[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 555
1. Kawakami H, Kuwatani M, Onodera M, Hirano S, Kondo S, Nakanishi Y, Itoh T, Asaka M: Primary acinar cell carcinoma of the ampulla of Vater. J Gastroenterol; 2007 Aug;42(8):694-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary acinar cell carcinoma of the ampulla of Vater.
  • Acinar cell carcinoma of the pancreatobiliary system is a relatively rare malignant neoplasm arising usually in the pancreatic parenchyma.
  • The patient underwent a curative surgical operation, and histopathological examination revealed that the tumor was confined to the ampulla of Vater with no continuity to the pancreatic parenchyma.
  • The tumor cells showed acinar or tubular arrangement with eosinophilic to basophilic granular cytoplasm, findings identical to those of acinar cell carcinoma of the pancreas.
  • Immunohistochemically, the tumor cells were positive for lipase.
  • From these findings, we concluded that the tumor was primary acinar cell carcinoma arising in the ampulla of Vater, probably originating from heterotopic pancreatic tissue.
  • This is the first reported case of primary acinar cell carcinoma in the ampulla of Vater.
  • [MeSH-major] Ampulla of Vater. Carcinoma, Acinar Cell / diagnosis. Common Bile Duct Neoplasms / diagnosis
  • [MeSH-minor] Biopsy. Diagnosis, Differential. Endosonography. Female. Follow-Up Studies. Humans. Middle Aged. Pancreaticoduodenectomy / methods. Tomography, X-Ray Computed

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Arch Pathol Lab Med. 2001 Aug;125(8):1127-8 [11473479.001]
  • [Cites] Dig Surg. 2005;22(5):377-9 [16432300.001]
  • [Cites] Arch Pathol Lab Med. 1994 May;118(5):568-71 [8192567.001]
  • [Cites] Hum Pathol. 2004 Feb;35(2):263-5 [14991547.001]
  • [Cites] Gastrointest Endosc. 2001 Jan;53(1):121-3 [11154509.001]
  • [Cites] Am J Surg Pathol. 1992 Sep;16(9):815-37 [1384374.001]
  • [Cites] Arch Pathol Lab Med. 1999 Aug;123(8):707-11 [10420228.001]
  • [Cites] Am J Clin Oncol. 1997 Feb;20(1):101-7 [9020300.001]
  • [Cites] Hum Pathol. 2002 Apr;33(4):449-51 [12055683.001]
  • (PMID = 17701134.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


2. Jorgenson TC, Williams BR, Wendland A, Bilger A, Sandgren EP, Drinkwater NR: Identification of susceptibility loci in a mouse model of KRASG12D-driven pancreatic cancer. Cancer Res; 2010 Nov 1;70(21):8398-406
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Genetic background affects susceptibility to pancreatic ductal adenocarcinoma in the Ela-KRAS(G12D) mouse model.
  • In this model, KRAS oncogene expression is driven by an elastase promoter in acinar cells of the pancreas on an FVB/NTac (FVB) background [FVB-Tg(Ela-KRAS(G12D))] with the transgene carried on the Y chromosome.
  • Markers on chromosome 2 segregated with high tumor multiplicity in all three strains; these loci were designated Prsq1-3 (pancreatic ras susceptibility quantitative trait loci 1-3; combined F2 and N2 LOD(W), 6.0, 4.1, and 2.7, respectively).
  • A marker on chromosome 12 segregated with tumor multiplicity in a BALB × FVB-Tg(Ela-KRAS(G12D)) cross and was designated Prsq6 (LOD(W), ∼2.5).
  • By 12 months of age, 10% of BALB-Chr Y(FVB-Tg(Ela-KRASG12D)) mice developed invasive carcinomas.

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] ©2010 AACR.
  • [Cites] Pancreas. 2008 Oct;37(3):e39-44 [18815537.001]
  • [Cites] Cancer Cell. 2009 Nov 6;16(5):379-89 [19878870.001]
  • [Cites] Nat Genet. 2000 Feb;24(2):144-52 [10655059.001]
  • [Cites] Oncogene. 2000 Jun 29;19(28):3182-92 [10918573.001]
  • [Cites] Mol Cell Biol. 2001 Jan;21(1):310-8 [11113205.001]
  • [Cites] Am J Surg Pathol. 2001 May;25(5):579-86 [11342768.001]
  • [Cites] Biochim Biophys Acta. 2002 Mar 14;1602(1):73-87 [11960696.001]
  • [Cites] Genome Biol. 2002 Jun 18;3(7):RESEARCH0034 [12184808.001]
  • [Cites] Oncogene. 2002 Aug 29;21(38):5960-6 [12185599.001]
  • [Cites] Genome Res. 2003 Mar;13(3):485-91 [12618379.001]
  • [Cites] Bioinformatics. 2003 May 1;19(7):889-90 [12724300.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2016-9 [12727811.001]
  • [Cites] Cell. 2003 Jun 13;113(6):685-700 [12809600.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] J Mol Biol. 2004 Jul 23;340(5):921-32 [15236956.001]
  • [Cites] Genetics. 2004 Jun;167(2):859-66 [15238534.001]
  • [Cites] Am J Surg Pathol. 2004 Aug;28(8):977-87 [15252303.001]
  • [Cites] Cell. 1988 May 20;53(4):549-54 [2453289.001]
  • [Cites] Genetics. 1994 Nov;138(3):963-71 [7851788.001]
  • [Cites] Genetics. 1995 Mar;139(3):1421-8 [7768449.001]
  • [Cites] Nature. 1996 Mar 14;380(6570):149-52 [8600386.001]
  • [Cites] J Cell Sci. 2005 Mar 1;118(Pt 5):843-6 [15731001.001]
  • [Cites] J Gastroenterol. 2005 May;40(5):511-7 [15942717.001]
  • [Cites] BMC Cancer. 2005;5:98 [16086840.001]
  • [Cites] Cancer Res. 2005 Nov 1;65(21):9637-42 [16266982.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):95-106 [16397221.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5947-52 [16585505.001]
  • [Cites] Genes Dev. 2006 May 15;20(10):1218-49 [16702400.001]
  • [Cites] Genes Chromosomes Cancer. 2006 Aug;45(8):721-30 [16688744.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]
  • [Cites] Nat Protoc. 2006;1(3):1559-82 [17406449.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):111-25 [18272835.001]
  • [Cites] Arch Pathol Lab Med. 2009 Mar;133(3):375-81 [19260743.001]
  • (PMID = 20959479.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA076361; United States / NCI NIH HHS / CA / P01 CA022484; United States / NCI NIH HHS / CA / P01CA022484; United States / NCI NIH HHS / CA / R01CA076361; United States / NCI NIH HHS / CA / T32 CA009135
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / RNA, Messenger; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ NIHMS305961; NLM/ PMC3141286
  •  go-up   go-down


3. Tonel E, Carbone A, Scirelli T, Bellone G, Emanuelli G: [Biological aspects of pancreatic cancer]. Minerva Med; 2005 Apr;96(2):87-94
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Aspetti bbiologici del carcinoma pancreatico.
  • Pancreatic ductal carcinoma still is an aggressive disease with a fatal prognosis due to late diagnosis and resistance to pharmacological and surgical treatments.
  • These molecular alterations, including overexpression of receptor-ligand systems, oncogene activation and loss of tumour suppressor genes, leads to a profound disturbance in cell cycle regulation and continuous growth.
  • However, it remains unclear whether the initial target cells of this cancer develop from ductal or acinar cells.
  • This review will present recent emerging questions on the biology of pancreatic cancer with particular emphasis on the cell origin and tumour microenvironment.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / genetics. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Cytokines / physiology. Genes, Tumor Suppressor / physiology. Humans

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16172578.001).
  • [ISSN] 0026-4806
  • [Journal-full-title] Minerva medica
  • [ISO-abbreviation] Minerva Med.
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Cytokines
  • [Number-of-references] 41
  •  go-up   go-down


Advertisement
4. Martínez-Romero C, Rooman I, Skoudy A, Guerra C, Molero X, González A, Iglesias M, Lobato T, Bosch A, Barbacid M, Real FX, Hernández-Muñoz I: The epigenetic regulators Bmi1 and Ring1B are differentially regulated in pancreatitis and pancreatic ductal adenocarcinoma. J Pathol; 2009 Oct;219(2):205-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • 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.
  • [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

  • Genetic Alliance. consumer health - Pancreatitis.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


5. Tonini G, Rosini R, Teppa A, Aulenti V, Kalantary F, Tosana M, Bianchi D, Zorzi F: [Adenoid cystic/basal cell carcinoma of the prostate:case report]. Urologia; 2008 Oct-Dec;75(4):245-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Adenoid cystic/basal cell carcinoma of the prostate:case report].
  • Although most prostate carcinomas belong to the conventional acinar type, unusual variants have been reported.
  • The adenoid cystic/basal cell carcinoma of the prostate is a rare tumor with distinctive histopathologic features.
  • There are quite few publications in the literature concerning the diagnosis, treatment, and prognosis of this neoplasm.
  • METHODS. A 71-year-old man had an increased PSA value (5.11 ng/dL); the prostatic biopsy examination was positive for adenoid cystic/basal cell carcinoma.
  • The histology examination showed an acinar conventional carcinoma and adenoid cystic/basal cell carcinoma.
  • CONCLUSIONS. Various histologic and immunohistochemical features are helpful in recognizing the adenoid cystic/basal cell carcinoma of the prostate.
  • Clinically, the only difference from a conventional adenocarcinoma is that the PSA value is usually normal or only slightly increased.
  • This tumor has a biological potential that can result in metastases in some cases; the current treatment consists primarily in the surgical resection.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21086341.001).
  • [ISSN] 0391-5603
  • [Journal-full-title] Urologia
  • [ISO-abbreviation] Urologia
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


6. Schaff Z, Kovalszky I, Lotz G, Kiss A: [Hepatocellular carcinoma--from macroscopy to molecular pathology]. Orv Hetil; 2010 Jun 13;151(24):982-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Hepatocellular carcinoma--from macroscopy to molecular pathology].
  • [Transliterated title] A hepatocellularis carcinoma--a makroszkópiától a molekuláris patológiáig.
  • Hepatocellular carcinoma (HCC) is a tumor with rather bad prognosis.
  • Recent years, however, have seen considerable progress in the diagnostics and treatment of this disease, contributing to better understanding of its molecular pathogenesis.
  • Microscopically the WHO distinguishes trabecular, acinar (pseudoglandular), scirrhous and solid forms.
  • Special histological subtypes are the clear cell, fibrolamellar and mixed hepato-cholangiocellular variants.
  • Certain tumor markers may help the diagnosis, such as alpha-fetoprotein (AFP), glypican-3, survivin, the recently described agrin and claudins, furthermore, the hepatocyte specific antigen (HSA), which confirms the hepatocytic origin of the tumor.
  • In addition to the Barcelona Clinic Liver Cancer (BCLC) staging classification which determines the course of therapy, the molecular classification of HCC is based on key molecular alterations, many of which are observable in all HCC cases, whereas some alterations are only detectable in certain tumors.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Hepatocellular / chemistry. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / chemistry. Liver Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20519181.001).
  • [ISSN] 0030-6002
  • [Journal-full-title] Orvosi hetilap
  • [ISO-abbreviation] Orv Hetil
  • [Language] hun
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Hungary
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 47
  •  go-up   go-down


7. Roldo C, Missiaglia E, Hagan JP, Falconi M, Capelli P, Bersani S, Calin GA, Volinia S, Liu CG, Scarpa A, Croce CM: MicroRNA expression abnormalities in pancreatic endocrine and acinar tumors are associated with distinctive pathologic features and clinical behavior. J Clin Oncol; 2006 Oct 10;24(29):4677-84
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] MicroRNA expression abnormalities in pancreatic endocrine and acinar tumors are associated with distinctive pathologic features and clinical behavior.
  • PURPOSE: We investigated the global microRNA expression patterns in normal pancreas, pancreatic endocrine tumors and acinar carcinomas to evaluate their involvement in transformation and malignant progression of these tumor types.
  • Recent evidence indicates that microRNAs can contribute to tumor development and progression and may have diagnostic and prognostic value in several human malignancies.
  • MATERIALS AND METHODS: Using a custom microarray, we studied the global microRNA expression in 12 nontumor pancreas and 44 pancreatic primary tumors, including 12 insulinomas, 28 nonfunctioning endocrine tumors, and four acinar carcinomas.
  • RESULTS: Our data showed that a common pattern of microRNA expression distinguishes any tumor type from normal pancreas, suggesting that this set of microRNAs might be involved in pancreatic tumorigenesis; the expression of miR-103 and miR-107, associated with lack of expression of miR-155, discriminates tumors from normal; a set of 10 microRNAs distinguishes endocrine from acinar tumors and is possibly associated with either normal endocrine differentiation or endocrine tumorigenesis; miR-204 is primarily expressed in insulinomas and correlates with immunohistochemical expression of insulin; and the overexpression of miR-21 is strongly associated with both a high Ki67 proliferation index and presence of liver metastasis.
  • CONCLUSION: These results suggest that alteration in microRNA expression is related to endocrine and acinar neoplastic transformation and progression of malignancy, and might prove useful in distinguishing tumors with different clinical behavior.
  • [MeSH-major] Carcinoma, Acinar Cell / genetics. Carcinoma, Acinar Cell / pathology. Insulinoma / genetics. Insulinoma / pathology. MicroRNAs / metabolism. Pancreatic Neoplasms / genetics. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Cell Transformation, Neoplastic. Gene Expression Profiling. Humans. Liver Neoplasms / secondary. Pancreas / metabolism. Prognosis. Survival

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16966691.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01CA76259; United States / NCI NIH HHS / CA / P01CA81534
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MicroRNAs
  •  go-up   go-down


8. Martin SK, Agarwal G, Lynch GR: Subcutaneous fat necrosis as the presenting feature of a pancreatic carcinoma: the challenge of differentiating endocrine and acinar pancreatic neoplasms. Pancreas; 2009 Mar;38(2):219-22
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Subcutaneous fat necrosis as the presenting feature of a pancreatic carcinoma: the challenge of differentiating endocrine and acinar pancreatic neoplasms.
  • The association between pancreatic panniculitis and pancreatic disease is well described, but differentiation among the neoplastic causes of the syndrome remains difficult due to substantial overlap in histological and immunohistochemical features.
  • We report a case of subcutaneous fat necrosis as the presenting feature in a 61-year-old man with metastatic carcinoma of pancreatic origin.
  • Previous pathological evaluation of the patient's liver biopsy led to an initial diagnosis of adenocarcinoma of unknown primary site.
  • Immunohistochemistry was consistent with neuroendocrine differentiation, but the patient rapidly decompensated and died before the evaluation was complete, leaving the definitive diagnosis in question.
  • In our review of the published reports of tumor types associated with pancreatic panniculitis, we found that immunohistochemical staining and electron microscopy can and should be used in conjunction with clinical correlation to accurately differentiate neuroendocrine tumors from carcinomas with acinar cell features.
  • Accurate diagnosis of these tumors is necessary to determine prognosis and define appropriate therapy.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Fat Necrosis / pathology. Neuroendocrine Tumors / pathology. Pancreatic Neoplasms / pathology. Panniculitis / pathology. Skin / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19238022.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


9. Tarasova MV, Pozharisskiĭ KM, Ten VP, Arzumanov AA, Kudaĭbergenova AG: [The proliferative properties and regulators of the mitotic cell cycle of prostate adenocarcinoma]. Arkh Patol; 2009 Nov-Dec;71(6):20-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The proliferative properties and regulators of the mitotic cell cycle of prostate adenocarcinoma].
  • The authors have made an immunohistochemical determination of Ki-67, topoisomerase IIalpha, cyclins D1, A, and B1, and calculated their indices in 145 acinar adenocarcinomas of the prostate.
  • This tumor is characterized by a wide range of Ki-67 index (from 3 to 90% or more) although 90% of cases are in the range of 5-35%.
  • The exception is cyclin D1 that shows high expression in intact and tumor tissues, which is frequently greater than that of Ki-67, and its stable expression independent of the Gleason score.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / biosynthesis. Cell Proliferation. Gene Expression Regulation, Neoplastic. Neoplasm Proteins / biosynthesis. Prostatic Neoplasms / metabolism

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20131501.001).
  • [ISSN] 0004-1955
  • [Journal-full-title] Arkhiv patologii
  • [ISO-abbreviation] Arkh. Patol.
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
  •  go-up   go-down


10. Omlie JE, Koutlas IG: Acinic cell carcinoma of minor salivary glands: a clinicopathologic study of 21 cases. J Oral Maxillofac Surg; 2010 Sep;68(9):2053-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinic cell carcinoma of minor salivary glands: a clinicopathologic study of 21 cases.
  • PURPOSE: Acinic cell carcinoma (ACC) is an infrequent type of malignant salivary gland tumor.
  • This study was undertaken to 1) report on the clinicopathologic characteristics of 21 intraoral examples, 2) reconfirm the reported indolent behavior of these tumors, and 3) verify the synchronous or metachronous occurrence of other malignancies with ACC.
  • The size of the tumors varied from 0.6 to 1.6 cm.
  • Eleven patients did not report recurrence or metastatic disease.
  • One patient had 2 recurrences due to erroneous diagnosis that led to inappropriate treatment.
  • After properly diagnosed and treated, this patient has been free of tumor for 4 years.
  • Of interest were the metachronous occurrence of lymphoma in 1 patient and the synchronous occurrence of renal cell carcinoma in another.
  • CONCLUSION: This study confirms the indolent behavior of ACC of minor salivary glands and previous reports on the occasional synchronous or metachronous association of malignant salivary gland tumors with other malignancies.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Neoplasms, Multiple Primary. Neoplasms, Second Primary. Salivary Gland Neoplasms / pathology. Salivary Glands, Minor / pathology
  • [MeSH-minor] Adolescent. Adult. Aged. Carcinoma, Renal Cell / parasitology. Female. Humans. Kidney Neoplasms / pathology. Lymph Nodes / pathology. Lymphoma / pathology. Male. Middle Aged. Young Adult

  • Genetic Alliance. consumer health - Acinic Cell Carcinoma.
  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 American Association of Oral and Maxillofacial Surgeons. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20576339.001).
  • [ISSN] 1531-5053
  • [Journal-full-title] Journal of oral and maxillofacial surgery : official journal of the American Association of Oral and Maxillofacial Surgeons
  • [ISO-abbreviation] J. Oral Maxillofac. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


11. Leivo I, Jee KJ, Heikinheimo K, Laine M, Ollila J, Nagy B, Knuutila S: Characterization of gene expression in major types of salivary gland carcinomas with epithelial differentiation. Cancer Genet Cytogenet; 2005 Jan 15;156(2):104-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Characterization of gene expression in major types of salivary gland carcinomas with epithelial differentiation.
  • Gene expression profiles were studied in 13 cases of salivary gland carcinoma including mucoepidermoid carcinoma (MEC), acinic cell carcinoma (ACC), and salivary duct carcinoma (SDC) using a cDNA array.
  • Only 5 genes were overexpressed in all carcinomas including fibronectin 1 (FN1), tissue metalloproteinase inhibitor 1 (TIMP1), biglycan (BGN), tenascin-C (HXB), and insulin-like growth factor binding protein 5 (IGFBP5), whereas 16 genes were underexpressed.
  • The small number of similarly deregulated genes in these carcinoma entities suggests an extensive genetic variation between them.
  • This result agrees with the great histopathological diversity of different entities of salivary gland carcinoma.
  • Furthermore, diversity in gene expression between the carcinoma types was identified also by hierarchical clustering.
  • Each carcinoma entity was clustered together but MEC, SDC, and ACC were separated from each other.
  • In MEC, overexpressed genes included those of cell proliferation (IL-6 and SFN) and cell adhesion (SEMA3F and COL6A3), whereas many underexpressed genes were related to DNA modification (NTHL1 and RBBP4).
  • Apoptosis-related genes CASP10 and MMP11 were overexpressed in SDC, in accordance with the typical tumor necrosis seen in this entity.
  • An intermediate filament protein of basal epithelial cells, cytokeratin 14 (KRT14) was clearly differently expressed between the 3 types of carcinoma, and can be used as an aid in their differential diagnosis.


