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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

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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

   

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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

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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

   

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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

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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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[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

   

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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

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[Cites] Gastrointest Endosc. 1997 May;45(5):387-93 [9165320.001]

[Cites] Am J Surg. 1994 Dec;168(6):571-3; discussion 573-5 [7977998.001]

[Cites] Hematol Oncol Clin North Am. 2002 Feb;16(1):81-94 [12063830.001]

[Cites] Dig Dis Sci. 1995 Mar;40(3):696-700 [7895567.001]

[Cites] Br J Surg. 1994 Apr;81(4):585-9 [7911387.001]

[Cites] Am J Gastroenterol. 2002 Jun;97(6):1386-91 [12094855.001]

[Cites] Gastrointest Endosc. 1992 Jan-Feb;38(1):27-34 [1612375.001]

[Cites] J Gastrointest Surg. 2003 Jan;7(1):118-26; discussion 127-8 [12559193.001]

[Cites] Gastrointest Endosc. 2000 Sep;52(3):367-71 [10968852.001]

[Cites] Cancer. 2006 Oct 15;107(8):1711-42 [16958083.001]

[Cites] Ann Intern Med. 2001 Mar 20;134(6):459-64 [11255521.001]

[Cites] Gastrointest Endosc. 2002 Feb;55(2):232-7 [11818928.001]

[Cites] Gastrointest Endosc. 2005 Nov;62(5):728-36; quiz 751, 753 [16246688.001]

[Cites] Gastrointest Endosc. 2005 Jan;61(1):76-9 [15672060.001]

[Cites] Am J Gastroenterol. 2004 May;99(5):844-50 [15128348.001]

[Cites] Diagn Cytopathol. 1986 Sep;2(3):221-7 [3533479.001]

[Cites] World J Gastroenterol. 2007 Mar 21;13(11):1701-5 [17461473.001]

[Cites] Gastrointest Endosc. 1997 Nov;46(5):417-23 [9402115.001]

[Cites] Ann Oncol. 1999;10 Suppl 4:85-8 [10436793.001]

[Cites] Gastrointest Endosc. 2003 Oct;58(4):510-5 [14520282.001]

[Cites] Am J Surg. 2006 Feb;191(2):191-7 [16442944.001]

[Cites] Acta Cytol. 1996 Jul-Aug;40(4):683-6 [8693886.001]

[Cites] Cancer. 2003 Oct 25;99(5):285-92 [14579295.001]

(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

   

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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

   

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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

   

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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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[Cites] Am J Surg Pathol. 2001 May;25(5):579-86 [11342768.001]

[Cites] Nat Med. 2002 Sep;8(9):979-86 [12185362.001]

[Cites] Cancer Res. 2003 May 1;63(9):2005-9 [12727809.001]

[Cites] Cancer Res. 2003 May 1;63(9):2016-9 [12727811.001]

[Cites] Lab Invest. 2003 Jun;83(6):853-9 [12808120.001]

[Cites] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]

[Cites] Cancer Cell. 2003 Aug;4(2):111-20 [12957286.001]

[Cites] Annu Rev Cell Dev Biol. 2003;19:71-89 [14570564.001]

[Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]

[Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]

[Cites] Mol Cancer. 2003 Jan 22;2:13 [12636873.001]

[Cites] Development. 2004 Sep;131(17):4213-24 [15280211.001]

[Cites] J Surg Oncol. 1975;7(2):139-41 [1097831.001]

[Cites] Cancer Res. 1976 Jul;36(7 PT 2):2690-8 [1277176.001]

[Cites] Nature. 1984 Nov 1-7;312(5989):71-5 [6092966.001]

[Cites] Yale J Biol Med. 1992 Sep-Oct;65(5):457-64; discussion 465-9 [1340063.001]

[Cites] Int J Pancreatol. 1999 Apr;25(2):77-87 [10360219.001]

[Cites] J Clin Gastroenterol. 2005 Apr;39(4 Suppl 2):S78-82 [15758664.001]

[Cites] Gastroenterology. 2005 Mar;128(3):728-41 [15765408.001]

[Cites] Cancer Cell. 2005 May;7(5):469-83 [15894267.001]

[Cites] Nature. 2005 Jun 16;435(7044):959-63 [15959515.001]

[Cites] Nature. 2005 Aug 4;436(7051):642 [16079833.001]

[Cites] Cancer Cell. 2005 Sep;8(3):185-95 [16169464.001]

[Cites] Cancer Res. 2006 Jan 1;66(1):95-106 [16397221.001]

[Cites] Cancer Res. 2006 Jan 1;66(1):242-7 [16397237.001]

[Cites] Cell Cycle. 2006 Jan;5(1):43-6 [16322695.001]

[Cites] Am J Surg Pathol. 2006 Sep;30(9):1067-76 [16931950.001]

[Cites] Genes Dev. 2006 Nov 15;20(22):3161-73 [17114586.001]

[Cites] Cancer Cell. 2006 Dec;10(6):451-3 [17157783.001]

[Cites] Cancer Cell. 2007 Mar;11(3):211-3 [17349578.001]

[Cites] Cancer Cell. 2007 Mar;11(3):229-43 [17349581.001]

[Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4419-24 [17360539.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4437-42 [17360542.001]

[Cites] Am J Pathol. 2007 Jul;171(1):263-73 [17591971.001]

[Cites] Gastroenterology. 2007 Dec;133(6):1999-2009 [18054571.001]

[Cites] Cell. 2008 Jan 25;132(2):197-207 [18243096.001]

[Cites] Gastroenterology. 2008 Aug;135(2):621-31 [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

   

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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

   

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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

   

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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

   

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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

   

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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

   

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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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[Cites] J Gastroenterol. 1995 Aug;30(4):529-33 [7550867.001]

