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1. Lewis RB, Lattin GE Jr, Paal E: Pancreatic endocrine tumors: radiologic-clinicopathologic correlation. Radiographics; 2010 Oct;30(6):1445-64
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic endocrine tumors: radiologic-clinicopathologic correlation.
  • Pancreatic endocrine tumors (PETs) are primarily well-differentiated tumors composed of cells that resemble normal islet cells but that arise from pancreatic ductal cells.
  • They are classified as functioning or nonfunctioning according to their associated clinical symptoms; insulinoma, gastrinoma, and glucagonoma are the most common functioning PETs.
  • Most are sporadic, but some are associated with familial syndromes such as multiple endocrine neoplasia type 1, von Hippel-Lindau syndrome, and neurofibromatosis type 1.
  • At imaging, PETs typically appear as well-defined hypervascular masses, a finding indicative of their rich capillary network.
  • Cystic change, calcification, and necrosis are common in large tumors, which are associated with a poorer prognosis and a higher prevalence of local and vascular invasion and metastases than are smaller tumors.
  • Poorly differentiated PETs are rare and have an infiltrative appearance; patients with such tumors have a poor prognosis.
  • Knowledge of the characteristic clinical, pathologic, and radiologic features of PETs is important in the evaluation and management of patients with a suspected clinical syndrome or a pancreatic mass.
  • [MeSH-major] Diagnostic Imaging. Pancreatic Neoplasms / diagnosis
  • [MeSH-minor] Adenoma, Islet Cell / diagnosis. Adenoma, Islet Cell / epidemiology. Adenoma, Islet Cell / pathology. Carcinoma, Islet Cell / diagnosis. Carcinoma, Islet Cell / epidemiology. Carcinoma, Islet Cell / pathology. Diagnosis, Differential. Humans. Multiple Endocrine Neoplasia Type 1 / pathology. Neurofibromatosis 1 / pathology. Prevalence. von Hippel-Lindau Disease / pathology

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  • [Copyright] © RSNA, 2010.
  • (PMID = 21071369.001).
  • [ISSN] 1527-1323
  • [Journal-full-title] Radiographics : a review publication of the Radiological Society of North America, Inc
  • [ISO-abbreviation] Radiographics
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
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2. Ju J, Hao X, Lee MJ, Lambert JD, Lu G, Xiao H, Newmark HL, Yang CS: A gamma-tocopherol-rich mixture of tocopherols inhibits colon inflammation and carcinogenesis in azoxymethane and dextran sulfate sodium-treated mice. Cancer Prev Res (Phila); 2009 Feb;2(2):143-52
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  • We investigated the effects of a gamma-tocopherol-rich mixture of tocopherols (gamma-TmT, containing 57% gamma-T, 24% delta-T, and 13% alpha-T) on colon carcinogenesis in azoxymethane (AOM)/dextran sulfate sodium (DSS)-treated mice.
  • In the AOM/DSS-treated mice, dietary gamma-TmT treatment resulted in a significantly lower colon inflammation index (52% of the control) on day 7 and number of colon adenomas (9% of the control) on week 7. gamma-TmT treatment also resulted in higher apoptotic index in adenomas, lower prostaglandin E2, leukotriene B4, and nitrotyrosine levels in the colon, and lower prostaglandin E2, leukotriene B4, and 8-isoprostane levels in the plasma on week 7.
  • In experiment 2 with AOM/DSS- treated mice sacrificed on week 21, dietary 0.17% or 0.3% gamma-TmT treatment, starting 1 week before the AOM injection, significantly inhibited adenocarcinoma and adenoma formation in the colon (to 17-33% of the control).

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  • (PMID = 19155443.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA072720; United States / NIEHS NIH HHS / ES / ES05022; United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NCI NIH HHS / CA / P30 CA072720-12; United States / NIEHS NIH HHS / ES / ES005022-109003; United States / NIEHS NIH HHS / ES / P30 ES005022-109003; United States / NCI NIH HHS / CA / CA72720; United States / NCI NIH HHS / CA / CA072720-12
  • [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 / Antioxidants; 0 / Carcinogens; 1HGW4DR56D / Leukotriene B4; 27415-26-5 / 8-epi-prostaglandin F2alpha; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; 8EF1Z1238F / gamma-Tocopherol; 9042-14-2 / Dextran Sulfate; B7IN85G1HY / Dinoprost; K7Q1JQR04M / Dinoprostone; MO0N1J0SEN / Azoxymethane
  • [Other-IDs] NLM/ NIHMS172441; NLM/ PMC2821738
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3. Wang XY, Degos F, Dubois S, Tessiore S, Allegretta M, Guttmann RD, Jothy S, Belghiti J, Bedossa P, Paradis V: Glypican-3 expression in hepatocellular tumors: diagnostic value for preneoplastic lesions and hepatocellular carcinomas. Hum Pathol; 2006 Nov;37(11):1435-41
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  • [Title] Glypican-3 expression in hepatocellular tumors: diagnostic value for preneoplastic lesions and hepatocellular carcinomas.
  • Glypican-3 (GPC3), a member of heparan sulfate proteoglycans, plays a role in cell growth, differentiation, and migration.
  • Fourteen typical liver cell adenomas and 5 with malignant foci were also included.
  • In cases of adenomas, only malignant foci were positive.
  • This study shows that GPC3 is an efficient diagnostic marker of HCC, potentially useful in the differential diagnosis of liver cell adenomas and well-differentiated HCC.
  • [MeSH-major] Biomarkers, Tumor. Carcinoma, Hepatocellular / metabolism. Glypicans / biosynthesis. Liver Neoplasms / metabolism. Precancerous Conditions / diagnosis
  • [MeSH-minor] Adult. Aged. Female. Humans. Liver Cirrhosis / metabolism. Male. Middle Aged. alpha-Fetoproteins / biosynthesis