12. Chandan VS, Iacobuzio-Donahue C, Abraham SC: Patchy distribution of pathologic abnormalities in autoimmune pancreatitis: implications for preoperative diagnosis. Am J Surg Pathol; 2008 Dec;32(12):1762-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patchy distribution of pathologic abnormalities in autoimmune pancreatitis: implications for preoperative diagnosis.
  • Autoimmune pancreatitis (AIP) is a distinctive form of chronic pancreatitis that can mimic pancreatic carcinoma.
  • In the past, AIP accounted for up to 27% of Whipple resections performed for suspected adenocarcinoma.
  • More recently, with increased awareness of AIP and reports of its steroid responsiveness, tru-cut needle biopsies are increasingly used as an aid in preoperative diagnosis.
  • We noticed a distinctive patchy distribution to the pathologic abnormalities in many cases of resected AIP that could potentially interfere with preoperative diagnosis by needle biopsy.
  • (1) lymphoplasmacytic infiltrates around ducts, (2) acinar lymphoplasmacytic inflammation with atrophy and fibrosis, and (3) obliterative phlebitis.
  • To be included as an area of sparing, both duct and acinar parenchyma had to be free of lymphoplasmacytic inflammation, and the focus had to be at least 0.5 cm in diameter.
  • In patients with radiologic and serologic features (eg, elevated serum IgG4 level) suspicious for AIP, this potential pitfall in pathologic diagnosis should be considered before proceeding to surgery.
  • [MeSH-major] Autoimmune Diseases / diagnosis. Pancreatitis / diagnosis
  • [MeSH-minor] Adenocarcinoma / pathology. Adolescent. Adult. Aged. Biopsy. Diagnosis, Differential. Female. Humans. Immunoglobulin G. Immunohistochemistry. Male. Middle Aged. Pancreatic Neoplasms / pathology. Preoperative Care


13. Gomez DR, Katabi N, Zhung J, Wolden SL, Zelefsky MJ, Kraus DH, Shah JP, Wong RJ, Ghossein RA, Lee NY: Clinical and pathologic prognostic features in acinic cell carcinoma of the parotid gland. Cancer; 2009 May 15;115(10):2128-37
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical and pathologic prognostic features in acinic cell carcinoma of the parotid gland.
  • BACKGROUND: To the authors' knowledge, the indications for adjuvant treatment in acinic cell carcinoma (AciCC) of the parotid gland have not been elucidated to date.
  • Five-year estimates of disease-free survival (DFS), overall survival (OS), and local control were 85%, 90%, and 90%, respectively.
  • If high-grade tumors were defined on the basis of high mitotic activity (>2 mitoses/10 HPF) and/or tumor necrosis, high-grade carcinomas had a significantly lower DFS and OS (P = .001).
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Parotid Neoplasms / diagnosis
  • [MeSH-minor] Adult. Combined Modality Therapy. Disease-Free Survival. Facial Nerve Injuries / etiology. Female. Humans. Male. Middle Aged. Neoplasm Metastasis. Neoplasm Recurrence, Local. Prognosis

  • Genetic Alliance. consumer health - Acinic Cell Carcinoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19309749.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


14. Machado MC, Machado MA, Perini MV, Herman P, Jukemura J, Leite KR, Bacchella T: Acinar cell carcinoma of the pancreas: is the absence of neuroendocrine component related to a more malignant behavior? Hepatogastroenterology; 2008 Mar-Apr;55(82-83):708-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cell carcinoma of the pancreas: is the absence of neuroendocrine component related to a more malignant behavior?
  • BACKGROUND/AIMS: Acinar cell carcinomas are uncommon malignant tumors of the pancreas, accounting for 1-2% of all the cases of exocrine pancreatic tumor.
  • Some authors have estimated acinar cell tumors to be as aggressive as ductal adenocarcinoma of the pancreas whereas other series showed acinar cell tumors to have a favorable clinical outcome.
  • This discrepancy in prognosis may be related to the cellular components of the tumor.
  • METHODOLOGY: With the aim to evaluate the possible relationship between the presence of neuroendocrine differentiation and behavior of these tumors, the authors reviewed all patients presenting acinar cell carcinoma of the pancreas in the last 5 years with emphasis in the immunohistochemical evaluation.
  • Two patients without neuroendocrine component had a disseminated disease at presentation.
  • This data suggests that this tumor is less aggressive than ductal adenocarcinoma and even with nodal involvement, long-term survival after complete resection can be achieved.
  • Due to the rarity of this pancreatic tumor, this relationship remains to be confirmed with a multicentric study including a larger number of patients.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Pancreatic Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18613439.001).
  • [ISSN] 0172-6390
  • [Journal-full-title] Hepato-gastroenterology
  • [ISO-abbreviation] Hepatogastroenterology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  •  go-up   go-down


15. Lomberk G: Funding opportunities for rare pancreatic diseases. Pancreatology; 2009;9(4):327-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Additional rare diseases which remain 'funding orphans' include certain cancers such as acinar carcinoma, autoimmune pancreatitis, and various types of diseases characterized by cysts, both benign and malignant, among others.

  • MedlinePlus Health Information. consumer health - Pancreatic Diseases.
  • MedlinePlus Health Information. consumer health - Rare Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2009 S. Karger AG, Basel.
  • (PMID = 19468246.001).
  • [ISSN] 1424-3911
  • [Journal-full-title] Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.]
  • [ISO-abbreviation] Pancreatology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  •  go-up   go-down


16. Ji B, Tsou L, Wang H, Gaiser S, Chang DZ, Daniluk J, Bi Y, Grote T, Longnecker DS, Logsdon CD: Ras activity levels control the development of pancreatic diseases. Gastroenterology; 2009 Sep;137(3):1072-82, 1082.e1-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND & AIMS: Differentiated pancreatic acinar cells expressing endogenous levels of mutant K-Ras do not spontaneously develop pancreatic ductal adenocarcinoma (PDAC).
  • However, we hypothesized that acinar cells would develop PDAC in the presence of Ras activity levels mimicking those of human tumor cells.
  • We compared the effects of acinar cell expression of mutant K-Ras at endogenous and elevated levels on Ras activity and on the development of PDAC.
  • Expression of endogenous levels of mutant K-Ras in differentiated acinar cells resulted in moderately elevated Ras activity and in sparse murine pancreatic intraepithelial neoplasias (mPanINs) that did not spontaneously advance to PDAC unless the tumor suppressor p53 was simultaneously deleted.
  • High Ras activity mimicking levels in PDAC led to acinar cell senescence and generated inflammation and fibrosis resembling the histologic features of chronic pancreatitis.
  • With higher Ras activity in acinar cells, abundant mPanINs formed and spontaneously progressed to both cystic papillary carcinoma and metastatic PDAC.
  • Sufficient Ras activity in pancreatic acinar induces several important pancreatic disease manifestations not previously reported and supports a potential direct linkage between chronic pancreatitis, cystic papillary carcinoma, and PDAC.

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 2000 Jun 1;88(11):2495-504 [10861425.001]
  • [Cites] Cell. 1988 May 20;53(4):549-54 [2453289.001]
  • [Cites] Am J Surg Pathol. 2001 May;25(5):579-86 [11342768.001]
  • [Cites] Gene. 1991 Dec 15;108(2):193-9 [1660837.001]
  • [Cites] Am J Pathol. 1993 Aug;143(2):545-54 [8342602.001]
  • [Cites] Am J Physiol. 1995 Jun;268(6 Pt 1):G1060-5 [7611406.001]
  • [Cites] Gastroenterology. 1996 Jan;110(1):227-31 [8536861.001]
  • [Cites] Gut. 1998 Jul;43(1):128-33 [9771417.001]
  • [Cites] Neoplasia. 2005 Jan;7(1):17-23 [15720814.001]
  • [Cites] Cancer Cell. 2005 May;7(5):469-83 [15894267.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):95-106 [16397221.001]
  • [Cites] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5947-52 [16585505.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]
  • [Cites] Nat Cell Biol. 2007 May;9(5):493-505 [17450133.001]
  • [Cites] Nat Cell Biol. 2007 May;9(5):483-5 [17473855.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4671-8 [17510393.001]
  • [Cites] Cancer Cell. 2007 Sep;12(3):266-79 [17785207.001]
  • [Cites] Gastroenterol Clin North Am. 2007 Dec;36(4):831-49, vi [17996793.001]
  • [Cites] J Biol Chem. 2008 Feb 1;283(5):2896-905 [18025081.001]
  • [Cites] Genesis. 2008 Aug;46(8):390-5 [18693271.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18913-8 [19028870.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18907-12 [19028876.001]
  • [Cites] PLoS Biol. 2008 Dec 2;6(12):2853-68 [19053174.001]
  • [Cites] Biochem Biophys Res Commun. 2009 May 8;382(3):561-5 [19292977.001]
  • [Cites] Gastroenterology. 2006 Jun;130(7):2165-78 [16762637.001]
  • [Cites] Genes Dev. 2001 Feb 1;15(3):286-93 [11159909.001]
  • [Cites] Nat Genet. 2001 Dec;29(4):418-25 [11694875.001]
  • [Cites] Gastroenterology. 2001 Dec;121(6):1380-90 [11729117.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630.001]
  • [Cites] Pancreatology. 2001;1(4):363-8 [12120215.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2016-9 [12727811.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14920-5 [14657333.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [ErratumIn] Gastroenterology. 2011 May;140(5):1696
  • (PMID = 19501586.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK052067-11; United States / NCI NIH HHS / CA / P30 CA016672; United States / NIDDK NIH HHS / DK / R21 DK068414; United States / NCI NIH HHS / CA / CA16672; United States / NIDDK NIH HHS / DK / R01 DK052067; United States / NIDDK NIH HHS / DK / R01 DK052067-11; United States / NIDDK NIH HHS / DK / 5R21DK068414; United States / NCI NIH HHS / CA / P20 CA101936; United States / NIAAA NIH HHS / AA / R01 AA020822; United States / NIDDK NIH HHS / DK / R01 DK052067-10; United States / NIDDK NIH HHS / DK / DK052067; United States / NIDDK NIH HHS / DK / DK052067-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS122586; NLM/ PMC2789008
  •  go-up   go-down


17. Ramachandra C, Manjunath S, Joseph B, Appaji L, Kumari BS, Rao CR, Prabhakaran PS: Mixed exocrine-endocrine pancreatic carcinoma in childhood. Indian J Gastroenterol; 2005 May-Jun;24(3):116
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mixed exocrine-endocrine pancreatic carcinoma in childhood.
  • This may be the second reported case of such a tumor in childhood.
  • [MeSH-major] Adenoma, Islet Cell / epidemiology. Carcinoma, Acinar Cell / epidemiology. Pancreatic Neoplasms / epidemiology

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16041106.001).
  • [ISSN] 0254-8860
  • [Journal-full-title] Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology
  • [ISO-abbreviation] Indian J Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] India
  • [Number-of-references] 5
  •  go-up   go-down


18. Lin HH, Xiong Y, Ho YS, Zhou B, Nguyen HV, Deng H, Lee R, Yen Y, Borok Z, Ann DK: Transcriptional regulation by targeted expression of architectural transcription factor high mobility group A2 in salivary glands of transgenic mice. Eur J Oral Sci; 2007 Feb;115(1):30-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Numerous studies have demonstrated that HMGA2 is exclusively expressed in the nucleus of embryonic, but not of terminally differentiated, cells, and aberrant expression of HMGA2 is associated with various benign tumors, including pleomorphic salivary adenoma.
  • Herein, we report the use of a 4.5-kb enhancer/promoter region of the aquaporin-5 (AQP-5) gene to target HMGA2 transgene expression in the mouse salivary acinar cells as a model to investigate the biochemical and biological role of ectopic HMGA2 expression.
  • Additionally, squamous carcinoma-like salivary tumors were observed in the AQP-5/HMGA2 transgenic mice, albeit at a low incidence.
  • [MeSH-minor] Animals. Carcinoma, Squamous Cell / genetics. Enhancer Elements, Genetic / physiology. Gene Expression Profiling. Lipid Metabolism / genetics. Mice. Mice, Transgenic. Oligonucleotide Array Sequence Analysis. Promoter Regions, Genetic / physiology. Reverse Transcriptase Polymerase Chain Reaction. Salivary Gland Neoplasms / genetics. Signal Transduction / genetics

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17305714.001).
  • [ISSN] 0909-8836
  • [Journal-full-title] European journal of oral sciences
  • [ISO-abbreviation] Eur. J. Oral Sci.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 72767; United States / NIDCR NIH HHS / DE / DE 14183; United States / NHLBI NIH HHS / HL / HL 38578; United States / NHLBI NIH HHS / HL / HL62569; United States / NIEHS NIH HHS / ES / P30 ES006639; United States / NIDCR NIH HHS / DE / R01 DE 10742
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Aqp5 protein, mouse; 0 / Aquaporin 5; 0 / HMGA2 Protein
  •  go-up   go-down


19. Du YC, Klimstra DS, Varmus H: Activation of PyMT in beta cells induces irreversible hyperplasia, but oncogene-dependent acinar cell carcinomas when activated in pancreatic progenitors. PLoS One; 2009 Sep 07;4(9):e6932
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • To ask whether PyMT transforms and transdifferentiates endocrine cells toward exocrine tumor phenotypes, we generated transgenic mice that carry tetracycline-inducible PyMT and a linked luciferase reporter.
  • 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.

  • Hazardous Substances Data Bank. TETRACYCLINE .
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • SciCrunch. The Antibody Registry: Reagent: Antibodies .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


20. Khanna AK, Yadav SK, Dixit VK, Kumar M: AgNOR count and subjective AgNOR pattern assessment (SAPA) score in carcinoma of the pancreatic head including periampullary tumors. JOP; 2005 Nov;6(6):575-80
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] AgNOR count and subjective AgNOR pattern assessment (SAPA) score in carcinoma of the pancreatic head including periampullary tumors.
  • CONTEXT: Only a few studies are available in the literature regarding the AgNOR (argyrophilic nucleolar organizer region) count in pancreatic adenocarcinoma but studies on the SAPA (subjective AgNOR pattern assessment) score are completely lacking.
  • OBJECTIVE: We attempted to estimate the AgNOR count and the SAPA score in carcinoma of the pancreatic head including periampullary tumors and to correlate them with other various clinico-histological parameters.
  • PATIENTS: Twenty-four cases of carcinoma of the pancreatic head including periampullary tumors.
  • MAIN OUTCOME MEASURES: Patients were studied for the AgNOR count and the SAPA score, and the values were correlated with the size of the tumor, the type of tumor and histological type and grade of tumor.
  • The AgNOR count was 1.6+/-0.1 in the healthy pancreas while it was 2.8+/-0.5 in cases of pancreatic carcinoma (P<0.001).
  • The SAPA score was 5.6+/-0.2 in the healthy pancreas while it was 8.0+/-1.4 in pancreatic carcinoma (P<0.001).
  • Tumors less than or equal to 2 cm in size had an AgNOR count of 2.6+/-0.08 while the AgNOR count was 3.4+/-0.02 in tumors larger than 2 cm (P<0.001).
  • The SAPA score was also higher in tumors greater than 2 cm in size (7.3+/-0.2 vs. 9.4+/-0.8; P<0.001).
  • Periampullary tumors had a significantly lower (P<0.001) AgNOR count (2.7+/-0.06) and SAPA score (7.8+/-0.2) as compared to carcinoma of the head of the pancreas (AgNOR count 3.3+/-0.03 and SAPA score 9.2+/-0.7).
  • Well-differentiated carcinomas had significantly lower AgNOR counts as compared to other tumors except acinar cell carcinomas since acinar cell carcinomas are also well-differentiated tumors.
  • The SAPA score was also higher in moderately-differentiated tumors and the difference between moderately-differentiated tumor and other types of tumors was significant although there was no significant difference between cystadenocarcinomas and unclassified tumors, and between acinar cell carcinomas and well-differentiated tumors on SAPA scoring.
  • CONCLUSIONS: The values of the AgNOR count and the SAPA score are well-correlated with the size of the tumor, the type of tumor and the histological grade.
  • [MeSH-minor] Adult. Aged. Cell Count. Female. Humans. Male. Middle Aged. Pancreatectomy

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16286708.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antigens, Nuclear; 0 / Nuclear Proteins; 0 / nucleolar organizer region associated proteins
  •  go-up   go-down


21. Schwartz AM, Man YG, Rezaei MK, Simmens SJ, Berg PE: BP1, a homeoprotein, is significantly expressed in prostate adenocarcinoma and is concordant with prostatic intraepithelial neoplasia. Mod Pathol; 2009 Jan;22(1):1-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] BP1, a homeoprotein, is significantly expressed in prostate adenocarcinoma and is concordant with prostatic intraepithelial neoplasia.
  • This study attempts to determine whether BP1 expression is detectable in prostate cancer, another hormone dependent solid tumor, and whether this expression correlates with histopathologic and prognostic factors.
  • Significant BP1 immunoreactivity (2+) was identified in approximately 70% of prostatic adenocarcinomas, whether the analysis was performed on tissue sections (50 cases) or tissue microarray platforms (123 cases).
  • BP1 immunoreactivity was seen in <5% of normal acinar cells.
  • In tissue sections, 12 cases with paired carcinoma and prostatic intraepithelial neoplasia (PIN) showed concordance with strong immunoreactivity.
  • Tumor proliferation, assayed with Ki-67 (MIB-1) immunoreactivity, was higher in cancer cells that were BP1 immunoreactive, relative to those that were BP1 non-reactive.
  • These findings suggest that BP1 is an important upstream factor in the carcinogenic pathway of prostate cancer and that the expression of BP1 may reflect or directly contribute to tumor progression and/or invasion.
  • [MeSH-major] Adenocarcinoma / pathology. Biomarkers, Tumor / analysis. Homeodomain Proteins / biosynthesis. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology. Transcription Factors / biosynthesis

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18931648.001).
  • [ISSN] 1530-0285
  • [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; 0 / DLX4 protein, human; 0 / Homeodomain Proteins; 0 / Transcription Factors; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


22. Rudomina DE, Lin O, Moreira AL: Cytologic diagnosis of pulmonary adenocarcinoma with micropapillary pattern: does it correlate with the histologic findings? Diagn Cytopathol; 2009 May;37(5):333-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytologic diagnosis of pulmonary adenocarcinoma with micropapillary pattern: does it correlate with the histologic findings?
  • Micropapillary adenocarcinoma is associated with poor-prognosis in several organs including the lung.
  • The presence of small tight balls of neoplastic cells devoid of fibrovascular core in cytological preparations (micropapillary tufts) has been described as characteristic of micropapillary adenocarcinoma.
  • The cytological material of 46 cases of histologically proven pulmonary adenocarcinoma with a micropapillary component was compared to 33 cases with no micropapillary component to determine the specificity of micropapillary tufts for the histologic diagnosis of micropapillary adenocarcinoma.
  • Other histologic patterns of invasive pulmonary adenocarcinomas (acinar, papillary, and solid) were also compared with patterns of neoplastic cell aggregates in cytological preparations.
  • The positive predictive value for the cytologic diagnosis of a micropapillary component in lung adenocarcinomas was of 64%.
  • Therefore, the detection of micropapillary tufts in cytology is not specific for the diagnosis of a pulmonary micropapillary adenocarcinoma in the lung.
  • [MeSH-major] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Lung Neoplasms / diagnosis. Lung Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Cell Nucleus / pathology. Female. Humans. Male. Middle Aged

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19191297.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


23. Hall DA, Pu RT: Acinic cell carcinoma of the salivary gland: a continuing medical education case. Diagn Cytopathol; 2008 Jun;36(6):379-85; quiz 386-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinic cell carcinoma of the salivary gland: a continuing medical education case.
  • [MeSH-major] Carcinoma, Acinar Cell. Salivary Gland Neoplasms
  • [MeSH-minor] Aged. Diagnosis, Differential. Education, Medical, Continuing. Female. Humans. Prognosis. Salivary Glands / pathology

  • Genetic Alliance. consumer health - Acinic Cell Carcinoma.
  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18478605.001).
  • [ISSN] 1097-0339
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


24. Wargo JA, Warshaw AL: Surgical approach to pancreatic exocrine neoplasms. Minerva Chir; 2005 Dec;60(6):445-68
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In this review, we will explore the contemporary clinical management of pancreatic adenocarcinoma, acinar cell carcinoma, and cystic neoplasms of the pancreas.
  • The pathogenesis and epidemiology of these tumors will also be examined.
  • [MeSH-minor] Adenocarcinoma / surgery. Algorithms. Carcinoma, Acinar Cell / surgery. Chemotherapy, Adjuvant. Cystadenocarcinoma / surgery. Cystadenoma / surgery. Decision Trees. Humans. Magnetic Resonance Imaging. Neoadjuvant Therapy / methods. Neoplasm Staging. Radiotherapy, Adjuvant. Tomography, X-Ray Computed. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16401999.001).
  • [ISSN] 0026-4733
  • [Journal-full-title] Minerva chirurgica
  • [ISO-abbreviation] Minerva Chir
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 181
  •  go-up   go-down


25. Asano T, Seya T, Tanaka N, Ooaki Y, Fujino O: A 13-year-old girl with a preoperatively diagnosed solid cystic tumor of the pancreas. J Nippon Med Sch; 2006 Aug;73(4):231-4
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A 13-year-old girl with a preoperatively diagnosed solid cystic tumor of the pancreas.
  • We report on a 13-year-old girl with a solid cystic tumor of the pancreas.
  • We diagnosed a solid and cystic tumor of the pancreas and subsequently performed distal pancreatectomy.
  • A firm, well-encapsulated tumor was found in the pancreas tail.
  • The cut surface of the tumor consisted of a solid area with hemorrhage and a cystic area.
  • Light microscopy of the tumor confirmed small neoplastic cells.
  • Pathological diagnosis was solid pseudopapillary tumor (solid cystic tumor) of the pancreas.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16936450.001).
  • [ISSN] 1345-4676
  • [Journal-full-title] Journal of Nippon Medical School = Nippon Ika Daigaku zasshi
  • [ISO-abbreviation] J Nippon Med Sch
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


26. Yamashita R, Matsuzaki M, Matsui T, Yamaguchi R, Yuen K, Niwakawa M, Tobisu K: [Clinical characteristics of prostatic adenocarcinoma with ductal features]. Nihon Hinyokika Gakkai Zasshi; 2008 Mar;99(3):525-30
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Clinical characteristics of prostatic adenocarcinoma with ductal features].
  • PURPOSE: To determine the incidence and prognosis of prostatic ductal adenocarcinoma.
  • We differentiated prostatic cases of ductal adenocarcinoma that were larger than 5 mm in diameter from cases of acinar adenocarcinomas.
  • RESULTS: We found eight cases (12%) of prostatic ductal adenocarcinoma among the 64 cases treated with radical prostatectomies.
  • Seven of the cases (11%) were mixed-type ductal adenocarcinomas, which contained acinar and ductal components.
  • In addition, one case was identified as pure ductal adenocarcinoma.
  • During the follow-up period, four of the eight cases of ductal adenocarcinoma (50%) and twelve of the 56 cases of acinar adenocarcinoma (21%) showed postoperative PSA failure.
  • CONCLUSIONS: We identified eight cases of ducal adenocarcinoma (12% of the examined cases), which suggests this disease is not as rare as previously reported.
  • Compared to the cases of acinar adenocarcinoma, the cases of ductal adenocarcinoma were at a more advanced pathological stage and resulted in a higher rate of postoperative PSA failure.
  • Therefore, we believe that patients that show even a limited degree of ductal adenocarcinoma should receive aggressive therapy.
  • [MeSH-major] Carcinoma, Ductal, Breast / pathology. Carcinoma, Ductal, Breast / therapy. Prostatic Neoplasms / pathology. Prostatic Neoplasms / therapy
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Carcinoma, Acinar Cell / diagnosis. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / therapy. Follow-Up Studies. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Recurrence, Local / epidemiology. Neoplasm Staging. Neoplasms, Multiple Primary. Prognosis. Prostate-Specific Antigen / blood

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18404881.001).
  • [ISSN] 0021-5287
  • [Journal-full-title] Nihon Hinyōkika Gakkai zasshi. The japanese journal of urology
  • [ISO-abbreviation] Nippon Hinyokika Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