[Cites] Hepatogastroenterology. 1996 Jul-Aug;43(10):1000-5 [8884328.001]

[Cites] Eur Radiol. 2001;11(9):1642-4 [11511884.001]

[Cites] Ultraschall Med. 2007 Feb;28(1):75-8 [17304414.001]

[Cites] Am J Gastroenterol. 1996 Jun;91(6):1268-9 [8651190.001]

[Cites] Surg Today. 2004;34(9):802-4 [15338361.001]

[Cites] Hepatogastroenterology. 2000 May-Jun;47(33):887-9 [10919054.001]

[Cites] ANZ J Surg. 2004 Apr;74(4):291-3 [15043751.001]

[Cites] J Assoc Physicians India. 1999 Jul;47(7):730-2 [10778598.001]

[Cites] Abdom Imaging. 2006 Mar-Apr;31(2):245-8 [16283584.001]

[Cites] J Hepatobiliary Pancreat Surg. 2006;13(3):256-9 [16708305.001]

[Cites] J Pediatr Surg. 2006 Mar;41(3):596-8 [16516645.001]

[Cites] J Hepatol. 1998 Sep;29(3):485-8 [9764999.001]

[Cites] Hepatogastroenterology. 2007 Jul-Aug;54(77):1585-8 [17708306.001]

[Cites] World J Surg. 2003 Mar;27(3):299-303 [12607055.001]

[Cites] J Comput Assist Tomogr. 1998 Mar-Apr;22(2):335-9 [9530406.001]

[Cites] Abdom Imaging. 2004 Jul-Aug;29(4):460-2 [15024520.001]

[Cites] N Engl J Med. 1968 Dec 5;279(23):1279-85 [4880017.001]

[Cites] Radiology. 1975 Nov;117(2):303-9 [170642.001]

[Cites] Am J Surg. 2005 Sep;190(3):364-5 [16105519.001]

[Cites] Magn Reson Imaging. 1999 Sep;17(7):1093-6 [10463662.001]

[Cites] J Gastroenterol. 2002;37(3):220-8 [11931537.001]

[Cites] Radiology. 1990 Mar;174(3 Pt 1):811-4 [1689502.001]

[Cites] Gastrointest Endosc. 2002 Feb;55(2):239-40 [11818930.001]

[Cites] Pancreas. 2003 Aug;27(2):201-3 [12883272.001]

[Cites] Surg Today. 1996;26(5):357-60 [8726623.001]

[Cites] Int J Hematol. 2006 Oct;84(3):282-3 [17050206.001]

[Cites] Hepatogastroenterology. 2003 Sep-Oct;50(53):1631-3 [14571802.001]

[Cites] Radiat Med. 1989 Mar-Apr;7(2):66-73 [2552504.001]

[Cites] Surg Today. 1992;22(1):62-5 [1312375.001]

[Cites] Eur J Gastroenterol Hepatol. 2007 Jun;19(6):519-20 [17489064.001]

[Cites] Gastroenterol Jpn. 1989 Aug;24(4):414-20 [2777018.001]

[Cites] AJR Am J Roentgenol. 1981 May;136(5):897-900 [6784524.001]

[Cites] Surg Today. 1998;28(10 ):1046-50 [9786577.001]

[Cites] Hepatogastroenterology. 2003 Sep-Oct;50(53):1693-6 [14571819.001]

[Cites] Gut. 1991 May;32(5):542-5 [1710199.001]

[Cites] Intern Med. 2007;46(6):273-7 [17379993.001]

(PMID = 26192173.001).

[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

   

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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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[Cites] Pathobiology. 1990;58(4):212-20 [1701303.001]

[Cites] Ear Nose Throat J. 2006 Aug;85(8):533-9 [16999063.001]

[Cites] APMIS. 2006 Oct;114(10):720-5 [17004975.001]

[Cites] Pancreas. 2009 Mar;38(2):219-22 [19238022.001]

[Cites] Mod Pathol. 2000 May;13(5):554-61 [10824928.001]

[Cites] Acta Pathol Jpn. 1990 Apr;40(4):279-87 [2371833.001]

[Cites] Am J Otolaryngol. 2004 Mar-Apr;25(2):129-33 [14976661.001]

[Cites] J Laryngol Otol. 1979 Apr;93(4):325-40 [438614.001]

[Cites] J Clin Pathol. 1982 Jun;35(6):611-6 [7085912.001]

[Cites] Cancer. 1987 Sep 1;60(5):962-8 [3300954.001]

[Cites] Cancer. 1987 Oct 1;60(7):1583-8 [2441846.001]

[Cites] Anticancer Res. 2001 May-Jun;21(3C):2131-4 [11501836.001]

(PMID = 19644544.001).

[ISSN] 1936-0568

[Journal-full-title] 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

   

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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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[Cites] Biochim Biophys Acta. 2004 Jun 1;1699(1-2):35-44 [15158710.001]

[Cites] Mol Endocrinol. 2006 Sep;20(9):1982-95 [16690750.001]

[Cites] J Clin Oncol. 2005 Jul 10;23(20):4524-31 [16002843.001]

[Cites] J Clin Invest. 1995 Feb;95(2):603-10 [7860744.001]

[Cites] J Steroid Biochem Mol Biol. 2008 Nov;112(1-3):127-37 [18840527.001]

[Cites] J Biol Chem. 2005 Sep 23;280(38):33066-75 [16012172.001]

[Cites] EMBO J. 1997 Feb 3;16(3):651-8 [9034346.001]

[Cites] J Endocrinol. 2006 Sep;190(3):749-57 [17003276.001]

[Cites] Nat Immunol. 2000 Aug;1(2):113-8 [11248802.001]

