecystokinin B; 0 / Receptors, G-Protein-Coupled; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein; 87299V3Q9W / Azaserine; G34N38R2N1 / Bromodeoxyuridine
93.
Antoine M, Khitrik-Palchuk M, Saif MW:
Long-term survival in a patient with acinar cell carcinoma of pancreas. A case report and review of literature.
JOP
; 2007;8(6):783-9
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[Title]
Long-term survival in a patient with
acinar cell carcinoma of pancreas
. A case report and review of literature.
CONTEXT:
Acinar cell carcinoma of
the
pancreas
is a rare malignancy that may have
acinar
and endocrine differentiation.
Clinical practice guidelines exist for
pancreatic
ductal
adenocarcinoma
.
However, treatment protocols for
acinar cell carcinoma of
the
pancreas
have not been standardized.
CASE REPORT: We describe a case of a 44-year-old woman presenting with low grade fever and mid-abdominal tenderness secondary to
a pancreatic
mass with
acinar
and endocrine differentiation metastatic to the liver.
The patient developed Clostridium difficile colitis and septic shock resulting in death 37 months after
the diagnosis
of acinar cell carcinoma
of the
pancreas
.
CONCLUSION: This is a case
of acinar cell carcinoma
of the
pancreas
with an endocrine component, treated with multiple chemotherapeutic agents, in which the patient survived 37 months after
diagnosis
.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Carcinoma
,
Acinar Cell
/ drug therapy.
Pancreatic
Neoplasms / drug therapy
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(PMID = 17993731.001).
[ISSN]
1590-8577
[Journal-full-title]
JOP : Journal of the pancreas
[ISO-abbreviation]
JOP
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
Italy
[Number-of-references]
28
94.
Yamaguchi H, Shimizu M, Ban S, Koyama I, Hatori T, Fujita I, Yamamoto M, Kawamura S, Kobayashi M, Ishida K, Morikawa T, Motoi F, Unno M, Kanno A, Satoh K, Shimosegawa T, Orikasa H, Watanabe T, Nishimura K, Ebihara Y, Koike N, Furukawa T:
Intraductal tubulopapillary neoplasms of the pancreas distinct from pancreatic intraepithelial neoplasia and intraductal papillary mucinous neoplasms.
Am J Surg Pathol
; 2009 Aug;33(8):1164-72
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[Title]
Intraductal tubulopapillary neoplasms of the
pancreas
distinct from
pancreatic
intraepithelial neoplasia and intraductal papillary mucinous neoplasms.
We have encountered cases of unusual intraductal
pancreatic
neoplasms with predominant tubulopapillary growth.
ITPNs were solid and nodular tumors obstructing dilated
pancreatic
ducts and did not contain any visible mucin.
All the features of ITPN were distinct from those of other known intraductal
pancreatic
neoplasms, including
pancreatic
intraepithelial neoplasia, intraductal papillary mucinous neoplasm, and the intraductal variant
of acinar cell carcinoma
.
In conclusion, ITPNs can be considered to represent a new disease entity encompassing intraductal tubular
carcinoma
as a
morphologic variant.
[MeSH-major]
Carcinoma
,
Pancreatic
Ductal / genetics.
Carcinoma
,
Pancreatic
Ductal / metabolism.
Carcinoma
,
Pancreatic
Ductal / pathology.
Pancreatic
Neoplasms / genetics.
Pancreatic
Neoplasms / metabolism.
Pancreatic
Neoplasms / pathology
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author profiles
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NCI CPTAC Assay Portal
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NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
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NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
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(PMID = 19440145.001).
[ISSN]
1532-0979
[Journal-full-title]
The American journal of surgical pathology
[ISO-abbreviation]
Am. J. Surg. Pathol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Biomarkers, Tumor
95.
Kataoka Y, Nio Y, Yano S, Koike M, Hashimoto K, Itakura M, Itagaki T, Nishi T, Endo S, Higami T:
[Pancreatic acinar cell carcinoma successfully treated with combination of oral TS-1 and intra-arterial cisplatin].
Gan To Kagaku Ryoho
; 2006 Apr;33(4):525-8
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[Title]
[
Pancreatic
acinar cell carcinoma
successfully treated with combination of oral TS-1 and intra-arterial cisplatin].
Pancreatic
acinar cell
carcinomas are rare, and little is reported on their chemotherapy.
We report a 49-year old male patient with
pancreatic
acinar cell carcinoma
and multiple liver metastases, which responded to oral TS-1 and hepatic arterial infusion of cisplatin.
The patient underwent a partial hepatectomy, MCT abrasions and excision of
the pancreatic
tumor.
Postoperative pathological studies revealed metastases
of acinar cell carcinoma
to the liver and lymph nodes; the primary lesion was undetermined.
Abdominal CT one year after surgery revealed
a pancreatic
body tumor, which was surgically removed.
Pathological studies showed primary
pancreatic
acinar cell carcinoma
, while previous metastases remained under control.
To summarize, TS-1 and cisplatin can be effective treatments for
pancreatic
acinar cell
carcinomas.
[MeSH-major]
Antineoplastic Combined Chemotherapy Protocols / therapeutic use.
Carcinoma
,
Acinar Cell
/ drug therapy.
Pancreatic
Neoplasms / drug therapy
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CIS-DIAMINEDICHLOROPLATINUM
.
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(PMID = 16612167.001).