27. Luukkaa H, Klemi P, Leivo I, Koivunen P, Laranne J, Mäkitie A, Virtaniemi J, Hinkka S, Grénman R: Salivary gland cancer in Finland 1991--96: an evaluation of 237 cases. Acta Otolaryngol; 2005 Feb;125(2):207-14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONCLUSION: In this material consisting of various salivary gland carcinomas, stage I, male gender and age were the most powerful predictors of patient outcome.
  • The commonest tumor location was the parotid gland (n = 152; 64%), followed by the minor salivary glands (n =46; 19%), the submandibular gland (n =38; 16%) and the sublingual gland (n = 1; 0.4%).
  • The most frequent histological types of SGC were adenoid cystic carcinoma (n =65; 27%), mucoepidermoid carcinoma (n =45; 19%) and acinic cell carcinoma (n =41; 17%).
  • Of the commonest tumor types, the best 5-year relative survival rate was for patients with acinic cell carcinoma (96%), followed by those with mucoepidermoid (79%) and adenoid cystic carcinoma (74%).
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Carcinoma / epidemiology. Carcinoma / mortality. Carcinoma / surgery. Female. Finland / epidemiology. Humans. Incidence. Male. Middle Aged. Neoplasm Staging. Parotid Neoplasms / epidemiology. Parotid Neoplasms / mortality. Parotid Neoplasms / surgery. Population Surveillance / methods. Survival Rate

  • Genetic Alliance. consumer health - Salivary Gland Cancer.
  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15880955.001).
  • [ISSN] 0001-6489
  • [Journal-full-title] Acta oto-laryngologica
  • [ISO-abbreviation] Acta Otolaryngol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  •  go-up   go-down


28. Komorski JA, Nienartowicz JM: [Acinic cell carcinoma of glandule parotidea presenting untypical clinical symptoms and their bad prognosis]. Otolaryngol Pol; 2009 Sep-Oct;63(5):442-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acinic cell carcinoma of glandule parotidea presenting untypical clinical symptoms and their bad prognosis].
  • [Transliterated title] Acinic cell carcinoma ślinianki przyusznej o nietypowym obrazie klinicznym i niekorzystnym przebiegu.
  • Differential diagnosis of neck tumours puts precedence on diagnosing neoplastic lesions.
  • In the case of neck tumours, these are unfortunately late signs, but in patients with a primary neoplastic focus within the head and neck, neck tumour is often the first sign of the disease.
  • The preoperative histopathological diagnosis using thin-needle biopsy: cellulae carcinomatosae and the clinical picture resulted in block operation with neck lymphatic system removal and tissue defect reconstruction by means of a pectoral flap.
  • The histopathological examination confirmed non-cornifying basal cell epithelioma only in the essential lesion with no metastases to lymph nodes and surrounding tissue margins free of infiltrates.
  • In the collected specimen of the tumour on the front thoracic wall, a diagnosis of acinic cell carcinoma was made.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / surgery. Parotid Neoplasms / pathology. Parotid Neoplasms / surgery

  • Genetic Alliance. consumer health - Acinic Cell Carcinoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20169911.001).
  • [ISSN] 0030-6657
  • [Journal-full-title] Otolaryngologia polska = The Polish otolaryngology
  • [ISO-abbreviation] Otolaryngol Pol
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Poland
  •  go-up   go-down


29. Kawano Y, Kitaoka M, Hamada Y, Walker MM, Waxman J, Kypta RM: Regulation of prostate cell growth and morphogenesis by Dickkopf-3. Oncogene; 2006 Oct 19;25(49):6528-37
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Regulation of prostate cell growth and morphogenesis by Dickkopf-3.
  • Ectopic expression of Dkk-3 inhibited colony formation in LNCaP and PC3 prostate cancer cell lines and inducible expression of Dkk-3 reduced LNCaP cell proliferation.
  • Moreover, small interfering RNA-mediated downregulation of Dkk-3 enhanced cell cycle progression in untransformed RWPE-1 prostate epithelial cells.
  • Consistent with this, depletion of Dkk-3 disrupted acinar morphogenesis of RWPE-1 cells in a three-dimensional cell culture model.
  • Our results are consistent with the loss of Dkk-3 expression resulting in impairment of glandular structure and uncontrolled prostate epithelial cell (PrEC) proliferation, both of which are crucial for prostate cancer progression.
  • [MeSH-major] Cell Differentiation. Cell Proliferation. Intercellular Signaling Peptides and Proteins / physiology. Prostate / growth & development
  • [MeSH-minor] Carcinoma / metabolism. Epithelial Cells / metabolism. Gene Expression Regulation, Developmental. Humans. Male. Morphogenesis / physiology. Prostatic Hyperplasia / metabolism. Prostatic Neoplasms / metabolism. RNA, Small Interfering / pharmacology. Transfection. Tumor Cells, Cultured

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16751809.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DKK3 protein, human; 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering
  •  go-up   go-down


30. Sakamoto N, Ohtsubo S, Iguchi A, Takeshita M, Kurozumi T: Intestinal-type mucinous adenocarcinoma arising from the prostatic duct. Int J Urol; 2005 May;12(5):509-12
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intestinal-type mucinous adenocarcinoma arising from the prostatic duct.
  • We present a case of mucinous adenocarcinoma of intestinal type arising from the prostatic duct in a 72-year-old Japanese man.
  • A transurethral biopsy specimen revealed mucinous adenocarcinoma.
  • The cancer cells resembled the intestinal epithelium rather than either the prostatic duct or the acinar epithelium, which showed diffusely positive immunohistochemical staining for carcinoembryonic antigen, but showed negative staining for prostate-specific antigen.
  • Therefore, these findings suggest mucinous adenocarcinoma of intestinal type arising from the prostatic duct.
  • A number of cases with mucinous adenocarcinoma arising from the prostatic urethra resembling the present case have been reported, but this is the first known case of carcinoma arising from the prostatic duct.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Aged. Biopsy / methods. Carcinoembryonic Antigen / metabolism. Cystoscopy. Diagnosis, Differential. Endosonography. Follow-Up Studies. Humans. Immunohistochemistry. Male. Prostatectomy

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15948756.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Carcinoembryonic Antigen
  •  go-up   go-down


31. Reis-Filho JS, Natrajan R, Vatcheva R, Lambros MB, Marchió C, Mahler-Araújo B, Paish C, Hodi Z, Eusebi V, Ellis IO: Is acinic cell carcinoma a variant of secretory carcinoma? A FISH study using ETV6'split apart' probes. Histopathology; 2008 Jun;52(7):840-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is acinic cell carcinoma a variant of secretory carcinoma? A FISH study using ETV6'split apart' probes.
  • AIMS: Acinic cell carcinomas (ACCs) and secretory carcinomas (SCs) of the breast are rare, low-grade malignancies that preferentially affect young female patients.
  • [MeSH-major] Breast Neoplasms / genetics. Carcinoma, Acinar Cell / genetics. Gene Rearrangement. In Situ Hybridization, Fluorescence. Proto-Oncogene Proteins c-ets / genetics. Repressor Proteins / genetics

  • Genetic Alliance. consumer health - Acinic Cell Carcinoma.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18462362.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / ETS translocation variant 6 protein; 0 / Proto-Oncogene Proteins c-ets; 0 / Repressor Proteins
  •  go-up   go-down


32. Li J, Yang SJ, Zhao XL, Zhang YQ, Li KN, Cui JH, Li J: [Significant increase of glucose transport activity in breast cancer]. Zhonghua Bing Li Xue Za Zhi; 2008 Feb;37(2):103-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To study the expression level and significance of glucose transporter 1 (Glut-1) in normal breast tissue, adenosis, adenoma and breast carcinoma.
  • METHODS: A total of 147 cases of female breast tissue samples, including 92 cases of invasive ductal carcinoma, 26 cases of breast fibroadenoma, 24 cases of breast adenosis and 5 cases of normal breast tissues, were collected for quantitative detection of the expression of Glut-1 protein by immunohistochemistry (EnVision method) and Western blot, and its mRNA by reverse transcriptase-polymerase chain reaction (RT-PCR).
  • RESULTS: In normal breast tissue and benign lesions of the breast, Glut-1 was undetectable or only weakly detectable in cytoplasm of ductal and acinar epithelia.
  • In contrast, the intensity of Glut-1 staining was significantly higher in invasive ductal carcinomas (P = 0.0002) with protein expression predominantly in cellular membrane and lesser in cytoplasm.
  • Western blot and RT-PCR analyses showed that the expression of Glut-1 protein and mRNA were significantly increased in invasive ductal carcinoma than fibroadenoma (P =0.001 for protein; P <0.05 for mRNA) and adenosis (P =0.001 for protein; P < 0.05 for mRNA).
  • CONCLUSIONS: Glucose transport activity, as indicated by Glut-1 protein and its mRNA expression, significantly increases in breast carcinoma than non-cancerous lesions.
  • The over-expression of Glut-1 in breast carcinoma is tightly coupled with tumor cell proliferation, invasion and metastasis, implying that Glut-1 may serve as a new marker in the early diagnosis and prognostication of breast malignancy as well as a new therapeutic target.
  • [MeSH-major] Breast Neoplasms / metabolism. Carcinoma, Ductal, Breast / metabolism. Gene Expression Regulation, Neoplastic. Glucose / physiology. Glucose Transporter Type 1 / metabolism

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. GLUCOSE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18681321.001).
  • [ISSN] 0529-5807
  • [Journal-full-title] Zhonghua bing li xue za zhi = Chinese journal of pathology
  • [ISO-abbreviation] Zhonghua Bing Li Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Glucose Transport Proteins, Facilitative; 0 / Glucose Transporter Type 1; IY9XDZ35W2 / Glucose
  •  go-up   go-down


33. Schwentner I, Obrist P, Thumfart W, Sprinzl G: Distant metastasis of parotid gland tumors. Acta Otolaryngol; 2006 Apr;126(4):340-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distant metastasis of parotid gland tumors.
  • Patients with malignant salivary gland tumors should have an X-ray or CT scan of the chest at their initial assessment to exclude the possibility of distant metastasis.
  • The likelihood of developing distant metastasis is associated with high-grade tumors, such as adenoid cystic carcinoma, salivary duct carcinoma, high-grade mucoepidermoid carcinoma and tumors located in the submandibular gland, posterior tongue and pharyngeal tumors.
  • A lower risk of developing distant metastasis is known for all other histological entities of salivary gland tumors.
  • Nevertheless all patients who have a histologically confirmed malignant salivary gland tumor should have lifelong follow-up.
  • [MeSH-minor] Aged. Bone Neoplasms / secondary. Brain Neoplasms / secondary. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / secondary. Carcinoma, Adenoid Cystic / pathology. Carcinoma, Adenoid Cystic / secondary. Carcinoma, Mucoepidermoid / pathology. Carcinoma, Mucoepidermoid / secondary. Fatal Outcome. Humans. Immunohistochemistry. Incidence. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Magnetic Resonance Imaging. Male. Parotid Gland / pathology. Parotid Gland / surgery. Salivary Ducts / pathology. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - Intestinal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16608783.001).
  • [ISSN] 0001-6489
  • [Journal-full-title] Acta oto-laryngologica
  • [ISO-abbreviation] Acta Otolaryngol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Norway
  • [Number-of-references] 32
  •  go-up   go-down


34. Yamada Y, Hiraoka N: A case of acinar cell adenocarcinoma in the pancreatic tail. Jpn J Clin Oncol; 2006 Jul;36(7):473
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of acinar cell adenocarcinoma in the pancreatic tail.
  • [MeSH-major] Carcinoma, Acinar Cell / radiography. Pancreatic Neoplasms / radiography. Tomography, X-Ray Computed

  • MedlinePlus Health Information. consumer health - CT Scans.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16887840.001).
  • [ISSN] 0368-2811
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


35. Scheble VJ, Braun M, Wilbertz T, Stiedl AC, Petersen K, Schilling D, Reischl M, Seitz G, Fend F, Kristiansen G, Perner S: ERG rearrangement in small cell prostatic and lung cancer. Histopathology; 2010 Jun;56(7):937-43
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] ERG rearrangement in small cell prostatic and lung cancer.
  • AIMS: Small cell prostatic cancer is a rare but aggressive disease.
  • Currently, its histogenetic origin is unclear and its distinction from metastatic small cell lung cancer is challenging.
  • The aim of our study was to determine whether the ERG rearrangement commonly observed in acinar prostatic cancer can distinguish small cell prostatic cancer from small cell lung cancer samples.
  • METHODS AND RESULTS: We assessed 15 small cell prostatic cancers and 22 small cell lung cancers for ERG rearrangement using fluorescence in situ hybridization.
  • ERG rearrangement occurred in 86% of small cell prostatic cancers but in none of the small cell lung cancers and was the best marker to differentiate between both tumours (P < 0.0001).
  • CONCLUSIONS: The ERG rearrangement is commonly observed in small cell prostatic cancer, supporting the hypothesis that ERG rearrangement occurs in aggressive prostatic cancers.
  • Furthermore, the ERG rearrangement is the most significant marker to differentiate between small cell prostatic cancer and small cell lung cancer.
  • Moreover, our data suggest that small cell prostatic cancer is not a tumour entity on its own, but a dedifferentiated variant of common acinar prostatic cancer.
  • [MeSH-major] Carcinoma, Small Cell / genetics. Gene Rearrangement. Lung Neoplasms / genetics. Prostatic Neoplasms / genetics. Trans-Activators / genetics
  • [MeSH-minor] Adult. Biomarkers, Tumor / genetics. Chi-Square Distribution. Diagnosis, Differential. Humans. Immunohistochemistry. In Situ Hybridization, Fluorescence. Male. Tissue Array Analysis


36. Mazzucchelli R, Barbisan F, Scarpelli M, Lopez-Beltran A, van der Kwast TH, Cheng L, Montironi R: Is incidentally detected prostate cancer in patients undergoing radical cystoprostatectomy clinically significant? Am J Clin Pathol; 2009 Feb;131(2):279-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cystoprostatectomy specimens obtained from patients with bladder cancer provide a unique opportunity to assess the features of silent prostate adenocarcinoma (PCa).
  • PCa was considered clinically significant if any of the following criteria were present: total tumor volume, 0.5 cc or more; Gleason grade, 4 or more; extraprostatic extension; seminal vesicle invasion; lymph node metastasis (of PCa); or positive surgical margins.
  • Features were as follows: acinar adenocarcinoma, 123 (100.0%); peripheral zone location, 98 (79.7%); pT2a, 96 (78.0%); pT2b, 11 (8.9%); pT2c, 9 (7.3%); pT3a, 5 (4.1%); pT3b, 2 (1.6%); pT4, 0 (0.0%); Gleason score 6 or less, 107 (87.0%); negative margins, 119 (96.7%); pN0 for PCa, 123 (100.0%); and tumor volume less than 0.5 cc, 116 (94.3%).
  • [MeSH-major] Adenocarcinoma / diagnosis. Incidental Findings. Prostatectomy. Prostatic Neoplasms / diagnosis

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19141388.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


37. Salgarelli AC, Capparè P, Bellini P, Collini M: Usefulness of fine-needle aspiration in parotid diagnostics. Oral Maxillofac Surg; 2009 Dec;13(4):185-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: This review presents an analysis of the usefulness of FNA in differential diagnosis of parotid pathologies.
  • FNA is notoriously unreliable in recognising the malignant nature of parotid carcinoma providing its precise classification and establishing its grade.
  • A few malignant neoplasms are particularly prone to diagnostic error: acinic cell carcinoma is frequently interpreted as benign, and low-grade lymphomas are often discounted as inflammatory processes.
  • For planning the extent of surgery of malignant parotid tumours, the histological subtype and/or grade should be determined; therefore, a histological diagnosis by frozen section analysis is required.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 1993 Oct 15;72(8):2306-11 [8402443.001]
  • [Cites] Laryngoscope. 2006 Apr;116(4):534-40 [16585855.001]
  • [Cites] Am J Surg. 2003 Jul;186(1):57-62 [12842751.001]
  • [Cites] J Pak Med Assoc. 2004 Dec;54(12):617-9 [16104489.001]
  • [Cites] Head Neck. 2005 Mar;27(3):217-23 [15672359.001]
  • [Cites] Curr Opin Otolaryngol Head Neck Surg. 2006 Apr;14(2):62-6 [16552260.001]
  • [Cites] Diagn Cytopathol. 1999 Sep;21(3):163-6 [10450099.001]
  • [Cites] Cytopathology. 1995 Oct;6(5):285-300 [8785366.001]
  • [Cites] Ear Nose Throat J. 1994 Jun;73(6):377-80 [8076536.001]
  • [Cites] Head Neck. 2002 Feb;24(2):191-7 [11891949.001]
  • [Cites] ANZ J Surg. 2005 Mar;75(3):144-6 [15777394.001]
  • [Cites] Laryngoscope. 2004 Apr;114(4):789 [15064645.001]
  • [Cites] Acta Otolaryngol. 2005 Dec;125(12):1318-22 [16303681.001]
  • [Cites] Acta Cytol. 1992 May-Jun;36(3):353-63 [1580118.001]
  • [Cites] Semin Surg Oncol. 1991 Jan-Feb;7(1):20-4 [2003181.001]
  • [Cites] Br J Surg. 1989 Dec;76(12 ):1273-4 [2605471.001]
  • [Cites] Eur J Surg Oncol. 1998 Jun;24(3):180-3 [9630856.001]
  • [Cites] Cancer. 1992 Feb 1;69(3):615-9 [1730113.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 2003 Jul;129(7):720-3 [12874071.001]
  • [Cites] Laryngoscope. 2002 Dec;112(12):2141-54 [12461331.001]
  • [Cites] Ann Otol Rhinol Laryngol. 1993 Jun;102(6):483-5 [8347239.001]
  • [Cites] Ann Surg. 1930 Aug;92(2):169-81 [17866350.001]
  • [Cites] Acta Cytol. 1997 Sep-Oct;41(5):1421-5 [9305379.001]
  • [Cites] J R Coll Surg Edinb. 2001 Apr;46(2):91-5 [11329749.001]
  • [Cites] Arch Pathol Lab Med. 1987 Apr;111(4):346-53 [3030228.001]
  • [Cites] Br J Cancer. 2003 Nov 3;89(9):1610-3 [14583757.001]
  • [Cites] Surg Gynecol Obstet. 1966 Apr;122(4):811-6 [4286811.001]
  • [Cites] Diagn Cytopathol. 2000 Mar;22(3):139-46 [10679992.001]
  • [Cites] Acta Otolaryngol. 1964 Dec;58:471-84 [14253066.001]
  • [Cites] Sao Paulo Med J. 1999 Nov 4;117(6):233-7 [10625885.001]
  • [Cites] Otolaryngol Head Neck Surg. 2008 May;138(5):601-5 [18439465.001]
  • [Cites] Otolaryngol Head Neck Surg. 2005 Mar;132(3):387-91 [15746848.001]
  • [Cites] J Laryngol Otol. 2005 Apr;119(4):289-92 [15949083.001]
  • [Cites] Med Princ Pract. 2004 Mar-Apr;13(2):95-106 [14755143.001]
  • [Cites] Laryngoscope. 2001 Sep;111(9):1551-7 [11568593.001]
  • [Cites] Arch Pathol Lab Med. 2005 Jan;129(1):26-31 [15628905.001]
  • [Cites] Ann Otol Rhinol Laryngol. 1992 Feb;101(2 Pt 1):185-8 [1739267.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 2004 Jun;130(6):773-8 [15210562.001]
  • [Cites] Otolaryngol Head Neck Surg. 2008 Dec;139(6):811-5 [19041508.001]
  • [Cites] Ear Nose Throat J. 2005 Aug;84(8):518, 520-2, 524 [16220858.001]
  • [Cites] Laryngoscope. 1991 Mar;101(3):245-9 [2000011.001]
  • [Cites] Surgeon. 2005 Apr;3(2):67-72 [15861939.001]
  • [Cites] Pathol Biol. 1959 Apr;7(7-8):785-91 [13667300.001]
  • [Cites] Otolaryngol Clin North Am. 1998 Oct;31(5):815-22 [9735109.001]
  • [Cites] Cancer. 1998 Jun 25;84(3):153-9 [9678729.001]
  • [Cites] Diagn Cytopathol. 1999 Sep;21(3):170-3 [10450101.001]
  • [Cites] Acta Cytol. 1985 Jul-Aug;29(4):503-12 [2992196.001]
  • [Cites] Cancer. 2004 May 1;100(9):1876-83 [15112268.001]
  • (PMID = 19821124.001).
  • [ISSN] 1865-1569
  • [Journal-full-title] Oral and maxillofacial surgery
  • [ISO-abbreviation] Oral Maxillofac Surg
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 51
  •  go-up   go-down


38. Negahban S, Daneshbod Y, Shishegar M: Clear cell carcinoma arising from pleomorphic adenoma of a minor salivary gland: Report of a case with fine needle aspiration, histologic and immunohistochemical findings. Acta Cytol; 2006 Nov-Dec;50(6):687-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clear cell carcinoma arising from pleomorphic adenoma of a minor salivary gland: Report of a case with fine needle aspiration, histologic and immunohistochemical findings.
  • BACKGROUND: Malignant changes in pleomorphic adenoma (PA) of the salivary gland (carcinoma ex pleomorphic adenoma) are not common.
  • Clear cell carcinoma is a rare form of salivary gland tumor and involves mostly minor salivary glands, especially those of the palate.
  • Only 3 cases of clear cell carcinoma arising in PA have been reported, 2 in submandibular glands and 1 in a minor salivary gland of the palate.
  • Since then the tumor had recurred twice in the same place; it had been excised and was diagnosed as PA again.
  • Glandlike and acinar structures with hyaline globule material resembling cannonballs were also noted.
  • The final diagnosis was clear cell carcinoma expleomorphic adenoma.
  • CONCLUSION: Due to nonspecific cytologic findings in clear cell carcinoma and a mixture of elements of PA in this case, we did not consider clear cell carcinoma as the malignant component.
  • [MeSH-major] Adenocarcinoma, Clear Cell / pathology. Adenoma, Pleomorphic / pathology. Neoplasms, Second Primary / pathology. Salivary Gland Neoplasms / pathology. Salivary Glands, Minor / pathology
  • [MeSH-minor] Biomarkers, Tumor / analysis. Biopsy, Fine-Needle. Humans. Immunohistochemistry. Male. Middle Aged. Periodic Acid-Schiff Reaction

  • Genetic Alliance. consumer health - Salivary gland adenoma, pleomorphic.
  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17152285.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


39. Wahid A, Ahmad S, Sajjad M: Pattern of carcinoma of oral cavity reporting at dental department of Ayub medical college. J Ayub Med Coll Abbottabad; 2005 Jan-Mar;17(1):65-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pattern of carcinoma of oral cavity reporting at dental department of Ayub medical college.
  • BACKGROUND: Carcinoma of oral cavity is amongst the first ten commonest malignancies in Pakistan.
  • METHODDS: This clinicopathological study consists of cases of carcinoma of oral cavity presenting to dentistry department of Ayub Medical College Abbottabad during 1993-2003.
  • RESULTS: There were 50 carcinoma cases in the study, including 30 (60%) males and 20 (40%) females.
  • Among these, 47 (94%,) were diagnosed as squamous cell carcinomas, that consisted 30 (63.82 %) males and 17 (36.17%) females.
  • The other 6 % lesions were histologically diagnosed as malignant melanoma, adenocarcinoma and acinar cell carcinoma.
  • The age of squamous cell carcinoma cases was 41-71 years.
  • The maximum number of squamous cell carcinomas (34%) effected buccal mucosa.
  • CONCLUSION: The results of this study are comparable with other such studies done in Pakistan and else where in the world showing commonality of factors associated with the development of the disease in this region of the country, which necessitates a detailed prospective study.