[Cites] EMBO Rep. 2002 Feb;3(2):136-40 [11839698.001]

[Cites] J Biol Chem. 2005 Jan 14;280(2):1376-83 [15475357.001]

[Cites] Theriogenology. 2006 Sep 1;66(4):755-65 [16530259.001]

[Cites] Arch Biochem Biophys. 2009 May 1;485(1):1-9 [19150607.001]

[Cites] Trends Biochem Sci. 1994 Mar;19(3):124-8 [8203019.001]

[Cites] Clin Exp Immunol. 2004 Feb;135(2):303-9 [14738460.001]

[Cites] Biochem Cell Biol. 2006 Dec;84(6):881-9 [17215875.001]

[Cites] EMBO Rep. 2005 Jan;6(1):28-32 [15643448.001]

[Cites] Science. 1999 Oct 1;286(5437):113-7 [10506557.001]

[Cites] Eur J Biochem. 1998 Mar 15;252(3):372-7 [9546651.001]

[Cites] Eur J Biochem. 1998 May 15;254(1):63-9 [9652395.001]

[Cites] Nat Rev Cancer. 2007 Aug;7(8):621-7 [17611544.001]

[Cites] DNA Cell Biol. 1996 Jan;15(1):9-16 [8561901.001]

[Cites] Brain Res. 2004 Oct 1;1022(1-2):164-72 [15353226.001]

[Cites] DNA Cell Biol. 1997 Mar;16(3):269-74 [9115635.001]

[Cites] Semin Oncol. 2007 Aug;34(4):303-10 [17674958.001]

[Cites] Trends Biochem Sci. 2006 Aug;31(8):455-64 [16815710.001]

[Cites] FASEB J. 1993 Dec;7(15):1515-7 [7903263.001]

[Cites] Domest Anim Endocrinol. 2007 Nov;33(4):451-9 [17034985.001]

[Cites] J Steroid Biochem Mol Biol. 2009 May;115(1-2):20-9 [19429457.001]

[Cites] Rev Invest Clin. 2007 Mar-Apr;59(2):124-9 [17633800.001]

[Cites] J Clin Invest. 2006 May;116(5):1292-301 [16628255.001]

[Cites] Histochem J. 1971 May;3(3):175-8 [4106573.001]

[Cites] EMBO J. 2002 Dec 16;21(24):6763-70 [12485997.001]

[Cites] Biochim Biophys Acta. 2008 Apr;1783(4):535-48 [18093543.001]

[Cites] Blood. 2009 Jan 22;113(4):856-65 [18796623.001]

[Cites] Am J Physiol Gastrointest Liver Physiol. 2005 Sep;289(3):G521-9 [15933222.001]

[Cites] Protein Sci. 2006 Dec;15(12):2749-60 [17088326.001]

(PMID = 19821078.001).

[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

   

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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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[Cites] Int J Cancer. 2008 Feb 15;122(4):742-50 [17943729.001]

[Cites] Ann Surg. 2007 Nov;246(5):786-93 [17968170.001]

[Cites] Lab Invest. 2003 Jun;83(6):853-9 [12808120.001]

[Cites] Nature. 2003 Oct 23;425(6960):851-6 [14520413.001]

[Cites] Int J Cancer. 2004 Jul 10;110(5):668-76 [15146555.001]

[Cites] Curr Gastroenterol Rep. 2004 Apr;6(2):111-8 [15191688.001]

[Cites] Pancreas. 2004 Jul;29(1):45-52 [15211111.001]

[Cites] Proc Natl Acad Sci U S A. 1976 May;73(5):1447-51 [1064018.001]

[Cites] J Biol Chem. 1980 Jul 25;255(14):6579-83 [6967067.001]

[Cites] Am J Surg. 1982 Aug;144(2):243-9 [7102934.001]

[Cites] Dtsch Med Wochenschr. 1985 Sep 20;110(38):1442-6 [3875469.001]

[Cites] Proc Natl Acad Sci U S A. 1985 Sep;82(18):6109-13 [3875856.001]

[Cites] Haemostasis. 1986;16(3-4):258-72 [3530901.001]

[Cites] Proc Natl Acad Sci U S A. 1989 Jun;86(12):4455-9 [2786632.001]

[Cites] Proc Natl Acad Sci U S A. 1992 Aug 1;89(15):6665-9 [1353882.001]

[Cites] Cancer Res. 1993 Jun 15;53(12):2704-7 [8389240.001]

[Cites] Gastroenterology. 1993 Dec;105(6):1846-56 [8253361.001]

[Cites] Biochem Biophys Res Commun. 1994 Dec 30;205(3):1815-21 [7529022.001]

[Cites] Br J Cancer. 1995 Oct;72(4):824-31 [7547227.001]

[Cites] Nature. 1996 Aug 1;382(6590):448-52 [8684484.001]

[Cites] Cancer Res. 1996 Oct 15;56(20):4614-9 [8840973.001]

[Cites] Mol Endocrinol. 1996 Nov;10(11):1444-56 [8923469.001]

[Cites] Eur J Haematol. 1997 Feb;58(2):104-8 [9111591.001]

[Cites] Cell. 1997 May 30;89(5):747-54 [9182762.001]

[Cites] Cell. 1997 May 30;89(5):755-64 [9182763.001]

[Cites] Int J Pancreatol. 1997 Apr;21(2):119-26 [9209953.001]

[Cites] Cancer Res. 1998 Apr 15;58(8):1677-83 [9563482.001]

[Cites] Bone. 1998 Sep;23(3):187-96 [9737340.001]

[Cites] Cancer Gene Ther. 1998 Sep-Oct;5(5):274-80 [9824046.001]

[Cites] Blood. 1998 Dec 15;92(12):4554-9 [9845520.001]