[ISSN]
0385-0684
[Journal-full-title]
Gan to kagaku ryoho. Cancer & chemotherapy
[ISO-abbreviation]
Gan To Kagaku Ryoho
[Language]
jpn
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
0 / Drug Combinations; 0 / Pyridines; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
96.
National Toxicology Program:
Toxicology and carcinogenesis studies of a binary mixture of 3,3',4,4',5-pentachlorobiphenyl (PCB 126) (Cas No. 57465-28-8) and 2,2',4,4',5,5'-hexachlorobiphenyl (PCB 153) (CAS No. 35065-27-1) in female Harlan Sprague-Dawley rats (gavage studies).
Natl Toxicol Program Tech Rep Ser
; 2006 Aug;(530):1-258
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Since human exposure to DLCs always occurs
as a
complex mixture, the toxic equivalency factor (TEF) methodology has been developed
as a
mathematical tool to assess the health risk posed by complex mixtures of these compounds.
The toxic equivalency of DLCs was nominated for evaluation because of the widespread human exposure to DLCs and the lack of data on the adequacy of the TEF methodology for predicting relative potency for
cancer
risk.
Hepatic
Cell
Proliferation Data: To evaluate hepatocyte replication, analysis of labeling of replicating hepatocytes with 5-bromo-2'-deoxyuridine was conducted at the 14-, 31-, and 53-week interim evaluations.
At the end of the 2-year study, there were significantly increased incidences and severities of toxic hepatopathy characterized by hepatocyte hypertrophy, multinucleated hepatocytes, pigmentation, diffuse and focal fatty change, eosinophilic focus, nodular hyperplasia, cholangiofibrosis, oval
cell
hyperplasia, bile duct cysts, bile duct hyperplasia, necrosis, and portal fibrosis.
In addition, two animals in the highest dose group had hepatocellular
carcinoma
.
In addition, single occurrences of squamous
cell carcinoma
were seen in the top two dose groups.
Significantly increased incidences of squamous
cell carcinoma
(gingival) of the oral mucosa were seen at the end of the 2-year study and were accompanied by increased incidences of gingival squamous hyperplasia.
In the
pancreas
at 53 weeks, the incidence
of acinar
cytoplasmic vacuolization was significantly increased in the highest dose group.
At 2 years, increased incidences
of acinar
atrophy and
acinar
cytoplasmic vacuolization were seen in addition to
pancreatic
acinar
neoplasms in dosed groups.
In the uterus at 2 years, there was a marginal increase in the incidence of squamous
cell carcinoma
in Group 5.
Numerous nonneoplastic effects were seen in other organs at the interim time points including atrophy of the thymus and follicular
cell
hypertrophy of the thyroid gland.
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(PMID = 17160104.001).
[ISSN]
0888-8051
[Journal-full-title]
National Toxicology Program technical report series
[ISO-abbreviation]
Natl Toxicol Program Tech Rep Ser
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Carcinogens; DFC2HB4I0K / Polychlorinated Biphenyls; TSH69IA9XF / 3,4,5,3',4'-pentachlorobiphenyl; ZRU0C9E32O / 2,4,5,2',4',5'-hexachlorobiphenyl
97.
Mortenson MM, Katz MH, Tamm EP, Bhutani MS, Wang H, Evans DB, Fleming JB:
Current diagnosis and management of unusual pancreatic tumors.
Am J Surg
; 2008 Jul;196(1):100-13
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[Title]
Current
diagnosis
and management of unusual
pancreatic
tumors.
BACKGROUND: The finding of a solid or cystic mass in the
pancreas
is becoming more common secondary to the increasing use of cross-sectional imaging and the improved sensitivity of such studies for the detection of
pancreatic
abnormalities.
Because of the aggressive natural history of
pancreatic cancer
, this has caused concern that all
pancreatic
abnormalities may be
cancer as
well as confusion over proper diagnostic and treatment algorithms.
This review provides an overview of the natural history, diagnostic considerations, and treatment recommendations for the less common tumors of the
pancreas
which can be misinterpreted
as pancreatic cancer
including: solid pseudopapillary tumors (SPT),
acinar cell carcinoma
(ACC), lymphoplasmacytic sclerosing pancreatitis (LPSP), primary
pancreatic
lymphoma (PPL), and metastatic renal
cell carcinoma
to the
pancreas
.
DATA SOURCES: A Medline search was conducted to identify studies investigating the clinicopathologic features, molecular genetics, pathogenesis,
diagnosis
, and treatment of SPT, ACC, LPSP, PPL, and
pancreatic
metastases.
CONCLUSIONS: It is often possible to obtain an accurate pretreatment
diagnosis
for these unusual
pancreatic
tumors and to successfully differentiate them from the more common
pancreatic
malignancies.
[MeSH-major]
Pancreatic
Neoplasms /
diagnosis
.
Pancreatic
Neoplasms / therapy. Pancreatitis /
diagnosis
. Pancreatitis / therapy
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(PMID = 18466869.001).
[ISSN]
1879-1883
[Journal-full-title]
American journal of surgery
[ISO-abbreviation]
Am. J. Surg.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
80
98.
Kawakami H, Kuwatani M, Onodera M, Hirano S, Kondo S, Nakanishi Y, Itoh T, Asaka M:
Primary acinar cell carcinoma of the ampulla of Vater.
J Gastroenterol
; 2007 Aug;42(8):694-7