  • MedlinePlus Health Information. consumer health - Oral Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15929532.001).
  • [ISSN] 1025-9589
  • [Journal-full-title] Journal of Ayub Medical College, Abbottabad : JAMC
  • [ISO-abbreviation] J Ayub Med Coll Abbottabad
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Pakistan
  •  go-up   go-down


40. Takazawa R, Kawakami S, Yamamoto K, Kubo Y, Kageyama Y, Kihara K: A case of prostatic duct adenocarcinoma: its clinical significance in comparison with typical acinar adenocarcinoma. Hinyokika Kiyo; 2008 Mar;54(3):243-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of prostatic duct adenocarcinoma: its clinical significance in comparison with typical acinar adenocarcinoma.
  • We report a case of prostatic duct adenocarcinoma treated with radical prostatectomy.
  • The main tumor of ductal adenocarcinoma was occupying the transitional zone and surrounded by scattered micro-foci of acinar adenocarcinoma.
  • We identified coexistence of ductal and acinar adenocarcinoma cells side by side in the same gland.
  • Pure ductal cancer cells were detected in the metastasized lymph node without acinar cancer cells.
  • Strong staining of PSA and loss of p63 expression by both types of adenocarcinoma cells were confirmed immunohistochemically.
  • We discuss the clinical significance of prostatic duct adenocarcinoma in comparision with typical acinar adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatic Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18411784.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


41. Basturk O, Khanani F, Sarkar F, Levi E, Cheng JD, Adsay NV: DeltaNp63 expression in pancreas and pancreatic neoplasia. Mod Pathol; 2005 Sep;18(9):1193-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • DeltaNp63 (DNp63) has become widely used, in particular, for distinguishing invasive carcinomas from noninvasive ducts by highlighting the myoepithelial or basal cells in the breast and prostate, respectively.
  • A total of 25 cases were non-neoplastic pancreata, 25 were pancreatic intraepithelial neoplasia (PanIN) of various grades, and 50 were examples of pancreatic ductal adenocarcinoma.
  • Among invasive carcinomas, DNp63 expression was detected only in areas of squamous differentiation and was completely absent in ordinary ductal areas.
  • Based on this observation, five additional cases of adenosquamous/squamous carcinoma was retrieved and stained, and the squamous components of all of these were also positive.
  • Among invasive carcinomas, it seems to be entirely specific for areas of squamous differentiation. (II) Those incidental microcysts seen in acinar lobules and lined by attenuated cells are also positive for DNp63, which suggests that they may be metaplastic in nature, and that they do not represent neoplastic cells. (III) Unlike the ducts of other exocrine organs, breast and prostate, there are no DNp63-expressing cells in the normal pancreatic ducts, and therefore, this marker cannot be used in distinguishing invasive carcinomas from the non-invasive ducts. (IV) No p63-expressing 'stem' cells are present in the pancreas.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma in Situ / pathology. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology. Phosphoproteins / biosynthesis. Trans-Activators / biosynthesis
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. DNA-Binding Proteins. Genes, Tumor Suppressor. Humans. Immunohistochemistry. Transcription Factors. Tumor Suppressor Proteins

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15976814.001).
  • [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
  • [Grant] United States / NIAMS NIH HHS / AR / PAR-02-068
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; 0 / Phosphoproteins; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
  •  go-up   go-down


42. Osunkoya AO, Hansel DE, Sun X, Netto GJ, Epstein JI: Aberrant diffuse expression of p63 in adenocarcinoma of the prostate on needle biopsy and radical prostatectomy: report of 21 cases. Am J Surg Pathol; 2008 Mar;32(3):461-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Aberrant diffuse expression of p63 in adenocarcinoma of the prostate on needle biopsy and radical prostatectomy: report of 21 cases.
  • Aberrant diffuse expression of p63 in prostate carcinoma cells is a rare and poorly understood phenomenon.
  • Needle biopsy cases ranged from Gleason patterns 3 to 5 with tumor identified on one or more cores, ranging from a minute focus to 80% of the core.
  • In all 8 radical prostatectomies p63 positive cancer was present, with in 2/8 cases both p63 positive cancer and usual p63 negative acinar prostate cancer.
  • In all 8 cases, the tumors were organ confined with negative margins and there was no seminal vesicle involvement or lymph node metastasis.
  • The presence of p63 positive atypical glands with an infiltrative pattern and perineural invasion on radical prostatectomy confirmed the needle biopsy diagnosis of carcinoma.
  • Rarely, prostate cancer can aberrantly express diffuse p63 staining in a nonbasal cell distribution leading to the erroneous diagnosis of atrophy or atypical basal cell proliferation.
  • The diagnosis of prostate cancer is based on the morphology and confirmed by the absence of high molecular weight cytokeratin staining and positivity for alpha-methylacyl-CoA racemase in the atypical glands.
  • Pathologists need to be aware of this rare and unusual phenomenon, which is a potential pitfall in prostate cancer diagnosis.
  • [MeSH-major] Adenocarcinoma / chemistry. Biopsy, Needle. Membrane Proteins / analysis. Prostatectomy. Prostatic Neoplasms / chemistry

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18300803.001).
  • [ISSN] 0147-5185
  • [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
  • [Chemical-registry-number] 0 / CKAP4 protein, human; 0 / Membrane Proteins
  •  go-up   go-down


43. Roskams T, Kojiro M: Pathology of early hepatocellular carcinoma: conventional and molecular diagnosis. Semin Liver Dis; 2010 Feb;30(1):17-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathology of early hepatocellular carcinoma: conventional and molecular diagnosis.
  • Recently, an East-West consensus on the histopathologic criteria for the diagnosis of high-grade dysplastic nodules (HGDN) versus early hepatocellular carcinoma (HCC) was reached.
  • Next to classical morphologic criteria such as nucleocytoplasmic ratio, thickness of cell plates, mitotic index, and architectural disturbance like acinar structures, one of the most relevant criteria to diagnose early HCC is stromal invasion.
  • Because a structured basement membrane is lacking along the hepatocytes in the liver, invasion cannot be defined as tumor growth through the basement membrane as in other tissues.
  • Based on molecular profiling, several additional markers for early malignant HCC have been found recently.
  • Glypican-3, heat shock protein 70, and glutamine synthetase have been already validated and can be used as a panel of stains to confirm the pathologist's histopathologic diagnosis and to solve difficult cases.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Hepatocellular / pathology. Liver Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20175030.001).
  • [ISSN] 1098-8971
  • [Journal-full-title] Seminars in liver disease
  • [ISO-abbreviation] Semin. Liver Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Glypicans; 0 / HSP70 Heat-Shock Proteins; EC 6.3.1.2 / Glutamate-Ammonia Ligase
  • [Number-of-references] 54
  •  go-up   go-down


44. Andreadis D, Epivatianos A, Poulopoulos A, Nomikos A, Papazoglou G, Antoniades D, Barbatis C: Detection of C-KIT (CD117) molecule in benign and malignant salivary gland tumours. Oral Oncol; 2006 Jan;42(1):57-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Detection of C-KIT (CD117) molecule in benign and malignant salivary gland tumours.
  • Archival formalin-fixed, paraffin-embedded sections of 40 benign and 57 malignant salivary gland tumours were retrieved and retrospectively studied immunohistochemically using a polyclonal C-KIT antibody in an Envision/HRP technique.
  • C-KIT expression was observed in cases of adenoid cystic, acinic cell polymorphous low grade, epithelial-myoepithelial, carcinosarcoma and basal cell adenocarcinomas, as in luminal cells of pleomorphic adenomas, in serous acinar and only in intercalated and a small number of striated ductal cells of inflammatory salivary gland tissue, whereas normal salivary lobules were generally negative except a weak positivity of intercalated cells.
  • Contrary to other reports, this study suggests that, C-KIT protein does not appear to be an exclusively specific marker for benign or malignant salivary gland neoplasms, but may be useful in differential diagnosis of adenoid cystic carcinoma from polymorphous low grade adenocarcinoma.
  • Furthermore its expression in serous acinar cells in sialadenitis and intercalated ductal cells in normal and inflammatory lesions may indicate a possible participation in pathogenesis of both neoplastic and non-neoplastic salivary gland diseases.
  • [MeSH-major] Biomarkers, Tumor / analysis. Carcinoma, Adenoid Cystic / chemistry. Proto-Oncogene Proteins c-kit / analysis. Salivary Gland Neoplasms / chemistry

  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16140564.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
  •  go-up   go-down


45. Sagi L, Amichai B, Barzilai A, Weitzen R, Trau H: Pancreatic panniculitis and carcinoma of the pancreas. Clin Exp Dermatol; 2009 Jul;34(5):e205-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic panniculitis and carcinoma of the pancreas.
  • Pancreatic panniculitis is a rare complication of carcinoma of the pancreas, most often accompanying the rare acinar cystadenocarcinoma.
  • We present a case of a 79-year-old man with neuroendocrine carcinoma of the pancreas and liver metastasis, who developed painful subcutaneous nodules on his shins.

  • Genetic Alliance. consumer health - Panniculitis.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19077093.001).
  • [ISSN] 1365-2230
  • [Journal-full-title] Clinical and experimental dermatology
  • [ISO-abbreviation] Clin. Exp. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


46. Chan WH, Lee KW, Chiang FY, Ho KY, Chai CY, Kuo WR: Features of parotid gland diseases and surgical results in southern Taiwan. Kaohsiung J Med Sci; 2010 Sep;26(9):483-92
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Various parotid gland diseases are seen clinically, including inflammation, sialolithiasis, and benign and malignant tumors.
  • It is important to differentiate between these to make a correct diagnosis and for proper management.
  • Here, we investigated the relationship between tumor characteristics and pathology, and considered whether the former could be used to differentiate malignant from benign parotid gland diseases.
  • Two hundred and eighty-one patients (88.9%) had benign disease, and 35 (11.1%) had malignant disease.
  • The most common benign disease was pleomorphic adenoma (115 cases, 36.4%), but the most common disease in male patients was Warthin's tumor, a finding which, as far as we aware, has not been previously been reported in the literature.
  • The incidence of Warthin's tumor seems to be increasing.
  • In malignant disease, the most common was acinic cell carcinoma (8 cases, 22.9%).
  • Compared with benign disease, malignant parotid gland disease more often presents as a hard, painful, fixed and large mass (> 3 cm), and more often involves the deep lobe of the parotid gland.
  • Partial parotidectomy was adequate for most tumors, including pleomorphic adenoma.
  • However, there was no difference in transient facial palsy rate between benign and malignant parotid gland disease, although parotid gland cancer had a higher incidence of permanent facial palsy postoperatively.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier. Published by Elsevier B.V. All rights reserved.
  • [CommentIn] Kaohsiung J Med Sci. 2012 Jun;28(6):350-1 [22632893.001]
  • (PMID = 20837345.001).
  • [ISSN] 1607-551X
  • [Journal-full-title] The Kaohsiung journal of medical sciences
  • [ISO-abbreviation] Kaohsiung J. Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China (Republic : 1949- )
  •  go-up   go-down


47. Sato T, Kamata SE, Kawabata K, Nigauri T, Mitani H, Beppu T, Sato M: Acinic cell carcinoma of the parotid gland in a child. Pediatr Surg Int; 2005 May;21(5):377-80
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinic cell carcinoma of the parotid gland in a child.
  • Acinic cell carcinoma of the parotid gland in children is an extremely rare occurrence.
  • We present a 13-year-old girl with acinic cell carcinoma of the parotid gland.
  • Removal of the superficial lobe of the parotid gland (superficial parotidectomy) was performed because the tumor was completely encapsulated by fibrous tissue and had not invaded the deep parotid gland.
  • In our view, when tumors are completely encapsulated and do not adhere to the facial nerves, superficial parotidectomy is the best surgical treatment in children.
  • [MeSH-major] Carcinoma, Acinar Cell / surgery. Parotid Neoplasms / surgery

  • Genetic Alliance. consumer health - Acinic Cell Carcinoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Pediatr Otorhinolaryngol. 1987 Oct;13(3):279-92 [3679684.001]
  • [Cites] Australas Radiol. 1997 Feb;41(1):44-8 [9125068.001]
  • [Cites] Int J Pediatr Otorhinolaryngol. 1993 Aug;27(2):187-91 [8258487.001]
  • [Cites] Mayo Clin Proc. 1975 May;50(5):279-83 [165335.001]
  • [Cites] Cancer. 1966 Dec;19(12):1761-72 [5927935.001]
  • [Cites] Cancer. 1983 Aug 1;52(3):542-9 [6861091.001]
  • [Cites] Rhinology. 1995 Sep;33(3):177-9 [8560174.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 1992 May;118(5):472-6 [1315140.001]
  • [Cites] Head Neck Surg. 1988 Mar-Apr;10(4):257-63 [3069812.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 1999 Sep;125(9):1025-8 [10488991.001]
  • (PMID = 15806422.001).
  • [ISSN] 0179-0358
  • [Journal-full-title] Pediatric surgery international
  • [ISO-abbreviation] Pediatr. Surg. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


48. Spanish National Registry of Laparoscopic Pancreatic Surgery, Fernández-Cruz L, Pardo F, Cugat E, Artigas V, Olsina J, Rotellar F, Carrillo A, Díaz H, Hernández J, Targarona E, Miras M, Morales-Conde S, Morales-Méndez S, Pereira F, Calafell J: [Analysis of the Spanish National Registry of Laparoscopic Pancreatic Surgery]. Cir Esp; 2006 May;79(5):293-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Análisis del Registro Nacional Español de la Cirugía Laparoscópica del Páncreas.
  • The final diagnosis included 42 neuroendocrine tumors, 40 cystic neoplasms, 24 cysts and pseudocysts, 8 inflammatory tumors, 8 ductal carcinomas, 7 intraductal papillary mucinous tumors, 1 acinar carcinoma and 2 solid pseudopapillary tumors.
  • Tumor enucleation was performed only in patients with insulinomas.

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Diseases.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16753119.001).
  • [ISSN] 0009-739X
  • [Journal-full-title] Cirugía española
  • [ISO-abbreviation] Cir Esp
  • [Language] spa
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Spain
  •  go-up   go-down


49. Robinson BD, Epstein JI: Intraductal carcinoma of the prostate without invasive carcinoma on needle biopsy: emphasis on radical prostatectomy findings. J Urol; 2010 Oct;184(4):1328-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intraductal carcinoma of the prostate without invasive carcinoma on needle biopsy: emphasis on radical prostatectomy findings.
  • PURPOSE: Limited information is available on radical prostatectomy findings in men with intraductal carcinoma of the prostate on needle core biopsy in the absence of invasive prostate cancer.
  • Of the 21 radical prostatectomies available for review findings revealed pathological stage pT3a in 8 (38%), pT3b in 3 (13%), pT2 in 8 (38%) and intraductal carcinoma without identifiable invasive cancer in 2 (10%).
  • In 15 prostatectomies (71%) there was extensive intraductal carcinoma, defined as greater than 10% of tumor being intraductal, including the 2 cases of intraductal carcinoma only.
  • Of the 19 prostatectomies with invasive adenocarcinoma 16 (84%) were conventional acinar adenocarcinoma, 2 (11%) ductal adenocarcinoma, and 1 (5%) mixed ductal and acinar adenocarcinoma.
  • CONCLUSIONS: At radical prostatectomy men in whom prior biopsies showed only intraductal carcinoma of the prostate typically have high grade (Gleason score 7 or greater) invasive adenocarcinoma and most have advanced stage disease (pT3).
  • Definitive therapy is recommended in men with intraductal carcinoma of the prostate on needle biopsy even in the absence of pathologically documented invasive prostate cancer.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma / surgery. Carcinoma, Intraductal, Noninfiltrating / pathology. Carcinoma, Intraductal, Noninfiltrating / surgery. Prostatectomy. Prostatic Neoplasms / pathology. Prostatic Neoplasms / surgery

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20723921.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


50. Kayed H, Bekasi S, Keleg S, Michalski CW, Giese T, Friess H, Kleeff J: BGLAP is expressed in pancreatic cancer cells and increases their growth and invasion. Mol Cancer; 2007;6:83
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.
  • 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

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


51. Li HC, Schmidt L, Greenson JK, Chang AC, Myers JL: Primary pulmonary adenocarcinoma with intestinal differentiation mimicking metastatic colorectal carcinoma: case report and review of literature. Am J Clin Pathol; 2009 Jan;131(1):129-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary pulmonary adenocarcinoma with intestinal differentiation mimicking metastatic colorectal carcinoma: case report and review of literature.
  • Pulmonary adenocarcinoma with intestinal differentiation is rare and typically expresses proteins common to lung primaries.
  • Additional clinical investigation, including positron emission tomography scan with fluorine 18-labeled fluorodeoxyglucose, colonoscopy, and capsule endoscopy of her small bowel, revealed no evidence of tumor elsewhere.
  • Histologic examination revealed tall columnar cells without goblet cell differentiation arranged in a cribriform and acinar pattern with extensive central necrosis.
  • Metastatic carcinoma was present in multiple hilar lymph nodes.
  • This is the first description of pulmonary adenocarcinoma with intestinal differentiation with histopathologic and immunophenotypic findings indistinguishable from metastatic colorectal adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Colorectal Neoplasms / secondary. Lung Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19095576.001).
  • [ISSN] 1943-7722
  • [Journal-full-title] American journal of clinical pathology
  • [ISO-abbreviation] Am. J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Keratin-20; 0 / Trans-Activators; 156560-97-3 / Cdx-2-3 protein
  • [Number-of-references] 18
  •  go-up   go-down


52. Awadallah NS, Shroyer KR, Langer DA, Torkko KC, Chen YK, Bentz JS, Papkoff J, Liu W, Nash SR, Shah RJ: Detection of B7-H4 and p53 in pancreatic cancer: potential role as a cytological diagnostic adjunct. Pancreas; 2008 Mar;36(2):200-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: This study compared p53 expression with B7-H4, a novel cancer biomarker, in pancreatic ductal adenocarcinoma (PDA) resection specimens and in a pilot series of endoscopic ultrasound-guided fine-needle aspirations (EUS-FNAs).
  • Some benign tissue components (intercalated cells/ducts, main pancreatic ducts, and acinar cells) were also positive for B7-H4 and/or p53.
  • Overall expression of B7-H4 in benign tissues, however, was relatively low compared with that seen in most carcinoma cases.
  • [MeSH-major] Antigens, CD80 / analysis. Biomarkers, Tumor / analysis. Carcinoma, Pancreatic Ductal / chemistry. Pancreatic Neoplasms / chemistry. Tumor Suppressor Protein p53 / analysis
  • [MeSH-minor] Adult. Aged. Biopsy, Fine-Needle / methods. Endosonography. Female. Humans. Immunoenzyme Techniques. Male. Middle Aged. Neoplasm Staging. Pancreas / chemistry. Pilot Projects. Predictive Value of Tests. Reproducibility of Results. Tissue Fixation. V-Set Domain-Containing T-Cell Activation Inhibitor 1

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18376314.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD80; 0 / Biomarkers, Tumor; 0 / TP53 protein, human; 0 / Tumor Suppressor Protein p53; 0 / V-Set Domain-Containing T-Cell Activation Inhibitor 1; 0 / VTCN1 protein, human
  •  go-up   go-down


53. Maruya S, Shirasaki T, Nagaki T, Kakehata S, Kurotaki H, Mizukami H, Shinkawa H: Differential expression of topoisomerase IIalpha protein in salivary gland carcinomas: histogenetic and prognostic implications. BMC Cancer; 2009;9:72
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Differential expression of topoisomerase IIalpha protein in salivary gland carcinomas: histogenetic and prognostic implications.
  • BACKGROUND: Salivary gland carcinomas are relatively uncommon heterogeneous malignancies characterized by locoregional invasion and distant metastasis.
  • Topoisomerase IIalpha (topoIIalpha), located at chromosome 17q21-22, is considered a major mediator of cell proliferation and DNA replication.
  • The purpose of this study was to evaluate the expression of topoIIalpha in various types of salivary gland tumors and its biological significance.
  • METHODS: The protein expression of topoIIalpha was evaluated immunohistochemically in formalin-fixed, paraffin-embedded tissue from 54 salivary gland carcinomas and 20 benign tumors (10 pleomorphic adenomas and 10 Warthin's tumors).
  • The primary salivary gland carcinoma specimens consisted of 17 adenoid cystic carcinomas, 7 adenocarcinomas not otherwise specified, 7 mucoepidermoid carcinomas, 6 salivary duct carcinomas, 3 acinic cell carcinomas, 3 carcinomas ex pleomorphic adenomas, 3 epithelial-myoepithelial carcinomas, 2 carcinosarcomas, 2 lymphoepithelial carcinomas, 2 myoepithelial carcinomas, 1 oncocytic carcinoma, and 1 squamous cell carcinoma.
  • RESULTS: Of the 54 primary salivary gland carcinomas, 38 (70%) showed positive expression (> or = 10%) of topoIIalpha protein, and 16 carcinomas (30%) and all benign tumors were negative (p < 0.001).
  • Expression of topoIIalpha was more frequently observed in salivary duct carcinoma, carcinoma ex pleomorphic adenoma, adenocarcinoma, and adenoid cystic carcinoma, solid type, and it was associated with advanced stage and shortened survival.
  • Furthermore, it may provide useful prognostic information and suggests the potential efficacy of topoIIalpha-targeting therapy in patients with salivary gland carcinoma.
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Carcinoma, Adenoid Cystic / enzymology. Carcinoma, Adenoid Cystic / pathology. Child. Female. Humans. Immunohistochemistry. Male. Middle Aged. Prognosis. Survival Rate. Young Adult