[Cites] Gastroenterology. 1999 May;116(5):1202-16 [10220513.001]

[Cites] Prostate. 1999 Jun 1;39(4):246-61 [10344214.001]

[Cites] Ann Surg. 2005 Aug;242(2):224-34 [16041213.001]

[Cites] Cancer Biol Ther. 2005 Jul;4(7):740-6 [15970685.001]

[Cites] Pol Merkur Lekarski. 2005 Jul;19(109):94-7 [16194038.001]

[Cites] Int J Biol Markers. 2005 Jul-Sep;20(3):146-55 [16240842.001]

[Cites] Clin Lymphoma Myeloma. 2007 Mar;7(5):346-53 [17562244.001]

[Cites] Int J Cancer. 2007 Jul 1;121(1):21-32 [17290391.001]

[Cites] Cancer Treat Rev. 2006;32 Suppl 1:15-9 [16680833.001]

[Cites] Br J Cancer. 2007 Oct 22;97(8):1106-15 [17876328.001]

[Cites] Mol Cell Biol. 2001 Apr;21(8):2891-905 [11283267.001]

(PMID = 18163903.001).

[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

   

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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

   

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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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[Cites] Microbiol Mol Biol Rev. 2001 Jun;65(2):288-318 ; second and third pages, table of contents [11381103.001]

[Cites] Nature. 2008 Oct 2;455(7213):627-32 [18754011.001]

[Cites] Nat Med. 2001 Oct;7(10):1133-7 [11590437.001]

[Cites] Cell Transplant. 2001;10(7):645-50 [11714200.001]

[Cites] J Clin Invest. 2001 Dec;108(11):1631-8 [11733558.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3818-23 [11904435.001]

[Cites] Cell. 2002 May 3;109(3):321-34 [12015982.001]

[Cites] Nat Rev Genet. 2002 Jul;3(7):524-32 [12094230.001]

[Cites] Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12236-41 [12221286.001]

[Cites] Nat Rev Cancer. 2002 Dec;2(12):951-6 [12459733.001]

[Cites] Genes Dev. 2003 Feb 15;17(4):488-501 [12600942.001]

[Cites] Genes Dev. 2003 Dec 15;17(24):3127-38 [14681205.001]

[Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]

[Cites] Nature. 2004 May 6;429(6987):41-6 [15129273.001]

[Cites] Nature. 1985 May 9-15;315(6015):115-22 [2986015.001]

[Cites] Proc Natl Acad Sci U S A. 1992 Feb 1;89(3):1128-32 [1371010.001]

[Cites] Am J Surg Pathol. 1992 Sep;16(9):815-37 [1384374.001]

[Cites] FASEB J. 1993 Jul;7(10):866-71 [8344486.001]

[Cites] Am J Pathol. 1994 Sep;145(3):671-84 [7521578.001]

[Cites] Nature. 1994 Oct 13;371(6498):606-9 [7935793.001]

[Cites] J Clin Invest. 1994 Dec;94(6):2421-5 [7989599.001]

[Cites] Genes Dev. 1996 Sep 1;10(17):2105-16 [8804306.001]

[Cites] Mol Cell Biol. 1997 Oct;17(10):6002-13 [9315659.001]

[Cites] Mol Cell Biol. 2005 Feb;25(4):1228-37 [15684377.001]

[Cites] Mol Cell Biol. 2006 Apr;26(7):2772-81 [16537919.001]

[Cites] Genes Dev. 2006 May 15;20(10):1218-49 [16702400.001]

[Cites] Mol Cell Biol. 2006 Jun;26(12):4511-8 [16738317.001]

[Cites] Cold Spring Harb Symp Quant Biol. 2005;70:1-9 [16869733.001]

[Cites] J Clin Invest. 2007 Apr;117(4):961-70 [17404619.001]

[Cites] Mod Pathol. 2007 Feb;20 Suppl 1:S94-112 [17486055.001]

[Cites] Cancer Res. 2008 May 1;68(9):3077-80; discussion 3080 [18451130.001]

[Cites] Science. 2008 Sep 26;321(5897):1841-4 [18755941.001]

[Cites] Diabetes. 2001 Oct;50(10):2260-7 [11574407.001]

(PMID = 19812721.001).

[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

   

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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

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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

   

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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

   

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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

   

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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

   

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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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[Cites] Intern Med. 2001 May;40(5):368-75 [11393404.001]

[Cites] Alcohol Clin Exp Res. 2009 Sep;33(9):1638-45 [19519715.001]

[Cites] Pancreatology. 2001;1(4):320-35 [12120211.001]

[Cites] Pancreatology. 2002;2(3):189-203 [12138724.001]

[Cites] Cancer Lett. 2002 Nov 28;185(2):123-30 [12169385.001]

[Cites] Pancreas. 2002 Nov;25(4):e71-6 [12409844.001]

[Cites] Eur J Pharmacol. 2004 Feb 13;486(1):107-19 [14751415.001]

[Cites] Gut. 1985 Sep;26(9):882-7 [4029715.001]

[Cites] Pancreas. 1989;4(4):486-91 [2762276.001]

[Cites] Gastroenterology. 1990 Jan;98(1):191-6 [2293577.001]

[Cites] N Engl J Med. 1993 May 20;328(20):1433-7 [8479461.001]

[Cites] Lancet. 1994 Jul 16;344(8916):193-4 [7912786.001]

[Cites] J Lab Clin Med. 1995 Mar;125(3):305-12 [7897296.001]

[Cites] Pancreas. 1995 Aug;11(2):127-31 [7479668.001]

[Cites] Dig Dis Sci. 1996 Jun;41(6):1216-24 [8654155.001]

[Cites] Biosci Rep. 1996 Aug;16(4):273-88 [8896787.001]