  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Head Neck. 2000 Aug;22(5):489-97 [10897109.001]
  • [Cites] Head Neck. 2008 May;30(5):680-3 [17972317.001]
  • [Cites] Clin Cancer Res. 2002 Apr;8(4):1061-7 [11948114.001]
  • [Cites] Clin Cancer Res. 2002 May;8(5):1107-16 [12006526.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Jun;3(6):430-40 [12042765.001]
  • [Cites] Lancet Oncol. 2002 Apr;3(4):235-43 [12067686.001]
  • [Cites] ORL J Otorhinolaryngol Relat Spec. 2003 Jan-Feb;65(1):26-32 [12624503.001]
  • [Cites] Am J Clin Pathol. 2003 May;119(5):715-22 [12760291.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4682-8 [14581337.001]
  • [Cites] Int J Oncol. 2004 Jan;24(1):201-9 [14654958.001]
  • [Cites] Anticancer Res. 2003 Sep-Oct;23(5A):3965-70 [14666704.001]
  • [Cites] Clin Cancer Res. 2004 Feb 1;10(3):944-6 [14871971.001]
  • [Cites] J Otolaryngol. 2003 Oct;32(5):328-31 [14974865.001]
  • [Cites] Mod Pathol. 2004 Jun;17(6):637-45 [15044918.001]
  • [Cites] Arch Otolaryngol. 1984 Mar;110(3):172-6 [6322732.001]
  • [Cites] Cancer. 1984 Sep 15;54(6):1062-9 [6088017.001]
  • [Cites] Oncology (Williston Park). 1998 May;12(5):671-80; discussion 683 [9597678.001]
  • [Cites] Pathol Res Pract. 2005;200(11-12):791-9 [15792122.001]
  • [Cites] Breast Cancer Res. 2005;7(3):R374-84 [15987433.001]
  • [Cites] J Clin Oncol. 2006 Jun 10;24(17):2673-8 [16763282.001]
  • [Cites] Cancer Treat Rev. 2007 Feb;33(1):64-77 [17113234.001]
  • [Cites] Oral Oncol. 2007 Sep;43(8):735-41 [17113340.001]
  • [Cites] Head Neck. 2007 Nov;29(11):1002-9 [17427971.001]
  • [Cites] Hum Pathol. 2001 Jun;32(6):596-604 [11431714.001]
  • (PMID = 19250538.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  • [Other-IDs] NLM/ PMC2654461
  •  go-up   go-down


54. Liu YL, Matsuzaki T, Nakazawa T, Murata S, Nakamura N, Kondo T, Iwashina M, Mochizuki K, Yamane T, Takata K, Katoh R: Expression of aquaporin 3 (AQP3) in normal and neoplastic lung tissues. Hum Pathol; 2007 Jan;38(1):171-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To investigate the expression of AQP3 in normal and neoplastic lung tissues, we studied a series of 149 lung carcinoma tissues and 2 cell lines by immunohistochemistry, Western blotting, and reverse transcriptase-polymerase chain reaction.
  • In lung carcinomas, AQP3 expression was observed in 59 (70.2%) of 84 adenocarcinomas.
  • Squamous cell carcinoma and large cell carcinoma had rather low positive ratios (35.8% and 13.4%, respectively).
  • No AQP3 expression was demonstrated in small cell carcinoma, pleomorphic carcinoma, or metastatic colon adenocarcinoma.
  • In adenocarcinomas, AQP3 was detected in all tumors of bronchioloalveolar subtype.
  • Papillary subtype also showed a higher positive ratio of AQP3 compared with that in acinar and solid with mucin subtypes.
  • In addition, AQP3 expression was related to tumor differentiation and clinical stage in adenocarcinomas.
  • Western blotting and reverse transcriptase-polymerase chain reaction analyses confirmed the expression of AQP3 protein and messenger RNA in cell lines and tissues of lung adenocarcinoma.
  • In addition, lung carcinomas, especially adenocarcinomas, can produce AQP3, possibly in connection with their functional and/or biological nature, although the detailed mechanism of AQP3 expression in lung carcinomas remains to be clarified.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Blotting, Western. Cell Line, Tumor. Female. Gene Expression. Humans. Immunohistochemistry. Male. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17056099.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 158801-98-0 / Aquaporin 3
  •  go-up   go-down


55. Shet T, Ghodke R, Kane S, Chinoy RN: Cytomorphologic patterns in papillary cystic variant of acinic cell carcinoma of the salivary gland. Acta Cytol; 2006 Jul-Aug;50(4):388-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytomorphologic patterns in papillary cystic variant of acinic cell carcinoma of the salivary gland.
  • OBJECTIVE: To study the cytomorphologic profile of the papillary and cystic variant of acinic cell carcinoma (ACC-PCV) of the salivary glands.
  • However, common to all was a papillary pattern and a cystic fluid background with or without mucin blobs; that led to misdiagnosing the tumor as mucoepidermoid carcinoma on 2 occasions.
  • The granular cells were similar to those seen in the usual acinic cell carcinoma but were smaller.
  • The tumor did not show any acinar pattern and lacked naked nuclei in the background.
  • CONCLUSION: ACC-PCV is papillary and cystic and hence is often not recognized as acinic cell carcinoma.
  • However, papillary fragments of vacuolated cells or histiocytelike cells and granular cells are clues to the diagnosis.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Cysts / pathology. Salivary Glands / pathology

  • Genetic Alliance. consumer health - Acinic Cell Carcinoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16901000.001).
  • [ISSN] 0001-5547
  • [Journal-full-title] Acta cytologica
  • [ISO-abbreviation] Acta Cytol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


56. Yoshida T, Shiraki N, Baba H, Goto M, Fujiwara S, Kume K, Kume S: Expression patterns of epiplakin1 in pancreas, pancreatic cancer and regenerating pancreas. Genes Cells; 2008 Jul;13(7):667-78
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Eppk1 is observed in pancreatic intraepithelial neoplasia (PanIN), previously identified as pancreatic ductal adenocarcinoma (PDAC) precursor lesions.
  • In addition, the expansion of Eppk1-positive cells occurs in a caerulein-induced acute pancreatitis, an acinar cell regeneration model.
  • [MeSH-minor] Animals. Biomarkers / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Carcinoma, Pancreatic Ductal / pathology. Gene Expression Regulation, Neoplastic / physiology. Mice. Mice, Knockout. Mice, Transgenic. Stem Cells / cytology. Stem Cells / metabolism


57. Li W, Nakagawa T, Koyama N, Wang X, Jin J, Mizuno-Horikawa Y, Gu J, Miyoshi E, Kato I, Honke K, Taniguchi N, Kondo A: Down-regulation of trypsinogen expression is associated with growth retardation in alpha1,6-fucosyltransferase-deficient mice: attenuation of proteinase-activated receptor 2 activity. Glycobiology; 2006 Oct;16(10):1007-19
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Trypsin, an active form of trypsinogen, regulates cell growth through a G-protein-coupled receptor, the proteinase-activated receptor 2 (PAR-2).
  • In a cell culture system, a Fut8 knockdown mouse pancreatic acinar cell carcinoma, TGP49-Fut8-KDs, showed decreased growth rate, similar to that seen in Fut8-/- mice, and the decreased growth rate was rescued by the application of the PAR-2-activating peptide (SLIGRL-NH2).
  • Our findings clearly demonstrate a relationship between Fut8 and the regulation of EGF receptor (EGFR)-trypsin-PAR-2 pathway in controlling cell growth and that the EGFR-trypsin-PAR-2 pathway is suppressed in TGP49-Fut8-KDs as well as in Fut8-/- mice.
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Down-Regulation. Embryo, Mammalian / metabolism. Male. Mice. Mice, Knockout. Oligopeptides / pharmacology. Phosphorylation. Receptor, Epidermal Growth Factor / metabolism. Tumor Cells, Cultured

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16861703.001).
  • [ISSN] 0959-6658
  • [Journal-full-title] Glycobiology
  • [ISO-abbreviation] Glycobiology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Oligopeptides; 0 / Receptor, PAR-2; 0 / seryl-leucyl-isoleucyl-glycyl--arginyl-leucinamide; 9002-08-8 / Trypsinogen; EC 2.4.1.- / Fucosyltransferases; EC 2.4.1.68 / Glycoprotein 6-alpha-L-fucosyltransferase; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


58. Vargas PA, Torres-Rendon A, Speight PM: DNA ploidy analysis in salivary gland tumours by image cytometry. J Oral Pathol Med; 2007 Jul;36(6):371-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIM: To determine whether DNA ploidy by image cytometry is a good diagnostic tool to distinguish benign and malignant salivary gland tumours.
  • According to the World Health Organization (WHO) classification, there were 14 mucoepidermoid carcinomas (MEC), 11 adenoid cystic carcinomas (ACC), 10 pleomorphic adenomas (PA), 10 carcinoma ex PA (CEPA), 9 acinic cell carcinomas (ACCa), 3 polymorphous low-grade adenocarcinomas (PLGA), 2 papillary cystadenocarcinomas (PC), 1 myoepithelial carcinoma (MC), 1 undifferentiated carcinoma (UC) and 1 mucinous adenocarcinoma (MA).
  • Paraffin sections (40 microm) were micro-dissected to isolate tumour areas; cell nuclei were extracted and Feulgen-stained cytospin monolayers were analysed using a DNA image cytometry system.
  • High-grade malignancies may be aneuploid, and ploidy may be useful to identify malignant change in atypical PA.

  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17559500.001).
  • [ISSN] 0904-2512
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / DNA, Neoplasm
  •  go-up   go-down


59. Shi G, Zhu L, Sun Y, Bettencourt R, Damsz B, Hruban RH, Konieczny SF: Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia. Gastroenterology; 2009 Apr;136(4):1368-78
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Loss of the acinar-restricted transcription factor Mist1 accelerates Kras-induced pancreatic intraepithelial neoplasia.
  • BACKGROUND & AIMS: Invasive pancreatic ductal adenocarcinoma is thought to originate from duct-like lesions called pancreatic intraepithelial neoplasia (PanIN).
  • METHODS: In this study, we examined the importance of the acinar-restricted transcription factor Mist1 to KrasG12D-induced mouse PanIN (mPanIN) formation in 3 different mouse models of pancreatic cancer.
  • RESULTS: In the absence of Mist1 (Mist1KO), KrasG12D-expressing mice exhibited severe exocrine pancreatic defects that were rescued by ectopic expression of Mist1 in acinar cells. mPanIN development was greatly accelerated in Mist1KO/KrasG12D/+ pancreata, and in vitro assays revealed that Mist1KO acinar cells were predisposed to convert to a ductal phenotype and activate epidermal growth factor receptor (EGFR) and Notch-signaling pathways.
  • CONCLUSIONS: We propose that convergence of EGFR, Notch, and Kras pathways in acinar cells lacking Mist1 leads to enhanced mPanIN formation.

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Anat Rec. 2000 Jun 1;259(2):157-67 [10820318.001]
  • [Cites] Clin Cancer Res. 2000 Aug;6(8):2969-72 [10955772.001]
  • [Cites] Genes Dev. 2001 Feb 1;15(3):286-93 [11159909.001]
  • [Cites] Am J Surg Pathol. 2001 May;25(5):579-86 [11342768.001]
  • [Cites] J Cell Biol. 2001 Nov 12;155(4):519-30 [11696558.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630.001]
  • [Cites] Gut. 2002 Dec;51(6):849-52 [12427788.001]
  • [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] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]
  • [Cites] J Cell Sci. 2003 Aug 15;116(Pt 16):3315-25 [12829745.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):111-20 [12957286.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] Mech Dev. 2004 Mar;121(3):261-72 [15003629.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(7):2673-81 [15024058.001]
  • [Cites] N Engl J Med. 2004 Sep 16;351(12):1218-26 [15371579.001]
  • [Cites] Cell. 1990 Jun 15;61(6):1121-35 [1693546.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Aug 28;237(3):752-7 [9299439.001]
  • [Cites] Adv Anat Pathol. 2005 Mar;12(2):81-91 [15731576.001]
  • [Cites] Cancer Res. 2005 Mar 1;65(5):1619-26 [15753353.001]
  • [Cites] J Biol Chem. 2005 Apr 1;280(13):12668-75 [15665001.001]
  • [Cites] Gastroenterology. 2005 May;128(6):1606-25 [15887154.001]
  • [Cites] Cancer Cell. 2005 May;7(5):469-83 [15894267.001]
  • [Cites] Development. 2005 Aug;132(16):3767-76 [16020518.001]
  • [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] CA Cancer J Clin. 2006 Mar-Apr;56(2):106-30 [16514137.001]
  • [Cites] Best Pract Res Clin Gastroenterol. 2006 Apr;20(2):211-26 [16549325.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4437-42 [17360542.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2007 Apr;292(4):G1123-32 [17170023.001]
  • [Cites] Am J Pathol. 2007 Jul;171(1):263-73 [17591971.001]
  • [Cites] Cancer Cell. 2007 Sep;12(3):266-79 [17785207.001]
  • [Cites] Cancer Res. 2007 Sep 1;67(17):8121-30 [17804724.001]
  • [Cites] Gastroenterology. 2007 Dec;133(6):1999-2009 [18054571.001]
  • [Cites] Annu Rev Pathol. 2008;3:157-88 [18039136.001]
  • [Cites] Gastroenterology. 2008 Nov;135(5):1687-97 [18762186.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18907-12 [19028876.001]
  • (PMID = 19249398.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK055489-10; United States / NCI NIH HHS / CA / P50CA62924; United States / NCI NIH HHS / CA / R01 CA124586-02; United States / NCI NIH HHS / CA / P50 CA062924; United States / NIDDK NIH HHS / DK / DK055489-10; United States / NCI NIH HHS / CA / CA124586-02; United States / NIDDK NIH HHS / DK / DK55489; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586; United States / NCI NIH HHS / CA / CA124586
  • [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 / Basic Helix-Loop-Helix Transcription Factors; 0 / Mist1 protein, mouse; 0 / Receptors, Notch; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ NIHMS182460; NLM/ PMC2845927
  •  go-up   go-down


60. Ohike N, Morohoshi T: Pathological assessment of pancreatic endocrine tumors for metastatic potential and clinical prognosis. Endocr Pathol; 2005;16(1):33-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pathological assessment of pancreatic endocrine tumors for metastatic potential and clinical prognosis.
  • The prognostic significance of several pathological factors (tumor size, mitotic index, Ki-67 labeling index, and vascular invasion) and expression of exocrine markers (CA19-9, CEA, AFP, and trypsin) in pancreatic endocrine tumors was studied.
  • A total of 20 specimens of metastasizing (n = 10) and non-metastasizing (n = 10) tumors were subjected to histological and immunohistochemical examination.
  • The metastasizing tumors showed significantly larger size, higher Ki-67 labeling index, increased number of mitotic cells, and more frequent vascular invasion in comparison with the non-metastasizing tumors.
  • It was difficult to determine the effect of individual factors on clinical outcome because of slow disease progression in almost all cases.
  • Numerous mitotic cells and widespread necrosis, however, were thought to indicate a poor prognosis, and tumors with these characteristics were regarded as high-grade malignant endocrine carcinomas.
  • In one case, one-third of the tumor tissue comprised trypsin-positive cells, the outcome was comparatively poor, and the behavior of the tumor resembled that of mixed acinar-endocrine carcinoma.
  • A simple multifactorial approach may be effective for the identification of tumors at increased risk of metastasis, but it remains difficult to determine clinical prognosis.
  • It is essential to at least distinguish high-grade endocrine carcinomas from the more common endocrine tumors.
  • [MeSH-major] Carcinoma, Islet Cell / secondary. Islets of Langerhans / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Disease-Free Survival. Female. Humans. Ki-67 Antigen / metabolism. Male. Middle Aged. Mitotic Index. Neoplasm Invasiveness. Prognosis

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2002 Jun 1;20(11):2633-42 [12039924.001]
  • [Cites] Semin Diagn Pathol. 2000 May;17(2):104-8 [10839610.001]
  • [Cites] Cancer. 1987 Feb 15;59(4):739-47 [3542187.001]
  • [Cites] Surgery. 1998 Dec;124(6):1153-9 [9854597.001]
  • [Cites] Cancer. 1985 Sep 15;56(6):1420-9 [2992737.001]
  • [Cites] Pathol Int. 2001 Oct;51(10):770-7 [11881729.001]
  • [Cites] Endocr Pathol. 1997 Autumn;8(3):181-187 [12114721.001]
  • [Cites] Am J Surg Pathol. 1992 Dec;16(12):1215-25 [1281387.001]
  • [Cites] Am J Clin Pathol. 1998 Mar;109(3):286-93 [9495200.001]
  • [Cites] Am J Surg Pathol. 1994 Aug;18(8):765-78 [8037290.001]
  • [Cites] Endocr Pathol. 2001 Fall;12(3):351-4 [11740056.001]
  • [Cites] Endocr Pathol. 2000 Autumn;11(3):229-241 [12114695.001]
  • [Cites] Virchows Arch. 2003 Mar;442(3):258-65 [12647216.001]
  • [Cites] Hum Pathol. 1996 Nov;27(11):1124-34 [8912819.001]
  • [Cites] Cancer Res. 2001 Jul 1;61(13):5186-92 [11431358.001]
  • [Cites] Cancer. 1983 Jan 15;51(2):277-82 [6821817.001]
  • [Cites] Cancer. 1992 Nov 1;70(9):2268-77 [1356613.001]
  • [Cites] Virchows Arch. 2004 Sep;445(3):231-5 [15517367.001]
  • [Cites] Pathol Res Pract. 1988 Apr;183(2):155-68 [2898775.001]
  • (PMID = 16000844.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen
  •  go-up   go-down


61. Hansel DE, Nadasdy T, Epstein JI: Fibromyxoid nephrogenic adenoma: a newly recognized variant mimicking mucinous adenocarcinoma. Am J Surg Pathol; 2007 Aug;31(8):1231-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Fibromyxoid nephrogenic adenoma: a newly recognized variant mimicking mucinous adenocarcinoma.
  • Nephrogenic adenomas demonstrate a variety of morphologic patterns that may occasionally be confused with malignant processes, including urothelial and prostatic carcinoma.
  • In this series, we describe 8 cases of nephrogenic adenoma that contain an admixture of the classic tubular form of nephrogenic adenoma and an unusual spindled and fibromyxoid form of nephrogenic adenoma that closely mimics infiltrating carcinoma.
  • All 8 patients were elderly men who had a prior or concurrent history of acinar prostate cancer (n=4), combined acinar prostate and urothelial carcinoma (n=1), urothelial-type adenocarcinoma of the prostate (n=1), bladder urothelial carcinoma (n=1), or no prior reported prostatic or urothelial abnormalities (n=1).
  • Awareness of this entity and the use of ancillary techniques can aid in the diagnosis of this unusual form of nephrogenic adenoma.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Adenoma / pathology. Fibroma / pathology. Urologic Neoplasms / pathology
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Diagnosis, Differential. Humans. Male. Middle Aged. Mucins / analysis. Neoplasms, Multiple Primary. Urothelium / chemistry. Urothelium / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17667548.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Mucins
  •  go-up   go-down


62. Luukkaa H, Klemi P, Hirsimäki P, Vahlberg T, Kivisaari A, Kähäri VM, Grénman R: Matrix metalloproteinase (MMP)-1, -9 and -13 as prognostic factors in salivary gland cancer. Acta Otolaryngol; 2008 Apr;128(4):482-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CONCLUSIONS: In the current study matrix metalloproteinases (MMPs)-9 and -13 were associated with the prognosis in salivary gland cancer (SGC), indicating that they contribute to the progression and invasion of these malignant tumours.
  • High MMP-13 intensity (2+3 vs 1; p=0.05), percentage (2 vs 1; p=0.03) and index (3 vs 1; p=0.02) were associated with poor survival in acinic cell carcinoma.
  • However, high MMP-9 index in adenoid cystic carcinoma (p=0.06) and the percentage of positively staining cells in salivary duct carcinoma patients (p=0.05) was associated with poor survival.
  • [MeSH-major] Carcinoma / enzymology. Matrix Metalloproteinase 1 / metabolism. Matrix Metalloproteinase 13 / metabolism. Matrix Metalloproteinase 9 / metabolism. Salivary Gland Neoplasms / enzymology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Female. Finland / epidemiology. Follow-Up Studies. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Staging. Prognosis. Retrospective Studies. Survival Rate / trends. Time Factors

  • Genetic Alliance. consumer health - Salivary Gland Cancer.
  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18368586.001).
  • [ISSN] 0001-6489
  • [Journal-full-title] Acta oto-laryngologica
  • [ISO-abbreviation] Acta Otolaryngol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 3.4.24.- / Matrix Metalloproteinase 13; EC 3.4.24.35 / Matrix Metalloproteinase 9; EC 3.4.24.7 / Matrix Metalloproteinase 1
  •  go-up   go-down


63. Ando K, Ohkuni Y, Kaneko N, Narita M: Spontaneous rupture of the splenic metastasis in acinar cell carcinoma. Pancreas; 2009 Oct;38(7):836-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spontaneous rupture of the splenic metastasis in acinar cell carcinoma.
  • [MeSH-major] Carcinoma, Acinar Cell / secondary. Pancreatic Neoplasms / pathology. Spleen / pathology. Splenic Neoplasms / secondary
  • [MeSH-minor] Diagnosis, Differential. Fatal Outcome. Humans. Immunohistochemistry. Lung Neoplasms / diagnosis. Lung Neoplasms / metabolism. Lung Neoplasms / secondary. Male. Middle Aged. Rupture, Spontaneous. alpha 1-Antichymotrypsin / metabolism. alpha 1-Antitrypsin / metabolism

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19893460.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / alpha 1-Antichymotrypsin; 0 / alpha 1-Antitrypsin
  •  go-up   go-down


64. Osumi D, Takahashi M, Miyoshi E, Yokoe S, Lee SH, Noda K, Nakamori S, Gu J, Ikeda Y, Kuroki Y, Sengoku K, Ishikawa M, Taniguchi N: Core fucosylation of E-cadherin enhances cell-cell adhesion in human colon carcinoma WiDr cells. Cancer Sci; 2009 May;100(5):888-95
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Core fucosylation of E-cadherin enhances cell-cell adhesion in human colon carcinoma WiDr cells.
  • To investigate the correlation between alpha1,6-fucosyltransferase and E-cadherin expression, we introduced alpha1,6-fucosyltransferase in WiDr human colon carcinoma cells.
  • It was revealed that the low molecular weight population of E-cadherin was significantly increased in alpha1,6-fucosyltransferase-transfected WiDr cells in dense culture, which resulted in an enhancement in cell-cell adhesion.
  • In alpha1,6-fucosyltransferase knock down mouse pancreatic acinar cell carcinoma TGP49 cells, the expression of E-cadherin and E-cadherin dependent cell-cell adhesion was decreased.
  • The introduction of alpha1,6-fucosyltransferase into kidney epithelial cells from alpha1,6-fucosyltransferase(-/-) mice restored the expression of E-cadherin and E-cadherin-dependent cell-cell adhesion.
  • These results suggest a possible role of core fucosylation in the regulation of cell-cell adhesion in cancer.
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Cell Adhesion. Cell Line, Tumor. Female. Fucosyltransferases / deficiency. Fucosyltransferases / genetics. Fucosyltransferases / metabolism. Humans. Male

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19302290.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cadherins; 3713-31-3 / Fucose; EC 2.4.1.- / Fucosyltransferases; EC 2.4.1.68 / Glycoprotein 6-alpha-L-fucosyltransferase
  •  go-up   go-down


65. Thomas JS, Kerr GR, Jack WJ, Campbell F, McKay L, Pedersen HC, Kunkler IH, Cameron DA, Chetty U, Bartlett JM: Histological grading of invasive breast carcinoma--a simplification of existing methods in a large conservation series with long-term follow-up. Histopathology; 2009 Dec;55(6):724-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Histological grading of invasive breast carcinoma--a simplification of existing methods in a large conservation series with long-term follow-up.
  • METHODS AND RESULTS: A single pathologist (J.St.J.T) graded 1650 cases using the Elston and Ellis method (EE) with particular reference to the component data: acinar differentiation, nuclear pleomorphism and mitotic counts.

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19845790.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


66. Yamaguchi R, Okabe Y, Jimi A, Shiota K, Kodama T, Naito Y, Yasunaga M, Kinoshita H, Kojiro M: Pancreatic acinar cell carcinoma extending into the common bile and main pancreatic ducts. Pathol Int; 2006 Oct;56(10):633-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic acinar cell carcinoma extending into the common bile and main pancreatic ducts.
  • Acinar cell carcinoma (ACC) of the pancreas is relatively rare, accounting for only approximately 1% of all exocrine pancreatic tumors.
  • Magnetic resonance cholangiopancreatography showed defect of the lower common bile duct (CBD) due to obstruction by the tumor cast.
  • Histopathologically, the pancreatic head tumor invaded the main pancreatic duct (MPD) and CBD with extension into the CBD in a form of tumor cast.
  • The tumor cells consisted of a solid proliferation with abundant eosinophilic cytoplasm and round nuclei in an acinar and trabecular fashion.
  • Histopathologically, the tumor was encapsulated by fibrous capsule and had extensive central necrosis with solid areas in the tumor periphery, and invaded with extension into the MPD in a form of tumor cast.
  • The tumor cells resembled acinar cells in solid growths.
  • Two resected cases of ACC with unusual tumor extension into the CBD and the MPD, respectively, are reported.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Common Bile Duct / pathology. Common Bile Duct Neoplasms / pathology. Pancreatic Ducts / pathology. Pancreatic Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16984622.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  •  go-up   go-down


67. Mazzullo G, Sfacteria A, Ianelli N, De Majo M, Pennisi MG: Carcinoma of the submandibular salivary glands with multiple metastases in a cat. Vet Clin Pathol; 2005;34(1):61-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carcinoma of the submandibular salivary glands with multiple metastases in a cat.
  • Slides were stained with May-Grünwald Giemsa, and a diagnosis of salivary gland carcinoma was made.
  • At surgery, the tumor was found to involve both submandibular salivary glands as well as adjacent lymph nodes and surrounding tissues.
  • The majority of tissues and organs examined histologically, including mandibular and retropharyngeal lymph nodes, soft palate, laryngopharynx and lungs, contained neoplastic cells whose appearance was consistent with adenocarcinoma.
  • Bilateral salivary adenocarcinoma has not previously been reported in cats, and extensive metastases are rare.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15732021.001).
  • [ISSN] 0275-6382
  • [Journal-full-title] Veterinary clinical pathology
  • [ISO-abbreviation] Vet Clin Pathol
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


68. Takechi Y, Shinozaki T, Fukuda T, Asami K, Yanagawa T, Takagishi K: Multiple subcutaneous inflammation, osteolysis, and polyarthritis. Skeletal Radiol; 2010 Jun;39(6):581-2, 601-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-major] Arthritis / diagnosis. Carcinoma, Acinar Cell / diagnosis. Dermatitis / diagnosis. Fat Necrosis / diagnosis. Osteolysis / diagnosis. Pancreatic Neoplasms / diagnosis. Pancreatitis / diagnosis

  • MedlinePlus Health Information. consumer health - Arthritis.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • MedlinePlus Health Information. consumer health - Pancreatitis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20174794.001).
  • [ISSN] 1432-2161
  • [Journal-full-title] Skeletal radiology
  • [ISO-abbreviation] Skeletal Radiol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


69. Gürbüz Y, Yildiz K, Aydin O, Almaç A: Immunophenotypical profiles of salivary gland tumours: a new evidence for their histogenetic origin. Pathologica; 2006 Apr;98(2):147-52
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 30 cases of salivary gland tumours (18 pleomorphic adenomas, 8 Warthin's tumours, 2 basal cell adenomas, 2 acinic cell carcinomas) were included in our study.
  • CK14 was found in all tumours except acinic cell carcinomas (p < 0.0001).
  • [MeSH-minor] Adenolymphoma / chemistry. Adenolymphoma / pathology. Adenoma / chemistry. Adenoma / pathology. Adenoma, Pleomorphic / chemistry. Adenoma, Pleomorphic / pathology. Carcinoma, Acinar Cell / chemistry. Carcinoma, Acinar Cell / pathology. Humans. Immunophenotyping. Organ Specificity. Protein Isoforms / analysis. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16929788.001).
  • [ISSN] 0031-2983
  • [Journal-full-title] Pathologica
  • [ISO-abbreviation] Pathologica
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Actins; 0 / Neoplasm Proteins; 0 / Protein Isoforms; 68238-35-7 / Keratins
  •  go-up   go-down


70. Tapia B, Ahrens W, Kenney B, Touloukian R, Reyes-Múgica M: Acinar cell carcinoma versus solid pseudopapillary tumor of the pancreas in children: a comparison of two rare and overlapping entities with review of the literature. Pediatr Dev Pathol; 2008 Sep-Oct;11(5):384-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • [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

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


71. National Toxicology Program: Toxicology and carcinogenesis studies of 2,3',4,4',5-pentachlorobiphenyl (PCB 118) (CAS No. 31508-00-6) in female harlan Sprague-Dawley rats (gavage studies). Natl Toxicol Program Tech Rep Ser; 2010 Nov;(559):1-174
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • There were increases in hepatic cell proliferation in the 4,600 g/kg group at 14, 31, and 53 weeks.
  • At 2 years, a significant dose-related increase in hepatic toxicity was observed and was characterized by increased incidences of numerous lesions including hepatocyte hypertrophy, inflammation, oval cell hyperplasia, pigmentation, multinucleated hepatocyte, eosinophilic and mixed cell foci, diffuse fatty change, toxic hepatopathy, nodular hyperplasia, necrosis, bile duct hyperplasia and cyst, and cholangiofibrosis.
  • The incidence of carcinoma of the uterus in the 4,600 g/kg stop-exposure group was significantly greater than those in the vehicle control and 4,600 g/kg core study groups at 2 years.
  • A marginal increase in squamous cell carcinoma occurred in the 220 g/kg group.
  • At 2 years, there were marginally increased incidences of exocrine pancreatic adenoma or carcinoma in the 460, 1,000, and 4,600 g/kg core study groups.
  • Numerous nonneoplastic effects were seen in other organs including: adrenal cortical atrophy and cytoplasmic vacuolization, pancreatic acinar cell cytoplasmic vacuolization and arterial chronic active inflammation, follicular cell hypertrophy of the thyroid gland, inflammation and respiratory epithelial hyperplasia of the nose, and kidney pigmentation.
  • Occurrences of carcinoma in the uterus were considered to be related to the administration of PCB 118.
  • Occurrences of squamous cell carcinoma of the uterus and acinar neoplasms of the pancreas may have been related to administration of PCB 118.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21383778.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 31508-00-6 / 2,3',4,4',5-pentachlorobiphenyl; DFC2HB4I0K / Polychlorinated Biphenyls; DO80M48B6O / Tetrachlorodibenzodioxin
  •  go-up   go-down


72. Zhu L, Shi G, Schmidt CM, Hruban RH, Konieczny SF: Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia. Am J Pathol; 2007 Jul;171(1):263-73
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinar cells contribute to the molecular heterogeneity of pancreatic intraepithelial neoplasia.
  • A number of studies have shown that pancreatic ductal adenocarcinoma develops through precursor lesions termed pancreatic intraepithelial neoplasia (PanIN).
  • What remains unanswered is the identification of the individual cell type(s) that contributes to pancreatic ductal adenocarcinoma formation.
  • To follow the cellular and molecular changes that occur in acinar and duct cell properties on Kras(G12D) expression, we took advantage of LSL-Kras(G12D/+)/p48(Cre/+) mice, which faithfully mimic the human disease.
  • In young animals (4 weeks), the predominant cellular alteration in the exocrine pancreas was acinar metaplasia in which individual acini consisted of acinar cells and duct-like cells.
  • Metaplastic acinar structures were highly proliferative, expressed Notch target genes, and exhibited mosaic expression patterns for epidermal growth factor receptor, ErbB2, and pErk.
  • This expression pattern paralleled the expression pattern detected in mouse PanINs, suggesting that mouse PanINs and acinar-ductal metaplasia follow similar molecular pathways.
  • Indeed, immunofluorescence studies confirmed the presence of acinar cells within mPanIN lesions, raising the possibility that Kras(G12D)-induced mPanINs develop from acinar cells that undergo acinar-ductal metaplasia.
  • Identification of an acinar contribution to PanIN formation offers new directions for successful targeted therapeutic approaches to combat this disease.

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Biol. 2001 Nov 12;155(4):519-30 [11696558.001]
  • [Cites] Curr Opin Genet Dev. 2001 Oct;11(5):581-6 [11532402.001]
  • [Cites] Nat Rev Mol Cell Biol. 2002 Mar;3(3):187-94 [11994739.001]
  • [Cites] Cancer Cell. 2002 Jul;2(1):25-8 [12150822.001]
  • [Cites] Nat Genet. 2002 Sep;32(1):128-34 [12185368.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2005-9 [12727809.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):565-76 [12842085.001]
  • [Cites] Dev Biol. 2003 Aug 15;260(2):426-37 [12921743.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 9;100(25):14920-5 [14657333.001]
  • [Cites] Genes Dev. 2003 Dec 15;17(24):3112-26 [14681207.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] CA Cancer J Clin. 2004 Jan-Feb;54(1):8-29 [14974761.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(7):2673-81 [15024058.001]
  • [Cites] Cancer Cell. 2004 Sep;6(3):251-61 [15380516.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Sep 30;203(3):1589-98 [7945309.001]
  • [Cites] Nature. 1999 Aug 26;400(6747):877-81 [10476967.001]
  • [Cites] Cancer Res. 2005 Mar 1;65(5):1619-26 [15753353.001]
  • [Cites] Gastroenterology. 2005 Mar;128(3):728-41 [15765408.001]
  • [Cites] Gastroenterology. 2005 May;128(6):1606-25 [15887154.001]
  • [Cites] Cancer Cell. 2005 May;7(5):469-83 [15894267.001]
  • [Cites] Methods Mol Med. 2005;103:1-13 [15542896.001]
  • [Cites] Development. 2005 Aug;132(16):3767-76 [16020518.001]
  • [Cites] J Cell Mol Med. 2005 Jul-Sep;9(3):569-82 [16202206.001]
  • [Cites] Virchows Arch. 2005 Nov;447(5):800-5 [16021508.001]
  • [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] Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5947-52 [16585505.001]
  • [Cites] Am J Surg Pathol. 2006 Sep;30(9):1067-76 [16931950.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):291-302 [17349585.001]
  • [Cites] Nat Genet. 2000 Jan;24(1):36-44 [10615124.001]
  • [Cites] Anat Rec. 2000 Jun 1;259(2):157-67 [10820318.001]
  • [Cites] Clin Cancer Res. 2000 Aug;6(8):2969-72 [10955772.001]
  • [Cites] Am J Surg Pathol. 2001 May;25(5):579-86 [11342768.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630.001]
  • (PMID = 17591971.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA062924; United States / NIDDK NIH HHS / DK / DK55489; United States / NCI NIH HHS / CA / P50 CA62924; United States / NIDDK NIH HHS / DK / R01 DK055489; United States / NCI NIH HHS / CA / R01 CA124586
  • [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 / Carrier Proteins; 0 / Erbb2ip protein, mouse; 0 / Interferon-Stimulated Gene Factor 3, gamma Subunit; 0 / Isgf3g protein, mouse; 0 / Receptors, Notch
  • [Other-IDs] NLM/ PMC1941579
  •  go-up   go-down


73. Hrabar D, Aralica G, Gomercic M, Ljubicic N, Kruslin B, Tomas D: Epithelial and stromal expression of syndecan-2 in pancreatic carcinoma. Anticancer Res; 2010 Jul;30(7):2749-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Epithelial and stromal expression of syndecan-2 in pancreatic carcinoma.
  • The aim of the study was to determine the expression and prognostic role of syndecan-2 in patients with pancreatic adenocarcinoma.
  • PATIENTS AND METHODS: Syndecan-2 expression and its relationship with established prognostic features were assessed in a series of 53 patients with pancreatic ductal adenocarcinoma.
  • RESULTS: Epithelial expression was observed in 23 (43.4%) and stromal in 30 (56.6%) pancreatic carcinomas, respectively.
  • In normal pancreatic tissue, the epithelial expression was moderate or strong in single or small clusters of acinar cells and negative in ductal cells.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Pancreatic Neoplasms / metabolism. Syndecan-2 / biosynthesis

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20683009.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 149769-25-5 / Syndecan-2
  •  go-up   go-down


74. Suzuki A, Sakaguchi T, Morita Y, Oishi K, Fukumoto K, Inaba K, Takehara Y, Baba S, Suzuki S, Konno H: Long-term survival after a repetitive surgical approach in a patient with acinar cell carcinoma of the pancreas and recurrent liver metastases: report of a case. Surg Today; 2010 Jul;40(7):679-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term survival after a repetitive surgical approach in a patient with acinar cell carcinoma of the pancreas and recurrent liver metastases: report of a case.
  • Acinar cell carcinoma is a relatively rare malignant neoplasm, which represents 1%-2% of all pancreatic exocrine tumors.
  • This report concerns a case of a long-term survivor of metastatic acinar cell carcinoma who was successfully treated with repetitive surgery.
  • A 62-year-old man underwent a distal pancreatectomy for a pancreatic tumor, which was histologically diagnosed as an acinar cell carcinoma.
  • The tumor recurred in the liver three times within 41 months.
  • The patient has remained disease-free for 22 months since the last surgery and has survived 65 months since the initial diagnosis.
  • Although no consensus has been reached on surgery for metastatic acinar cell carcinoma, the current case has important implications for establishing an appropriate treatment strategy.
  • [MeSH-major] Carcinoma, Acinar Cell / surgery. Hepatectomy. Liver Neoplasms / surgery. Neoplasm Recurrence, Local / surgery. Pancreatectomy. Pancreatic Neoplasms / surgery

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] JOP. 2007 Nov 09;8(6):783-9 [17993731.001]
  • [Cites] J Comput Assist Tomogr. 2004 Mar-Apr;28(2):180-6 [15091120.001]
  • [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] Surgery. 2008 Aug;144(2):141-8 [18656619.001]
  • [Cites] Pancreas. 2007 Jul;35(1):42-6 [17575544.001]
  • [Cites] Surg Today. 2007;37(8):704-7 [17643220.001]
  • [Cites] Surg Today. 1996;26(5):357-60 [8726623.001]
  • [Cites] Am J Surg Pathol. 1987 Feb;11(2):85-93 [3812876.001]
  • [Cites] Pancreas. 2001 Jul;23(1):109-12 [11451140.001]
  • [Cites] Surg Today. 1996;26(9):762-4 [8883259.001]
  • [Cites] Am J Surg Pathol. 1992 Sep;16(9):815-37 [1384374.001]
  • [Cites] Pancreas. 2007 Mar;34(2):271-2 [17312470.001]
  • (PMID = 20582524.001).
  • [ISSN] 1436-2813
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


75. Valentich MA, Eynard AR, Barotto NN, Díaz MP, Bongiovanni GA: Effect of the co-administration of phenobarbital, quercetin and mancozeb on nitrosomethylurea-induced pancreatic tumors in rats. Food Chem Toxicol; 2006 Dec;44(12):2101-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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
  • [MeSH-minor] Alkylating Agents / toxicity. Animals. Animals, Newborn. Disease Models, Animal. Drug Interactions. Drug Therapy, Combination. Female. Hyperplasia / chemically induced. Hyperplasia / pathology. Maternal Exposure. Maternal-Fetal Exchange. Methylnitrosourea / toxicity. Pregnancy. Rats. Rats, Wistar

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • Hazardous Substances Data Bank. QUERCETIN .
  • Hazardous Substances Data Bank. Zineb .
  • Hazardous Substances Data Bank. Maneb .
  • Hazardous Substances Data Bank. Phenobarbital .
  • Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .
  • Hazardous Substances Data Bank. Mancozeb .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


76. La Rosa S, Franzi F, Marchet S, Finzi G, Clerici M, Vigetti D, Chiaravalli AM, Sessa F, Capella C: The monoclonal anti-BCL10 antibody (clone 331.1) is a sensitive and specific marker of pancreatic acinar cell carcinoma and pancreatic metaplasia. Virchows Arch; 2009 Feb;454(2):133-42
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The monoclonal anti-BCL10 antibody (clone 331.1) is a sensitive and specific marker of pancreatic acinar cell carcinoma and pancreatic metaplasia.
  • Acinar cell carcinoma (ACC) is a rare pancreatic cancer which may be difficult to distinguish from other solid nonadenocarcinoma tumors.
  • The diagnosis depends on the demonstration of acinar differentiation, obtained with antibodies recognizing various pancreatic enzymes that, although specific, show different sensitivity.
  • The C-terminal portion of the BCL10 protein shows homology with carboxyl ester hydrolase (CEH), an enzyme produced by pancreatic acinar cells.
  • We investigated the usefulness of a C-terminal BCL10 monoclonal antibody in the diagnosis of ACCs.
  • We examined normal pancreases and different pancreatic tumors including ACCs, mixed acinar-endocrine carcinomas, ductal adenocarcinomas, mucinous, serous, solid pseudopapillary, and endocrine neoplasms.
  • In addition, various normal tissues and cases of pancreatic metaplasia of the gastroesophageal mucosa, cases of ectopic pancreas, gastrointestinal endocrine tumors, salivary and breast acinic cell carcinomas, gastric adenocarcinomas with and without acinar differentiation, and hepatocellular carcinomas were studied.
  • BCL10 immunoreactivity paralleled that of CEH and was restricted to acinar cells of normal and ectopic pancreas, of pancreatic metaplasia, and of ACCs.
  • We suggest using BCL10 antibody for diagnosing pancreatic tumors and whenever an acinar differentiation is suspected in gastrointestinal neoplastic and metaplastic lesions.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / analysis. Antibodies, Monoclonal / immunology. Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / diagnosis. Pancreas / pathology. Pancreatic Neoplasms / diagnosis

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem J. 1998 Feb 1;329 ( Pt 3):675-9 [9445398.001]
  • [Cites] Semin Diagn Pathol. 2000 May;17(2):104-8 [10839610.001]
  • [Cites] Cancer. 1987 Feb 15;59(4):739-47 [3542187.001]
  • [Cites] FEBS Lett. 1991 Jan 28;278(2):190-4 [1991511.001]
  • [Cites] Int J Oncol. 2006 Sep;29(3):649-54 [16865281.001]
  • [Cites] Virchows Arch. 2004 Sep;445(3):248-54 [15517368.001]
  • [Cites] Differentiation. 1992 Sep;51(1):55-60 [1451962.001]
  • [Cites] Am J Pathol. 1993 Sep;143(3):685-98 [8362971.001]
  • [Cites] J Clin Oncol. 2002 Dec 15;20(24):4673-8 [12488412.001]
  • [Cites] Hum Pathol. 1997 Jul;28(7):869-73 [9224759.001]
  • [Cites] Biochem Biophys Res Commun. 1988 Sep 15;155(2):950-5 [3421974.001]
  • [Cites] Eur J Biochem. 1990 Sep 11;192(2):543-50 [1698625.001]
  • [Cites] Biochim Biophys Acta. 1995 Oct 17;1272(2):69-72 [7548236.001]
  • [Cites] Adv Anat Pathol. 2001 May;8(3):144-59 [11345238.001]
  • [Cites] Int J Pancreatol. 1989 Sep;5(2):123-34 [2689525.001]
  • [Cites] Virchows Arch. 2007 Aug;451 Suppl 1:S61-9 [17684764.001]
  • [Cites] Virchows Arch. 2004 Sep;445(3):231-5 [15517367.001]
  • [Cites] Cell. 1999 Jan 8;96(1):35-45 [9989495.001]
  • [Cites] Am J Surg Pathol. 1992 Sep;16(9):815-37 [1384374.001]
  • [Cites] J Clin Invest. 1990 Apr;85(4):1221-6 [2318975.001]
  • [Cites] Biochim Biophys Acta. 1978 Nov 10;527(1):142-9 [718955.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12641-6 [9770539.001]
  • [Cites] APMIS. 1995 Jan;103(1):69-78 [7695893.001]
  • [Cites] Am J Surg Pathol. 2007 Mar;31(3):363-70 [17325477.001]
  • [Cites] Genomics. 1993 Aug;17(2):416-22 [7691717.001]
  • (PMID = 19066953.001).
  • [ISSN] 1432-2307
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Antibodies, Monoclonal; 0 / BCL10 protein, human; 0 / Biomarkers, Tumor; EC 3.1.1.1 / Carboxylesterase
  •  go-up   go-down


77. Bandyopadhyay A, Das TK, Raha K, Hati GC, Mitra PK, Dasgupta A: A study of fine needle aspiration cytology of salivary gland lesions with histopathological corroboration. J Indian Med Assoc; 2005 Jun;103(6):312-4, 316
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • All smears were evaluated according to cell size, amount of cytoplasm, cytologic atypia and presence of lymphocytes. (a) Variable cytologic appearances of pleomorphic salivary adenoma were observed. (b) Cellular pleomorphic adenoma and adenoid cystic carcinoma showed basaloid cell features. (c) Tumours with intermediate size cells and bland cytology included low grade muco-epidermoid carcinoma and cystic lesions. (d) Warthin's tumour, oncocytoma, salivary duct carcinoma and high grade muco-epidermoid carcinoma revealed large cells and abundant cytoplasm with or without atypia.
  • A major diagnostic categories were inflammatory lesions (n = 7 5), cystic lesions (n = 9), benign tumours (n = 81), malignant neoplasms (n = 1 8) and normal acinar pattern (n = 2).
  • Malignant tumours included muco-epidermoid carcinoma (n = 5), adenoid cystic carcinoma (n = 3), acinic cell carcinoma (n = 2), adenocarcinoma (n= 2), squamous cell carcinoma (n = 1), undifferentiated carcinoma (n= 4) and malignant lymphoma (n = 1).
  • Histopathological correlation was possible in 40% of benign and 80% of malignant neoplasms.
  • So it can be concluded that fine needle aspiration cytology can play important role in early diagnosis and subsequent therapeutic planning of salivary gland lesions.