[Cites] Pancreas. 1997 Apr;14(3):276-9 [9094158.001]

[Cites] Inflamm Res. 1997 May;46(5):159-65 [9197985.001]

[Cites] Pancreas. 1997 Aug;15(2):109-12 [9260194.001]

[Cites] Alcohol Clin Exp Res. 1998 Oct;22(7):1570-83 [9802544.001]

[Cites] J Gastroenterol. 2004 Sep;39(9):879-87 [15565408.001]

[Cites] Biofactors. 2004;21(1-4):335-7 [15630222.001]

[Cites] World J Gastroenterol. 2005 Jan 28;11(4):525-8 [15641139.001]

[Cites] Pancreas. 2005 Jul;31(1):43-7 [15968246.001]

[Cites] Alcohol. 2005 Apr;35(3):205-11 [16054982.001]

[Cites] Biochem Pharmacol. 2005 Sep 15;70(6):869-78 [16023081.001]

[Cites] Inflamm Res. 2005 Dec;54(12):522-7 [16389574.001]

[Cites] World J Gastroenterol. 2006 Jan 7;12(1):137-40 [16440434.001]

[Cites] Dig Dis. 2005;23(3-4):232-40 [16508287.001]

[Cites] J Clin Invest. 2000 Jul;106(1):81-9 [10880051.001]

[Cites] Eur J Pharmacol. 2006 Feb 17;532(1-2):187-93 [16499907.001]

[Cites] J Gastroenterol Hepatol. 2006 Oct;21 Suppl 3:S97-S101 [16958684.001]

[Cites] World J Gastroenterol. 2006 Dec 14;12(46):7421-7 [17167828.001]

[Cites] J Physiol. 2007 Apr 1;580(Pt 1):31-7 [17218353.001]

[Cites] Am J Epidemiol. 2007 Oct 15;166(8):924-31 [17690219.001]

[Cites] Eur J Pharmacol. 2008 Feb 2;580(1-2):271-6 [18031730.001]

[Cites] Best Pract Res Clin Gastroenterol. 2008;22(1):45-63 [18206812.001]

[Cites] J Physiol Pharmacol. 2007 Dec;58 Suppl 6:65-80 [18212401.001]

[Cites] Adv Exp Med Biol. 2008;614:179-86 [18290328.001]

[Cites] J Gastroenterol Hepatol. 2008 Mar;23 Suppl 1:S63-8 [18336667.001]

[Cites] World J Gastroenterol. 2008 Jun 21;14(23):3672-80 [18595134.001]

[Cites] Am J Epidemiol. 2008 Oct 15;168(8):932-7 [18779386.001]

[Cites] Cell Biol Int. 2009 Jan;33(1):1-9 [18948215.001]

[Cites] Cancer Epidemiol Biomarkers Prev. 2009 Mar;18(3):765-76 [19258474.001]

[Cites] Alcohol Clin Exp Res. 2009 Sep;33(9):1545-54 [19485972.001]

[Cites] Int J Cancer. 2002 Apr 10;98(5):761-9 [11920648.001]

(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)

   

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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

   

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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

   

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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

   

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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 [11222142.001]

[Cites] Mod Pathol. 2007 Feb;20 Suppl 1:S94-112 [17486055.001]

[Cites] Am J Pathol. 1993 Sep;143(3):685-98 [8362971.001]

[Cites] Am J Clin Pathol. 2004 Nov;122(5):721-7 [15491968.001]

[Cites] World J Gastroenterol. 2006 May 28;12(20):3180-5 [16718837.001]

[Cites] Pancreas. 2007 Jul;35(1):42-6 [17575544.001]

[Cites] Indian J Med Sci. 1979 Jun;33(6):157-9 [521108.001]

[Cites] Surg Today. 2007;37(8):704-7 [17643220.001]

[Cites] Am J Surg Pathol. 2005 Nov;29(11):1524-9 [16224221.001]

[Cites] Hum Pathol. 2004 Feb;35(2):263-5 [14991547.001]

[Cites] Pediatr Dev Pathol. 2006 Jul-Aug;9(4):312-5 [16944990.001]

[Cites] Appl Immunohistochem Mol Morphol. 2000 Sep;8(3):203-9 [10981872.001]

[Cites] Hum Pathol. 2002 May;33(5):569-73 [12094386.001]

[Cites] Am J Surg Pathol. 1992 Sep;16(9):815-37 [1384374.001]

[Cites] Hum Pathol. 2000 Aug;31(8):938-44 [10987254.001]

[Cites] Trends Endocrinol Metab. 2003 Dec;14(10):460-6 [14643061.001]

[Cites] Hepatogastroenterology. 1992 Jun;39(3):282-6 [1380476.001]

[Cites] Arch Pathol Lab Med. 1999 Aug;123(8):707-11 [10420228.001]

[Cites] J Biol Chem. 2003 Aug 22;278(34):31950-7 [12775714.001]

[Cites] 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

   

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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

   

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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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(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

   

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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

   

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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

   

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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

   

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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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[Cites] Gastroenterology. 1999 Dec;117(6):1416-26 [10579983.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4437-42 [17360542.001]

[Cites] Mol Cell Biol. 2000 Mar;20(5):1825-35 [10669757.001]

[Cites] Mol Cell. 2000 Feb;5(2):207-16 [10882063.001]

[Cites] Int J Cancer. 2000 Oct 1;88(1):12-20 [10962434.001]

[Cites] Anticancer Res. 2001 Mar-Apr;21(2B):1355-8 [11396212.001]

[Cites] Mod Pathol. 2002 Apr;15(4):441-7 [11950919.001]

[Cites] J Clin Invest. 2002 Jun;109(11):1437-44 [12045257.001]