  • MedlinePlus Health Information. consumer health - Salivary Gland Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16225156.001).
  • [ISSN] 0019-5847
  • [Journal-full-title] Journal of the Indian Medical Association
  • [ISO-abbreviation] J Indian Med Assoc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  •  go-up   go-down


78. Chang F, Chandra A, Culora G, Mahadeva U, Meenan J, Herbert A: Cytologic diagnosis of pancreatic endocrine tumors by endoscopic ultrasound-guided fine-needle aspiration: a review. Diagn Cytopathol; 2006 Sep;34(9):649-58
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytologic diagnosis of pancreatic endocrine tumors by endoscopic ultrasound-guided fine-needle aspiration: a review.
  • Precise localization and diagnosis of pancreatic endocrine tumors (PETs) is important, because pancreatic PETs have different clinical and biological behavior and treatment modalities than do exocrine pancreatic tumors.
  • In contrast to the much more common exocrine adenocarcinomas, cytologic studies of PET are relatively rare and many cytopathologists lack experience with the cytomorphologic features of these tumors.During the last 10 yr, endoscopic ultrasound (EUS)-guided fine-needle aspiration (FNA) has matured into an accurate, highly sensitive, and cost-effective modality for the preoperative localization of pancreatic PETs.
  • This manuscript focuses on the cytomorphologic features most suggestive of pancreatic PETs, differential diagnosis, and diagnostic pitfalls of PETs.
  • The data summarized in this review indicate that EUS-FNA is a valuable method in the recognition of pancreatic PETs and in most cases cytopathologists could reach a correct diagnosis of these tumors, including their hormone producing capability on aspirated cytologic material.
  • [MeSH-major] Biopsy, Fine-Needle / methods. Carcinoma, Islet Cell / pathology. Endoscopy, Digestive System / methods. Insulinoma / pathology. Pancreatic Neoplasms / pathology. Ultrasonography / methods
  • [MeSH-minor] Adenocarcinoma, Papillary / pathology. Biomarkers, Tumor / analysis. Carcinoma, Acinar Cell / pathology. Carcinoma, Pancreatic Ductal / pathology. Diagnosis, Differential. Gastrinoma / chemistry. Gastrinoma / pathology. Glucagonoma / chemistry. Glucagonoma / pathology. Humans. Immunohistochemistry. Lymphoma / pathology

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • MedlinePlus Health Information. consumer health - Ultrasound.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2006 Wiley-Liss, Inc.
  • (PMID = 16900463.001).
  • [ISSN] 8755-1039
  • [Journal-full-title] Diagnostic cytopathology
  • [ISO-abbreviation] Diagn. Cytopathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 74
  •  go-up   go-down


79. Psalla D, Geigy C, Konar M, Café Marçal V, Oevermann A: Nasal acinic cell carcinoma in a cat. Vet Pathol; 2008 May;45(3):365-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nasal acinic cell carcinoma in a cat.
  • This case report describes the clinical, magnetic resonance imaging (MRI)-related, and pathologic features of a nasal acinic cell carcinoma in a cat.
  • Evaluation by MRI revealed an heterogeneous, space-occupying lesion that filled the left nasal cavity and was diagnosed by histopathologic examination as an acinic cell carcinoma arising from a minor salivary gland of the nasal cavity.
  • Acinic cell carcinoma is a rare tumor in veterinary medicine.
  • The tumor is composed mainly of cells resembling serous cells of salivary glands and originates from major or minor salivary glands.
  • Clinicians and pathologists should be aware of the occurrence of acinic cell carcinoma in the sinonasal tract and include the tumor in the differential diagnosis of feline nasal diseases.
  • [MeSH-major] Carcinoma, Acinar Cell / veterinary. Paranasal Sinus Neoplasms / veterinary

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18487495.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 68238-35-7 / Keratins
  •  go-up   go-down


80. Grapin-Botton A: Ductal cells of the pancreas. Int J Biochem Cell Biol; 2005 Mar;37(3):504-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Ductal cells of the pancreas form the epithelial lining of the branched tubes that deliver enzymes produced by pancreatic acinar cells into the duodenum.
  • All endocrine, acinar and ductal cells arise from common precursors in this epithelial structure.
  • Based on challenged pancreas regeneration experiments, the adult ductal cells have been proposed to be pancreatic stem cells but their role in normal endocrine cell turnover has recently been challenged.
  • In addition, in the main form of pancreatic cancer, pancreas adenocarcinoma, tumor cells share similarities with ductal cells.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. Pancreas / cytology. Pancreas / physiology. Pancreatic Ducts / metabolism. Pancreatic Neoplasms / metabolism. Stem Cells / cytology
  • [MeSH-minor] Animals. Cell Differentiation. Humans. Models, Biological

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • MedlinePlus Health Information. consumer health - Stem Cells.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15618005.001).
  • [ISSN] 1357-2725
  • [Journal-full-title] The international journal of biochemistry & cell biology
  • [ISO-abbreviation] Int. J. Biochem. Cell Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 34
  •  go-up   go-down


81. Gologan A, Bastacky S, McHale T, Yu J, Cai C, Monzon-Bordonaba F, Dhir R: Age-associated changes in alpha-methyl CoA racemase (AMACR) expression in nonneoplastic prostatic tissues. Am J Surg Pathol; 2005 Nov;29(11):1435-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AMACR expression in the prostate has been investigated primarily in patients, in an older age group, treated for prostatic carcinoma and benign prostatic hypertrophy.
  • Semi-quantitative analysis of staining in acinar cells was used to generate a composite score (CS) [Sigma(% area x intensity)] for each case.
  • Acinar cells showed granular cytoplasmic staining.
  • Most cases in the control set of prostatic adenocarcinoma cases showed moderate to strong staining.
  • However, AMACR staining should be interpreted with caution and the diagnosis of PIN or prostate cancer should be rendered only with convincing histologic evidence.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16224209.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01-CA 86735-05; United States / NCI NIH HHS / CA / U01-CA 88110-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  •  go-up   go-down


82. Chen AM, Garcia J, Granchi PJ, Johnson J, Eisele DW: Late recurrence from salivary gland cancer: when does "cure" mean cure? Cancer; 2008 Jan 15;112(2):340-4
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Between 1960 and 2000, 145 patients underwent definitive therapy for localized carcinomas of the salivary glands and were clinically without evidence of disease at 5 years of follow-up.
  • RESULTS: The 10-year and 15-year cumulative probabilities of late recurrence in patients who were free of disease at 5 years were 13% and 18%, respectively.
  • The crude rates of late recurrence by histologic subtype were adenoid cystic carcinoma (26%), mixed malignant tumor (25%), mucoepidermoid carcinoma (17%), adenocarcinoma (10%), and acinic cell carcinoma (8%).
  • Salvage treatment varied according to location of disease recurrence and initial treatment characteristics.
  • The 15-year estimate of overall survival was 39% for patients who experienced a late recurrence compared with 71% for those who remained free of disease (P= .001).
  • CONCLUSIONS: A significant proportion of patients who are presumed to be cured of their disease at 5 years after initial treatment for salivary gland cancer will be found to develop late disease recurrence with additional follow-up.


83. Newman K, Stahl-Herz J, Kabiawu O, Newman E, Wieczorek R, Wang B, Pei Z, Bannan M, Lee P, Xu R: Pancreatic carcinoma with multilineage (acinar, neuroendocrine, and ductal) differentiation. Int J Clin Exp Pathol; 2009;2(6):602-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic carcinoma with multilineage (acinar, neuroendocrine, and ductal) differentiation.
  • The preponderance of pancreatic tumors is adenocarcinoma of the ductal type; carcinomas with multiple lineage differentiation are extremely rare.
  • We report an unusual case of pancreatic carcinoma with combined acinar and neuroendocrine differentiation and minor ductal component with concurrent acinar-ductal metaplasia (ADM), an early lesion implicated in ductal carcinogenesis.
  • Histologic examination revealed a pancreatic carcinoma with cellular features of eosinophilic granular cytoplasm and salt-pepper nuclei.
  • The acinar differentiation of the carcinoma was confirmed by positivity on periodic acid-Schiff stain resistant to diastase digestion (dPAS), positivity for antitrypsin on immunohistochemistry (IHC), and presence of zymogen granules on electron microscopy (EM).
  • The ductal component was only visible by PAS stain and immunostains for CEA and CK19A and accompanied by a number of the acinar-ductal metaplasia lesions adjacent to the main tumor.
  • Thus, the histological, histochemical, immunohistochemical and electron-microscopic evidence all suggested that the pancreatic carcinoma underwent trilineage differentiation.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pathol Int. 1995 Sep;45(9):669-76 [8548040.001]
  • [Cites] Am J Surg Pathol. 1994 Aug;18(8):765-78 [8037290.001]
  • [Cites] Am J Surg Pathol. 1992 Sep;16(9):815-37 [1384374.001]
  • [Cites] Ultrastruct Pathol. 1992 May-Jun;16(3):317-29 [1316659.001]
  • [Cites] Cancer. 1984 Nov 1;54(9):1766-70 [6089999.001]
  • [Cites] Mod Pathol. 2007 Feb;20 Suppl 1:S94-112 [17486055.001]
  • [Cites] J Clin Oncol. 2002 Dec 15;20(24):4673-8 [12488412.001]
  • [Cites] Am J Surg Pathol. 2002 Jul;26(7):893-901 [12131156.001]
  • [Cites] Pancreas. 2002 Mar;24(2):111-20 [11854615.001]
  • [Cites] Surg Today. 2001;31(2):177-9 [11291717.001]
  • [Cites] Hepatogastroenterology. 2008 Mar-Apr;55(82-83):708-10 [18613439.001]
  • [Cites] Pathol Int. 2002 Nov;52(11):740-6 [12685552.001]
  • (PMID = 19636408.001).
  • [ISSN] 1936-2625
  • [Journal-full-title] International journal of clinical and experimental pathology
  • [ISO-abbreviation] Int J Clin Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2713457
  • [Keywords] NOTNLM ; Adenocarcinoma / metaplasia / neuroendocrine differentiation / pancreas
  •  go-up   go-down


84. Uzaslan E, Stuempel T, Ebsen M, Freudenberg N, Nakamura S, Costabel U, Guzman J: Surfactant protein A detection in primary pulmonary adenocarcinoma without bronchioloalveolar pattern. Respiration; 2005 May-Jun;72(3):249-53
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surfactant protein A detection in primary pulmonary adenocarcinoma without bronchioloalveolar pattern.
  • BACKGROUND: Immunohistochemical studies in human lung carcinoma reported positive staining of tumor cells for surfactant protein A (SP-A), especially in peripheral airway cell carcinoma, which include bronchioloalveolar carcinoma and in some reports also papillary subtypes.
  • OBJECTIVE: The purpose of this study was to determine the SP-A expression in tumor cells of lung adenocarcinoma without a bronchioloalveolar pattern, classified according to the WHO.
  • METHODS: In total, 169 primary adenocarcinomas of the lung (109 acinar, 32 solid with mucin, 24 papillary and 4 mucinous) were examined by immunohistochemistry for SP-A expression.
  • RESULTS: Twenty-five percent of acinar, 38% of papillary and 3% of solid adenocarcinoma with mucin showed a positive intracytoplasmic SP-A reaction of the tumor cells.
  • None of the mucinous adenocarcinomas stained for SP-A.
  • This study included the largest number of acinar adenocarcinomas and solid adenocarcinomas with mucin studied for SP-A.
  • We clearly demonstrated that also primary lung adenocarcinoma without a bronchioloalveolar pattern can express SP-A.
  • A positive staining of hyperplastic type II cells surrounding the tumors or entrapped in the tumor could clearly be differentiated from the SP-A-positive stain of tumor cells.
  • CONCLUSION: These results support the theory that SP-A-producing cells may generate not only bronchioloalveolar and papillary carcinoma, but also other subtypes of lung adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Biomarkers, Tumor / metabolism. Lung Neoplasms / metabolism. Pulmonary Surfactant-Associated Protein A / metabolism
  • [MeSH-minor] Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / pathology. Adenocarcinoma, Papillary / metabolism. Adenocarcinoma, Papillary / pathology. Carcinoma, Acinar Cell / metabolism. Carcinoma, Acinar Cell / pathology. Humans

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 S. Karger AG, Basel
  • (PMID = 15942293.001).
  • [ISSN] 0025-7931
  • [Journal-full-title] Respiration; international review of thoracic diseases
  • [ISO-abbreviation] Respiration
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Pulmonary Surfactant-Associated Protein A
  •  go-up   go-down


85. van Tongeren J, Creytens DH, Meulemans EV, de Bondt RB, de Jong J, Manni JJ: Synchronous bilateral epithelial-myoepithelial carcinoma of the parotid gland: case report and review of the literature. Eur Arch Otorhinolaryngol; 2009 Sep;266(9):1495-500
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synchronous bilateral epithelial-myoepithelial carcinoma of the parotid gland: case report and review of the literature.
  • The most common synchronous bilateral malignancies are acinic cell carcinoma.
  • Epithelial-myoepithelial carcinoma is an uncommon neoplasm comprising 1% of all salivary gland tumours.
  • In this case report, we describe, to our best of knowledge, the first case of a patient with a synchronous bilateral epithelial-myoepithelial carcinoma of the parotid gland.
  • [MeSH-major] Carcinoma / pathology. Neoplasms, Multiple Primary / pathology. Parotid Neoplasms / pathology

  • Genetic Alliance. consumer health - Epithelial-Myoepithelial Carcinoma.
  • Genetic Alliance. consumer health - Myoepithelial carcinoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Oral Maxillofac Surg. 2006 Oct;44(5):397-401 [16207507.001]
  • [Cites] Oral Oncol. 2006 Feb;42(2):154-60 [16256413.001]
  • [Cites] Am J Surg Pathol. 2007 Jan;31(1):44-57 [17197918.001]
  • [Cites] Arch Surg. 1975 Jan;110(1):64-8 [1090282.001]
  • [Cites] Cancer. 2000 Aug 25;90(4):258-63 [10966568.001]
  • [Cites] J Laryngol Otol. 2001 May;115(5):434-6 [11410145.001]
  • [Cites] Am J Clin Pathol. 2001 Dec;116(6):823-30 [11764070.001]
  • [Cites] Virchows Arch. 2002 Nov;441(5):428-36 [12447671.001]
  • [Cites] J Histochem Cytochem. 2003 Feb;51(2):133-9 [12533521.001]
  • [Cites] Auris Nasus Larynx. 2003 May;30(2):201-3 [12753995.001]
  • [Cites] J Laryngol Otol. 2003 May;117(5):419-21 [12803799.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 May;97(5):613-9 [15153875.001]
  • [Cites] Int J Oral Maxillofac Surg. 2004 Sep;33(6):531-4 [15308250.001]
  • [Cites] Am J Surg. 1969 Nov;118(5):787-9 [4310431.001]
  • [Cites] Ann Surg. 1969 Nov;170(5):866-9 [5347563.001]
  • [Cites] Virchows Arch A Pathol Pathol Anat. 1972;356(1):16-31 [4340536.001]
  • [Cites] ORL J Otorhinolaryngol Relat Spec. 1978;40(2):120-6 [570688.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1982 Mar;53(3):280-7 [6950345.001]
  • [Cites] Laryngoscope. 1988 Jan;98(1):99-105 [3336269.001]
  • [Cites] Ann Otol Rhinol Laryngol. 1992 Jun;101(6):540-2 [1376977.001]
  • [Cites] Acta Pathol Jpn. 1992 May;42(5):358-63 [1322017.001]
  • [Cites] Virchows Arch A Pathol Anat Histopathol. 1993;422(5):389-96 [8322454.001]
  • [Cites] Am J Surg Pathol. 1994 Apr;18(4):421-5 [7511356.001]
  • [Cites] Am J Clin Pathol. 1995 Apr;103(4):432-7 [7726139.001]
  • [Cites] Eur J Cancer B Oral Oncol. 1996 Jul;32B(4):251-9 [8776422.001]
  • [Cites] Surg Oncol. 1997 Dec;6(4):209-13 [9775407.001]
  • [Cites] AMA Arch Pathol. 1953 Apr;55(4):328-46 [13030050.001]
  • [Cites] Plast Reconstr Surg Transplant Bull. 1959 Jan;23(1):55-63 [13633480.001]
  • [Cites] J Laryngol Otol. 1961 Jul;75:699-702 [13722582.001]
  • [Cites] Mod Pathol. 2005 May;18(5):645-50 [15529180.001]
  • [Cites] Head Neck. 2005 Sep;27(9):825-8 [15920750.001]
  • [Cites] Oral Oncol. 2006 Jan;42(1):57-65 [16140564.001]
  • [Cites] Int J Surg Pathol. 2006 Jul;14(3):212-7 [16959701.001]
  • (PMID = 18841376.001).
  • [ISSN] 1434-4726
  • [Journal-full-title] European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery
  • [ISO-abbreviation] Eur Arch Otorhinolaryngol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Germany
  • [Number-of-references] 35
  • [Other-IDs] NLM/ PMC2718197
  •  go-up   go-down


86. Lin J, Jing X: Fine-needle aspiration of intrapancreatic accessory spleen, mimic of pancreatic neoplasms. Arch Pathol Lab Med; 2010 Oct;134(10):1474-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Intrapancreatic accessory spleen (IPAS) is a congenital abnormality, which mimics neoplasm.
  • Hematoxylin-eosin–stained cell block sections showed conspicuous thin-walled blood vessels in addition to inflammatory cells.
  • By correlating the cytologic findings with the result of immunostaining, we rendered the diagnosis of IPAS.
  • Our experience supports the view that endoscopic ultrasound-guided fine-needle aspiration may enable a reliable, preoperative diagnosis of IPAS and thus prevent unnecessary surgery.
  • [MeSH-minor] Adenocarcinoma / pathology. Adenocarcinoma / ultrasonography. Aged. Animals. Carcinoma, Acinar Cell / pathology. Carcinoma, Acinar Cell / ultrasonography. Coloring Agents. Diagnosis, Differential. Humans. Inflammation / pathology. Inflammation / ultrasonography. Lymphocytes / pathology. Lymphocytes / ultrasonography. Male. Pancreas / anatomy & histology. Pancreas / ultrasonography

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20923303.001).
  • [ISSN] 1543-2165
  • [Journal-full-title] Archives of pathology & laboratory medicine
  • [ISO-abbreviation] Arch. Pathol. Lab. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Coloring Agents
  •  go-up   go-down


87. Lee JH, Lee KG, Park HK, Lee KS: [Acinar cell carcinoma of the pancreas in Korea--clinicopathologic analysis of 27 patients from korean literature and 2 cases from our hospital--]. Korean J Gastroenterol; 2010 Apr;55(4):245-51
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Acinar cell carcinoma of the pancreas in Korea--clinicopathologic analysis of 27 patients from korean literature and 2 cases from our hospital--].
  • BACKGROUND/AIMS: Acinar cell carcinoma (ACC) of the pancreas is a rare malignancy.
  • RESULTS: ACC was more common in male, and age at diagnosis ranged from 25 to 68 years (median 54).
  • Liver was most common organ of metastasis at diagnosis and recurrence after operation.
  • The mean tumor size was 7.0 cm, and most common location was tail.
  • CONCLUSIONS: In Korea, the clinical features of ACC include young age, large size, tail location, and nonspecific tumor markers.
  • [MeSH-major] Carcinoma, Acinar Cell / diagnosis. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adult. Age Factors. Aged. Biomarkers, Tumor / analysis. Female. Humans. Male. Middle Aged. Prognosis. Republic of Korea. Survival Analysis

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20389178.001).
  • [ISSN] 1598-9992
  • [Journal-full-title] The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi
  • [ISO-abbreviation] Korean J Gastroenterol
  • [Language] kor
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 22
  •  go-up   go-down