[Cites] Hum Mol Genet. 2002 Oct 1;11(21):2615-24 [12354787.001]

[Cites] Cell. 2002 Nov 27;111(5):635-46 [12464176.001]

[Cites] Am J Pathol. 2003 Jun;162(6):1831-43 [12759241.001]

[Cites] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]

[Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14920-5 [14657333.001]

[Cites] Clin Cancer Res. 2004 Feb 15;10(4):1235-40 [14977820.001]

[Cites] Development. 2004 Sep;131(17):4213-24 [15280211.001]

[Cites] Cancer Res. 1985 Mar;45(3):1285-90 [2982487.001]

[Cites] Eur J Cell Biol. 1990 Feb;51(1):64-75 [2184038.001]

[Cites] Mol Carcinog. 1991;4(6):527-33 [1793490.001]

[Cites] Princess Takamatsu Symp. 1994;24:152-61 [8983072.001]

[Cites] Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1402-7 [9037065.001]

[Cites] Cell. 1997 Jul 25;90(2):271-80 [9244301.001]

[Cites] J Natl Cancer Inst. 1997 Sep 3;89(17):1260-70 [9293916.001]

[Cites] Development. 1997 Oct;124(20):4133-41 [9374409.001]

[Cites] FEBS Lett. 1998 Sep 11;435(1):39-44 [9755855.001]

[Cites] Gastroenterology. 1998 Nov;115(5):1254-62 [9797382.001]

[Cites] Cancer Res. 1998 Dec 1;58(23):5500-6 [9850086.001]

[Cites] Nature. 2005 Jun 16;435(7044):959-63 [15959515.001]

[Cites] Development. 2005 Aug;132(16):3767-76 [16020518.001]

[Cites] Mol Cell Biol. 2006 Jan;26(1):117-30 [16354684.001]

[Cites] Biochem J. 2006 Feb 1;393(Pt 3):679-85 [16201968.001]

[Cites] Best Pract Res Clin Gastroenterol. 2006 Apr;20(2):197-209 [16549324.001]

[Cites] J Cell Biol. 2007 Feb 12;176(4):445-58 [17296795.001]

[Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]

[Cites] J Clin Invest. 2000 Jan;105(2):143-50 [10642592.001]

(PMID = 18042722.001).

[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 / 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

   

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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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[Cites] Histol Histopathol. 1994 Jan;9(1):53-8 [8003821.001]

[Cites] Pancreas. 2001 Apr;22(3):326-9 [11291937.001]

[Cites] Can Med Assoc J. 1962 Nov 3;87:970-3 [14011794.001]

[Cites] AJR Am J Roentgenol. 2005 Feb;184(2):511-9 [15671372.001]

[Cites] Br Med J. 1970 Jun 20;2(5711):708-9 [5429656.001]

[Cites] Mayo Clin Proc. 1979 Jul;54(7):449-58 [221755.001]

[Cites] Cancer. 1987 Feb 15;59(4):739-47 [3542187.001]

[Cites] Int Surg. 1984 Oct-Dec;69(4):361-4 [6084650.001]

[Cites] J Comput Assist Tomogr. 2004 Mar-Apr;28(2):180-6 [15091120.001]

[Cites] Ann Surg. 1995 Jun;221(6):721-31; discussion 731-3 [7794076.001]

[Cites] Am J Pathol. 1993 Sep;143(3):685-98 [8362971.001]

[Cites] J Pathol. 1985 May;146(1):17-29 [2989468.001]

[Cites] Int J Gastrointest Cancer. 2003;34(2-3):67-72 [15361637.001]

[Cites] J Clin Oncol. 2002 Dec 15;20(24):4673-8 [12488412.001]

[Cites] World J Gastroenterol. 2006 May 28;12(20):3180-5 [16718837.001]

[Cites] Hum Pathol. 2004 Dec;35(12):1568-71 [15619219.001]

[Cites] Gut. 1990 Aug;31(8):953-5 [2387523.001]

[Cites] Ultrastruct Pathol. 2000 Jul-Aug;24(4):227-41 [11013963.001]

[Cites] Virchows Arch. 2001 Mar;438(3):312-5 [11315630.001]

[Cites] Hum Pathol. 2004 Feb;35(2):263-5 [14991547.001]

[Cites] Adv Anat Pathol. 2001 May;8(3):144-59 [11345238.001]

[Cites] J Clin Pathol. 1977 Feb;30(2):103-12 [845259.001]

[Cites] Am J Surg Pathol. 1987 Feb;11(2):85-93 [3812876.001]

[Cites] Gastroenterol Jpn. 1992 Dec;27(6):785-91 [1281798.001]

[Cites] Acta Cytol. 1996 May-Jun;40(3):585-91 [8669201.001]

[Cites] Virchows Arch. 2004 Sep;445(3):231-5 [15517367.001]

[Cites] J Hepatobiliary Pancreat Surg. 2000;7(2):222-5 [10982618.001]

[Cites] Am J Surg Pathol. 1992 Sep;16(9):815-37 [1384374.001]

[Cites] Hum Pathol. 2000 Aug;31(8):938-44 [10987254.001]

[Cites] Int J Cancer. 2000 Dec 1;88(5):772-7 [11072247.001]

[Cites] Cancer. 1985 Jul 15;56(2):397-402 [4005804.001]

[Cites] Cancer. 1974 Apr;33(4):1002-9 [4819206.001]

[Cites] Diagn Cytopathol. 1994;10(4):362-4 [7924811.001]

[Cites] Gastroenterology. 1965 Nov;49(5):555-9 [5853162.001]

[Cites] Cancer Res. 1975 Aug;35(8):2234-48 [167949.001]

[Cites] Am J Surg. 2006 Feb;191(2):191-7 [16442944.001]

(PMID = 17957440.001).

[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

   

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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

   

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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

   

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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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[Cites] Arch Pathol Lab Med. 2001 Aug;125(8):1127-8 [11473479.001]

[Cites] Br Med J. 1970 Jun 20;2(5711):708-9 [5429656.001]

[Cites] JAMA. 2007 Jan 17;297(3):267-77 [17227978.001]

[Cites] Ann Surg Oncol. 2001 Mar;8(2):123-32 [11258776.001]

[Cites] Mayo Clin Proc. 1979 Jul;54(7):449-58 [221755.001]

[Cites] Cancer. 1987 Feb 15;59(4):739-47 [3542187.001]

[Cites] Clin Imaging. 2006 Sep-Oct;30(5):343-6 [16919557.001]

[Cites] Gastroenterol Clin Biol. 2007 May;31(5):543-6 [17541347.001]

[Cites] J Pathol. 1985 May;146(1):17-29 [2989468.001]

[Cites] Am J Surg Pathol. 1994 Aug;18(8):765-78 [8037290.001]

[Cites] J Clin Oncol. 2008 Jul 20;26(21):3496-502 [18640930.001]

[Cites] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19327-32 [18042722.001]

[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] J Clin Invest. 2002 Jun;109(11):1403-4 [12045253.001]

[Cites] J Gastrointest Surg. 2000 Nov-Dec;4(6):567-79 [11307091.001]

[Cites] World J Gastroenterol. 2006 May 28;12(20):3180-5 [16718837.001]

[Cites] Surgery. 2008 Aug;144(2):141-8 [18656619.001]

[Cites] Pancreas. 2007 Jul;35(1):42-6 [17575544.001]

[Cites] J Clin Oncol. 2008 Jul 20;26(21):3487-95 [18640929.001]

[Cites] Ultrastruct Pathol. 2000 Jul-Aug;24(4):227-41 [11013963.001]

[Cites] Virchows Arch. 2001 Mar;438(3):312-5 [11315630.001]

[Cites] Adv Anat Pathol. 2001 May;8(3):144-59 [11345238.001]

[Cites] Curr Opin Gastroenterol. 2006 Sep;22(5):498-504 [16891880.001]

[Cites] J Clin Pathol. 1977 Feb;30(2):103-12 [845259.001]

[Cites] Pancreas. 2003 Apr;26(3):306-8 [12657959.001]

[Cites] Ann Surg Oncol. 2009 Apr;16(4):836-47 [19194760.001]

[Cites] Virchows Arch. 2004 Sep;445(3):231-5 [15517367.001]

[Cites] J Gastrointest Surg. 2008 Dec;12(12):2078-86 [18836784.001]

[Cites] Am J Surg Pathol. 1992 Sep;16(9):815-37 [1384374.001]

[Cites] Mol Cell Biol. 2004 Apr;24(7):2673-81 [15024058.001]

[Cites] Development. 2005 Aug;132(16):3767-76 [16020518.001]

[Cites] Ann Surg. 1995 Jan;221(1):59-66 [7826162.001]

[Cites] Am J Surg Pathol. 2007 Mar;31(3):363-70 [17325477.001]

(PMID = 19495891.001).

[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; Multicenter Study

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents

   

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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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[Cites] Gastroenterology. 2003 May;124(5):1292-9 [12730869.001]

[Cites] Pancreatology. 2001;1(1):43-7 [12120267.001]

[Cites] FASEB J. 2003 Aug;17(11):1441-50 [12890698.001]

[Cites] FEBS Lett. 1994 Jan 3;337(1):114-8 [8276102.001]

[Cites] J Cereb Blood Flow Metab. 1996 Sep;16(5):834-40 [8784228.001]

[Cites] J Natl Cancer Inst. 1997 Mar 19;89(6):442-6 [9091646.001]

[Cites] Ann Surg. 1997 Sep;226(3):248-57; discussion 257-60 [9339931.001]

[Cites] Ann Intern Med. 1999 Aug 17;131(4):247-55 [10454945.001]

[Cites] Curr Opin Struct Biol. 1999 Oct;9(5):585-90 [10508765.001]

[Cites] Mod Pathol. 2005 Jun;18(6):779-87 [15791284.001]

[Cites] Biochim Biophys Acta. 2005 May 25;1723(1-3):8-18 [15715980.001]

[Cites] World J Gastroenterol. 2005 Sep 7;11(33):5199-202 [16127752.001]

[Cites] Int J Oncol. 2005 Nov;27(5):1361-9 [16211233.001]

[Cites] Cancer Res. 2005 Nov 15;65(22):10613-22 [16288055.001]

[Cites] J Clin Oncol. 2006 Jan 10;24(2):252-8 [16344318.001]

[Cites] Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):2066-9 [16609017.001]

[Cites] Semin Nucl Med. 2006 Jul;36(3):248-56 [16762614.001]

[Cites] Hum Pathol. 2006 Aug;37(8):1066-75 [16867870.001]

[Cites] Cancer Biol Ther. 2007 Jun;6(6):948-56 [17611392.001]

[Cites] Eur J Nucl Med Mol Imaging. 2008 May;35(5):990-8 [18057932.001]

[Cites] Pancreatology. 2008;8(2):110-25 [18382097.001]

[Cites] Cancer Res. 2008 Jun 15;68(12):4819-26 [18559529.001]

[Cites] Pancreas. 2009 Jul;38(5):527-33 [19342980.001]

[Cites] Mol Imaging Biol. 2011 Jun;13(3):536-46 [20593279.001]

[Cites] Am J Pathol. 1999 Nov;155(5):1525-33 [10550309.001]