88. Ikezoe M, Nishihara T, Yanagawa K, Kohro T, Yamai T, Ikezoe S, Yasunaga Y, Inui Y, Nishikawa M: A case of pancreatic acinar cell carcinoma metastatic to skin. Rare Tumors; 2010;2(4):e62
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A case of pancreatic acinar cell carcinoma metastatic to skin.
  • We report a rare case of pancreatic acinar cell carcinoma with widespread metastases in a 68-year-old woman who presented with subcutaneous nodules as the initial symptom.
  • Computed tomography showed a pancreatic mass with hepatic tumors and enlarged lymph nodes besides ring-enhanced subcutaneous nodules.
  • Histological analysis of a colonic polypoid lesion revealed carcinoma with endocrine and acinar differentiation compatible with pancreatic origin.
  • Regrettably, she died of a cerebral infarction without any treatment, and autopsy findings confirmed our diagnosis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2002 Dec 15;20(24):4673-8 [12488412.001]
  • [Cites] J Clin Pathol. 1977 Feb;30(2):103-12 [845259.001]
  • [Cites] Am J Surg Pathol. 1992 Sep;16(9):815-37 [1384374.001]
  • [Cites] Semin Neurol. 2004 Dec;24(4):453-60 [15637656.001]
  • [Cites] Pancreas. 2007 Jul;35(1):42-6 [17575544.001]
  • [Cites] Surgery. 2008 Aug;144(2):141-8 [18656619.001]
  • [Cites] J Pathol. 1985 May;146(1):17-29 [2989468.001]
  • [Cites] Cancer. 1987 Feb 15;59(4):739-47 [3542187.001]
  • [Cites] Radiology. 1986 Jan;158(1):67-8 [3940400.001]
  • [Cites] Am J Dig Dis. 1976 Nov;21(11):978-87 [984019.001]
  • [Cites] J Gastrointest Surg. 2008 Jun;12(6):1061-7 [17957440.001]
  • [Cites] J Stroke Cerebrovasc Dis. 2008 Jul-Aug;17(4):169-74 [18589335.001]
  • [Cites] Virchows Arch. 1995;426(4):419-23 [7541276.001]
  • [Cites] Histol Histopathol. 1994 Jan;9(1):53-8 [8003821.001]
  • [Cites] Pancreas. 2003 Jul;27(1):e18-22 [12826914.001]
  • (PMID = 21234254.001).
  • [ISSN] 2036-3613
  • [Journal-full-title] Rare tumors
  • [ISO-abbreviation] Rare Tumors
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Other-IDs] NLM/ PMC3019597
  • [Keywords] NOTNLM ; magnetic resonance diffusion-weighted imaging. / pancreatic acinar cell carcinoma / subcutaneous nodules / widespread metastases
  •  go-up   go-down


89. Luna MA: Sinonasal tubulopapillary low-grade adenocarcinoma: a specific diagnosis or just another seromucous adenocarcinoma? Adv Anat Pathol; 2005 May;12(3):109-15
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sinonasal tubulopapillary low-grade adenocarcinoma: a specific diagnosis or just another seromucous adenocarcinoma?
  • Histopathologically, sinonasal adenocarcinomas fall into four categories: the intestinal type, the conventional salivary gland type (eg, adenoid cystic carcinoma, acinic cell carcinoma), the seromucous type, and the low-grade not otherwise specified type.
  • Recently, a new type of sinonasal adenocarcinoma has been described, called tubulopapillary low-grade adenocarcinoma.
  • In this commentary, the histologic features of this type of tumor are compared with those of the other types of sinonasal adenocarcinoma.
  • The clinicopathologic characteristics and probable origin of this type of adenocarcinoma are also discussed.
  • [MeSH-major] Adenocarcinoma / pathology. Adenocarcinoma, Papillary / pathology. Paranasal Sinus Neoplasms / pathology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Virchows Arch. 2003 Aug;443(2):152-8 [12827515.001]
  • (PMID = 15900111.001).
  • [ISSN] 1072-4109
  • [Journal-full-title] Advances in anatomic pathology
  • [ISO-abbreviation] Adv Anat Pathol
  • [Language] eng
  • [Publication-type] Comment; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


90. Shen JX, Fan WJ, Lu YC, Xiao P: [Malignant epithelial parotid tumors: CT imaging and histopathologic correlation]. Ai Zheng; 2007 Jul;26(7):762-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Malignant epithelial parotid tumors: CT imaging and histopathologic correlation].
  • BACKGROUND & OBJECTIVE: Malignant epithelial parotid tumors have various histopathologic types.
  • This study was to analyze CT features of malignant epithelial parotid tumors to evaluate the diagnostic value of CT in the characterization of malignant epithelial parotid tumors.
  • METHODS: CT reports of 29 patients with malignant epithelial parotid tumors (8 at low grade and 21 at intermediate or high grade), confirmed by histopathology in Cancer Center of Sun Yat-sen University, were reviewed.
  • RESULTS: Of the 8 cases at low grade, 4 were well-differentiated mucoepidermoid carcinoma, 3 were acinic cell carcinoma, and 1 was epithelial-myoepithelial carcinoma; 3 had sharp margin, 3 had partly unsharp margin, and 2 had unsharp margin; 5 had regular contour, and 3 had irregular contour; all were enhanced obviously; 2 showed homogeneous appearance, and 6 showed inhomogeneous appearance with low-density areas; none had adjacent infiltration; 3 had lymph node metastasis.
  • Of the 21 cases at intermediate or high grade, 5 were poorly-differentiated squamous cell carcinoma, 8 were malignant pleomorphic adenoma, 2 were adenocarcinoma, 1 was lymph-epithelial carcinoma, 4 were mucoepidermoid carcinoma, and 1 was adenoidcystic carcinoma; 5 had sharp margin, 7 had partly unsharp margin, and 9 had unsharp margin; 10 had regular contour, and 11 had irregular contour; 17 were enhanced obviously, and the 4 cases of malignant pleomorphic adenoma were enhanced slightly; 9 showed homogeneous appearance, and 12 showed inhomogeneous appearance with low-density areas; 8 had adjacent infiltration (the fat space between tumor and the parotid bed disappeared); 6 had lymph node metastasis.
  • CONCLUSIONS: To some extent, CT features of malignant epithelial parotid tumors are correlated to the differentiation of tumor cells.
  • Moreover, tumor size and histologic subtype should be considered to make a more accurate imaging diagnosis.
  • [MeSH-major] Carcinoma / pathology. Carcinoma / radiography. Parotid Neoplasms / pathology. Parotid Neoplasms / radiography. Tomography, X-Ray Computed
  • [MeSH-minor] Adenoma, Pleomorphic / pathology. Adenoma, Pleomorphic / radiography. Adolescent. Adult. Aged. Aged, 80 and over. Carcinoma, Mucoepidermoid / pathology. Carcinoma, Mucoepidermoid / radiography. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / radiography. Female. Follow-Up Studies. Humans. Lymphatic Metastasis. Male. Middle Aged. Neoplasm Invasiveness. Neoplasm Recurrence, Local. Neoplasm Staging. Parotid Gland / pathology. Parotid Gland / radiography. Young Adult

  • MedlinePlus Health Information. consumer health - CT Scans.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17626755.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  •  go-up   go-down


91. Nishikawa S, Sano F, Takagi K, Okada M, Sugimoto J, Takagi S: Spontaneous poorly differentiated carcinoma with cells positive for vimentin in a salivary gland of a young rat. Toxicol Pathol; 2010 Feb;38(2):315-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spontaneous poorly differentiated carcinoma with cells positive for vimentin in a salivary gland of a young rat.
  • Spontaneous salivary gland tumors in rats are rare.
  • The authors report a poorly differentiated carcinoma of a submandibular gland in a ten-week-old rat that was positive for vimentin.
  • Microscopically, the neoplastic cells showed a diffuse growth pattern in most areas of the tumor mass and a nestlike structure in a part of the peripheral area.
  • Based on these findings, the tumor was diagnosed as a poorly differentiated carcinoma.
  • The origin of the neoplastic cells would be either acinar or ductal cells.
  • This suggests that acinar or ductal cells have the potential to transform into vimentin-expressing cells.
  • [MeSH-major] Carcinoma / veterinary. Rats, Sprague-Dawley. Rodent Diseases / pathology. Submandibular Gland Neoplasms / veterinary. Vimentin / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20124499.001).
  • [ISSN] 1533-1601
  • [Journal-full-title] Toxicologic pathology
  • [ISO-abbreviation] Toxicol Pathol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vimentin; 68238-35-7 / Keratins
  •  go-up   go-down


92. Kuo FY, Swanson PE, Yeh MM: Pancreatic acinar tissue in liver explants: a morphologic and immunohistochemical study. Am J Surg Pathol; 2009 Jan;33(1):66-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic acinar tissue in liver explants: a morphologic and immunohistochemical study.
  • To gain further insight into this issue, we performed a pathologic and immunohistochemical study in liver explants to identify pancreatic acinar 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 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

  • MedlinePlus Health Information. consumer health - Liver Diseases.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


93. Samaratunga H, Delahunt B: Ductal adenocarcinoma of the prostate: current opinion and controversies. Anal Quant Cytol Histol; 2008 Aug;30(4):237-46
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ductal adenocarcinoma of the prostate: current opinion and controversies.
  • OBJECTIVE: To evaluate the morphologic spectrum and clinical significance of ductal adenocarcinoma of the prostate (DAP).
  • STUDY DESIGN: We reviewed diagnostic criteria, including the value of immunohistochemistry, and outlined the prognostic implications of a diagnosis of DAP.
  • Immunostaining for prostatic-specific antigen and prostate-specific acid phosphatase is present in these tumors, a high percentage of which overexpress alpha-methylacyl-coenzyme A racemase.
  • A basal cell layer can be seen in some of these tumors, which is probably due to tumor growth into preexisting ducts.
  • This usually represents an advanced stage of tumor progression and is not a precursor of invasive carcinoma.
  • CONCLUSION: DAP are neoplasms of prostatic origin, and the terms endometrioid or endometrial adenocarcinoma are best avoided.
  • The term ductal carcinoma is also inappropriate because this includes some urothelial carcinomas of ductal origin.
  • DAP are aggressive tumors with a shortened average time to progression compared with acinar adenocarcinoma.

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18773743.001).
  • [ISSN] 0884-6812
  • [Journal-full-title] Analytical and quantitative cytology and histology
  • [ISO-abbreviation] Anal. Quant. Cytol. Histol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 36
  •  go-up   go-down


94. Parikh B, Jojo A, Shah B, Bansal R, Trivedi P, Shah MJ: Fine needle aspiration cytology of hepatoblastoma: a study of 20 cases. Indian J Pathol Microbiol; 2005 Jul;48(3):331-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hepatoblastoma (HBL) is the most common primary malignant hepatic tumor in children.
  • Morphologically, the tumor cells were commonly arranged in acinar pattern, papillary pattern, or in sheets.
  • FNA cytology alone had some limitations in the diagnosis of HBL.
  • Hence, cytoarchitecture in combination with clinicalfeatures, imaging techniques and serum a-fetoprotein levels were helpful for specific diagnosis of HBL and to rule out various others differential diagnosis of small round cell tumor.
  • The cytological differential diagnosis between differentiated HBL and Hepatocellular carcinoma (HCC) was found to be very difficult.
  • [MeSH-minor] Adolescent. Biopsy, Fine-Needle. Carcinoma, Hepatocellular / diagnosis. Carcinoma, Hepatocellular / pathology. Child. Child, Preschool. Cytodiagnosis. Diagnosis, Differential. Female. Humans. Infant. Male

  • Genetic Alliance. consumer health - Hepatoblastoma.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16761744.001).
  • [ISSN] 0377-4929
  • [Journal-full-title] Indian journal of pathology & microbiology
  • [ISO-abbreviation] Indian J Pathol Microbiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
  •  go-up   go-down


95. Neto AG, Pineda-Daboin K, Spencer ML, Luna MA: Sinonasal acinic cell carcinoma: a clinicopathologic study of four cases. Head Neck; 2005 Jul;27(7):603-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sinonasal acinic cell carcinoma: a clinicopathologic study of four cases.
  • BACKGROUND: Acinic cell carcinoma is a low-grade malignant epithelial salivary gland neoplasm with a predilection for the parotid gland.
  • To date, only 11 cases of sinonasal acinic cell carcinomas have been reported in the English-language literature.
  • We present the clinicopathologic features of four sinonasal acinic cell carcinomas.
  • METHODS: The demographic data and pathologic material of four patients with sinonasal acinic cell carcinoma identified from the files of the Department of Pathology at The University of Texas M. D.
  • Histologically, all tumors were composed of round to ovoid cells with clear and/or basophilic granular cytoplasm and round, hyperchromatic, small, eccentrically located nuclei.
  • CONCLUSIONS: Sinonasal acinic cell carcinoma is a distinct low-grade carcinoma that can be distinguished from other neoplasms by light microscopy and histochemical staining methods.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Nose Neoplasms / pathology

  • Genetic Alliance. consumer health - Acinic Cell Carcinoma.
  • MedlinePlus Health Information. consumer health - Nasal Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15900565.001).
  • [ISSN] 1043-3074
  • [Journal-full-title] Head & neck
  • [ISO-abbreviation] Head Neck
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 23
  •  go-up   go-down


96. Luebke AM, Schlomm T, Gunawan B, Bonkhoff H, Füzesi L, Erbersdobler A: Simultaneous tumour-like, atypical basal cell hyperplasia and acinar adenocarcinoma of the prostate: a comparative morphological and genetic approach. Virchows Arch; 2005 Mar;446(3):338-41
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Simultaneous tumour-like, atypical basal cell hyperplasia and acinar adenocarcinoma of the prostate: a comparative morphological and genetic approach.
  • Basal cell tumours of the prostatic gland are rare, and the classification is difficult.
  • In the present case report, a large, tumour-like proliferation of atypical basaloid cells was found incidentally in a prostatectomy specimen that otherwise contained a conventional acinar adenocarcinoma.
  • A high Ki-67 index was recorded within the atypical basaloid cells, by far exceeding the one counted in the conventional adenocarcinoma.
  • However, there were no definite criteria for a malignant behaviour of the basal cell tumour.
  • Comparative genomic hybridisation from microdissected tumour cells yielded losses at the short arms of chromosomes 8 and 12 in the conventional adenocarcinoma and a normal karyotype in the basal cell tumour.
  • The pathological findings favoured the diagnosis of an atypical basal cell hyperplasia.
  • [MeSH-major] Carcinoma, Acinar Cell / complications. Carcinoma, Acinar Cell / pathology. Prostatic Hyperplasia / complications. Prostatic Hyperplasia / pathology. Prostatic Neoplasms / complications. Prostatic Neoplasms / pathology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasms, Basal Cell / genetics. Neoplasms, Basal Cell / pathology. Nucleic Acid Hybridization

  • MedlinePlus Health Information. consumer health - Enlarged Prostate (BPH).
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Arch Pathol Lab Med. 1993 Aug;117(8):799-801 [8343043.001]
  • [Cites] Cancer Res. 1995 Jan 15;55(2):342-7 [7529134.001]
  • [Cites] Eur Urol. 1999;36(1):21-30 [10364651.001]
  • [Cites] Int J Cancer. 2004 May 1;109(5):668-72 [14999772.001]
  • [Cites] Histopathology. 1992 Feb;20(2):151-5 [1559669.001]
  • [Cites] Pathol Res Pract. 1990 Feb;186(1):28-36 [2179908.001]
  • [Cites] Am J Surg Pathol. 1993 Jul;17(7):645-59 [7686348.001]
  • [Cites] Genes Chromosomes Cancer. 1994 Aug;10(4):231-43 [7522536.001]
  • [Cites] Br J Cancer. 2001 Jan;84(2):202-8 [11161378.001]
  • [Cites] Mod Pathol. 1997 Jun;10(6):612-29 [9195581.001]
  • [Cites] Virchows Arch. 2003 Dec;443(6):787-91 [14756145.001]
  • [Cites] Hum Pathol. 1988 Dec;19(12):1425-33 [2461340.001]
  • [Cites] Am J Surg Pathol. 2003 Dec;27(12):1523-9 [14657711.001]
  • [Cites] Am J Pathol. 2001 Feb;158(2):399-406 [11159178.001]
  • [Cites] Am J Pathol. 2002 Jul;161(1):43-51 [12107088.001]
  • [Cites] Am J Surg Pathol. 1992 Dec;16(12):1205-14 [1281386.001]
  • [Cites] Cancer. 1990 Sep 15;66(6):1225-33 [2400973.001]
  • [Cites] Hum Pathol. 1998 Dec;29(12):1447-50 [9865831.001]
  • (PMID = 15726402.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Comparative Study; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


97. Bangari DS, Stevenson GW: Carcinoma in a mixed mammary tumor in a llama (Lama glama). J Vet Diagn Invest; 2007 Jul;19(4):450-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carcinoma in a mixed mammary tumor in a llama (Lama glama).
  • A formalin-fixed wedge biopsy specimen from the affected quarter was submitted to Purdue University Animal Disease Diagnostic Laboratory for histopathology.
  • Histopathologic examination revealed tubulopapillary acinar or solid nest-like clusters of neoplastic epithelial cells surrounded by whorls and sheets of proliferative myoepithelial cells.
  • The presence of osseous metaplasia in the proliferative mesenchymal component justified classification as a mixed tumor.
  • Positive immunohistochemical staining of neoplastic epithelial cells with anticytokeratin antibody, and proliferative spindloid cells with antiviemtin and antismooth muscle actin antibodies supported the histopathologic diagnosis.
  • To the authors' knowledge, this is the first report of a carcinoma in a mixed mammary tumor in a llama.
  • [MeSH-major] Camelids, New World. Carcinoma / veterinary. Mammary Neoplasms, Animal / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17609363.001).
  • [ISSN] 1040-6387
  • [Journal-full-title] Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
  • [ISO-abbreviation] J. Vet. Diagn. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


98. Zou YP, Li WM, Liu HR, Li N: Primary carcinoid tumor of the gallbladder: a case report and brief review of the literature. World J Surg Oncol; 2010;8:12
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary carcinoid tumor of the gallbladder: a case report and brief review of the literature.
  • BACKGROUND: Primary carcinoid tumor of the gallbladder is rare and comprises less than 1% of all carcinoid tumors.
  • Preoperative diagnosis of carcinoid tumor of the gallbladder is difficult.
  • CASE PRESENTATION: A 46-year-old woman was hospitalized with a preoperative diagnosis of gallbladder carcinoma, The patient was referred for surgical opinion and laparotomy was subsequently performed.
  • Histologically, the tumor consisted of small oval cells with round-to-oval neclei and tumor cells formed small nodular, trabeculare and acinar structures.
  • The tumor showed moderate pleomorphism with scattered mitotic figures, but no definite evidence of vascular permeation, perineural invasion or lymphatic permeation was seen.
  • The tumor cells invaded the mucosa extensively, and some penetrated the muscular layer but not through the serosa of the gallbladder into the liver.
  • This lesion was proved to be a primary carcinoid tumor of the gallbladder.
  • A brief review of literature, clinical feature, pathology and treatment of this rare disease was discussed.
  • CONCLUSION: Primary carcinoid tumor of the gallbladder is uncommon.
  • The definite diagnosis is often made on histopathological results after surgery.
  • [MeSH-major] Carcinoid Tumor / pathology. Gallbladder Neoplasms / pathology


99. Michail P, Karavokyros I, Pikoulis E, Arvelakis A, Charminis G, Michail O, Theodoros D: Acinic cell carcinoma of the parotid gland in children: a case report and literature review. West Indian Med J; 2008 Jan;57(1):70-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acinic cell carcinoma of the parotid gland in children: a case report and literature review.
  • Parotid acinic cell carcinoma is a rare malignancy in childhood.
  • Tumour resection revealed acinic cell carcinoma of the parotid gland.
  • The patient has been disease-free for the last five years.
  • We review the literature on acinic cell carcinomas of parotid glands in childhood.
  • [MeSH-major] Carcinoma, Acinar Cell / pathology. Parotid Neoplasms / pathology

  • Genetic Alliance. consumer health - Acinic Cell Carcinoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19565943.001).
  • [ISSN] 0043-3144
  • [Journal-full-title] The West Indian medical journal
  • [ISO-abbreviation] West Indian Med J
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] Jamaica
  • [Number-of-references] 26
  •  go-up   go-down


100. Dobashi Y, Suzuki S, Matsubara H, Kimura M, Endo S, Ooi A: Critical and diverse involvement of Akt/mammalian target of rapamycin signaling in human lung carcinomas. Cancer; 2009 Jan 1;115(1):107-18
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Critical and diverse involvement of Akt/mammalian target of rapamycin signaling in human lung carcinomas.
  • BACKGROUND: Aberrant signaling cascades emanating from epidermal growth factor receptor (EGFR) are involved in the complex network of oncogenic signaling in lung carcinomas.
  • METHODS: The authors investigated the involvement of mTOR in the pathobiologic profiles of 150 specimens of lung carcinoma by immunohistochemistry and immunoblotting in correlation with the upstream and downstream proteins Akt and p70S6-kinase (S6K), respectively.
  • RESULTS: Immunohistochemistry revealed Akt activation in 44% of tumors and mTOR expression in 68.7% of tumors, and the preponderance of activation was observed in adenocarcinoma (AC) (100%).
  • Phosphorylated mTOR (p-mTOR) was observed in 53.3% of tumors and had the highest frequency in AC (89.7%).
  • In AC, the frequency of p-mTOR staining was higher in the well differentiated subtype, in particular, in the acinar structure.
  • However, little correlation was observed between the activation of mTOR and Akt, except in the 5 AC specimens that harbored an EGFR gene mutation, which exhibited constitutive activation of both Akt and mTOR.
  • Conversely, in squamous cell carcinomas, mTOR activation was associated with a significantly higher frequency of lymph node metastasis.
  • First, mTOR may function not only in the proliferation of tumor cells as an effector molecule downstream of EGFR but also possibly in the morphogenesis of AC.
  • Second, the activation of mTOR may play a key role in metastasis in squamous cell carcinoma.
  • Overall, the current results demonstrated the potential for the application of rapamycin, an mTOR inhibitor, as an additional novel component of chemotherapy for a defined subset of patients with lung carcinoma.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Humans. Neoplasm Metastasis. Neoplasms, Squamous Cell / metabolism. Neoplasms, Squamous Cell / pathology. Phosphorylation. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction. TOR Serine-Threonine Kinases






Advertisement