[Cites] Cancer Res. 2000 Jan 15;60(2):409-16 [10667595.001]

[Cites] Neoplasia. 1999 Apr;1(1):50-62 [10935470.001]

[Cites] J Surg Oncol. 2000 Aug;74(4):243-8 [10962454.001]

[Cites] Gastroenterology. 2000 Dec;119(6):1447-53 [11113065.001]

[Cites] Dig Dis. 2001;19(1):76-84 [11385254.001]

[Cites] Anticancer Res. 2001 Mar-Apr;21(2B):1471-4 [11396234.001]

[Cites] Cancer Res. 2002 Mar 15;62(6):1868-75 [11912167.001]

[Cites] Dig Dis Sci. 2003 Mar;48(3):459-64 [12757156.001]

(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

   

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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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(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

   

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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

   

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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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[Cites] J Hepatobiliary Pancreat Surg. 2000;7(2):222-5 [10982618.001]

[Cites] J Gastrointest Surg. 2008 Jun;12(6):1061-7 [17957440.001]

[Cites] Adv Anat Pathol. 2001 May;8(3):144-59 [11345238.001]

[Cites] Lancet. 2001 Nov 10;358(9293):1576-85 [11716884.001]

[Cites] J Clin Oncol. 2002 Dec 15;20(24):4673-8 [12488412.001]

[Cites] Pathol Res Pract. 2002;198(12):777-83 [12608654.001]

[Cites] Pancreas. 2003 Jul;27(1):e18-22 [12826914.001]

[Cites] Int J Gastrointest Cancer. 2003;34(2-3):67-72 [15361637.001]

[Cites] Br Med J. 1970 Jun 20;2(5711):708-9 [5429656.001]

[Cites] Cancer. 1974 Apr;33(4):1002-9 [4819206.001]

[Cites] J Clin Pathol. 1977 Feb;30(2):103-12 [845259.001]

[Cites] Radiology. 1979 Feb;130(2):345-6 [760147.001]

[Cites] Am J Surg Pathol. 1992 Sep;16(9):815-37 [1384374.001]

[Cites] Gastroenterol Jpn. 1992 Dec;27(6):785-91 [1281798.001]

[Cites] Dig Surg. 1999;16(1):76-9 [9949272.001]

[Cites] AJR Am J Roentgenol. 2005 Feb;184(2):511-9 [15671372.001]

[Cites] Pancreas. 2007 Jul;35(1):42-6 [17575544.001]

[Cites] JOP. 2007;8(6):783-9 [17993731.001]

[Cites] 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

   

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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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(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

   

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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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[Cites] Development. 2001 Mar;128(6):871-81 [11222142.001]

[Cites] Differentiation. 1996 Oct;61(1):67-75 [8921586.001]

[Cites] Genes Dev. 2001 Jan 15;15(2):111-27 [11157769.001]

[Cites] Diabetes. 2001 Feb;50 Suppl 1:S5-9 [11272202.001]

[Cites] J Cell Biochem. 2005 Jul 1;95(4):649-56 [15849724.001]

[Cites] Dig Dis Sci. 1989 Jan;34(1):46-55 [2535980.001]

[Cites] Am J Surg. 1982 Aug;144(2):243-9 [7102934.001]

[Cites] Pancreas. 2005 Aug;31(2):108-18 [16024996.001]

[Cites] J Pathol. 1992 Feb;166(2):97-103 [1373187.001]

[Cites] Diabetologia. 2000 Jul;43(7):907-14 [10952464.001]

[Cites] J Endocrinol. 2001 Nov;171(2):309-18 [11691651.001]

[Cites] Lab Invest. 2003 Jun;83(6):853-9 [12808120.001]

[Cites] Development. 1995 Jun;121(6):1569-80 [7600975.001]

[Cites] Lab Invest. 2005 May;85(5):675-88 [15765120.001]

[Cites] J Natl Cancer Inst. 1976 Oct;57(4):931-6 [187782.001]

[Cites] Genes Dev. 1998 Jun 1;12(11):1705-13 [9620856.001]

[Cites] Pancreas. 2006 Mar;32(2):119-29 [16552330.001]

[Cites] Am J Pathol. 1999 Apr;154(4):1223-9 [10233860.001]

[Cites] Nature. 1999 Aug 26;400(6747):877-81 [10476967.001]

[Cites] Genes Dev. 2001 Feb 1;15(3):286-93 [11159909.001]

[Cites] Gastroenterology. 2005 Mar;128(3):728-41 [15765408.001]

[Cites] Annu Rev Cell Dev Biol. 2003;19:71-89 [14570564.001]

[Cites] Nature. 2003 Oct 23;425(6960):851-6 [14520413.001]

[Cites] J Natl Cancer Inst. 1975 Oct;55(4):857-64 [810597.001]

[Cites] Am J Pathol. 1978 Mar;90(3):645-58 [415616.001]

[Cites] Gastroenterology. 1998 Nov;115(5):1254-62 [9797382.001]

[Cites] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]

[Cites] Cell. 1990 Jun 15;61(6):1121-35 [1693546.001]

[Cites] Science. 2001 Oct 19;294(5542):564-7 [11577200.001]

[Cites] Cancer. 1981 Mar 15;47(6 Suppl):1528-34 [6268274.001]

[Cites] Eur J Cell Biol. 1990 Feb;51(1):64-75 [2184038.001]

[Cites] Lab Invest. 1993 Nov;69(5):518-30 [8246444.001]

[Cites] Dev Dyn. 2004 Jan;229(1):176-200 [14699589.001]

[Cites] Gastroenterology. 1992 Dec;103(6):1883-92 [1451981.001]

[Cites] Surgery. 1997 Jul;122(1):82-90 [9225919.001]

(PMID = 18189145.001).

[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