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  • (PMID = 16949914.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / GPC3 protein, human; 0 / Glypicans; 0 / alpha-Fetoproteins
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4. Jain S, Singhal S, Lee P, Xu R: Molecular genetics of hepatocellular neoplasia. Am J Transl Res; 2010;2(1):105-18
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Recent molecular genetic, pathologic, and clinical data have led to the stratification of hepatic adenomas into three subgroups: those with mutant TCF1/HNF1 alpha gene, those with mutant beta-catenin, and those without mutations in either of these loci.
  • Hepatic adenomas with alpha-catenin mutations have a significantly greater risk for malignant transformation in comparison with the other two subgroups.
  • Telangiectatic focal nodular hyperplasia has now been reclassified as telangiectatic adenoma due to the presence of non-random methylation patterns, consistent with the monoclonal origin which is similar to hepatic adenoma and HCC.
  • HCC precursor lesions demonstrate unique molecular alterations of HSP70, CAP2, glypican 3, and glutamine synthetase that have proven useful in the histologic diagnosis of early HCC.
  • Though specific genetic alterations depend on HCC etiology, the main proteins affected include cell membrane receptors (in particular tyrosine kinase receptors) as well as proteins involved in cell signaling (specifically Wnt/beta-catenin, Ras/Raf/MEK/ERK and PI3K/Akt/mTOR pathways), cell cycle regulation (i.e. p53, p16/INK4, cyclin/cdk complex), invasiveness (EMT, TGF-beta) and DNA metabolism.
  • HCCs can now be stratified into two clinically relevant groups: Class A, the low survival subclass (overall survival time 30.3+/- 8.02 months), shows strong expression signatures of cell proliferation and antiapoptosis genes (such as PNCA and cell cycle regulators CDK4, CCNB1, CCNA2, and CKS2) as well as genes involving ubiquitination and sumoylation; Class B, the high survival subclass (overall survival time 83.7 +/-10.3 months), does not have the above expression signature.



5. Zatelli MC, Piccin D, Vignali C, Tagliati F, Ambrosio MR, Bondanelli M, Cimino V, Bianchi A, Schmid HA, Scanarini M, Pontecorvi A, De Marinis L, Maira G, degli Uberti EC: Pasireotide, a multiple somatostatin receptor subtypes ligand, reduces cell viability in non-functioning pituitary adenomas by inhibiting vascular endothelial growth factor secretion. Endocr Relat Cancer; 2007 Mar;14(1):91-102
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pasireotide, a multiple somatostatin receptor subtypes ligand, reduces cell viability in non-functioning pituitary adenomas by inhibiting vascular endothelial growth factor secretion.
  • Somatostatin (SRIF) analogs have been employed in medical therapy of non-functioning pituitary adenomas (NFA), with contrasting results.
  • Previous evidence showed that SRIF can exert its antiproliferative effects by reducing vascular endothelial growth factor (VEGF) secretion and action, and that VEGF expression may be related to pituitary tumor growth.
  • The aim of our study was to clarify the possible effects of a multireceptor SRIF ligand on VEGF secretion and cell proliferation in human NFA primary cultures.
  • We assessed the expression of SRIF receptors (SSTR1-5), the in vitro effects on VEGF secretion, and on cell viability of SRIF and of the stable SRIF analog pasireotide (SOM230), which activates SSTR1, 2, 3, and 5.
  • Twenty-five NFA were examined by RT-PCR for expression of alpha-subunit, SSTR, VEGF, and VEGF receptors 1 (VEGF-R1) and 2 (VEGF-R2).
  • All NFA samples expressed alpha-sub, VEGF and VEGFR-1 and 2, while SSTR expression pattern was highly variable.
  • VEGF secretion and cell viability were reduced by SRIF and pasireotide in the 'responder' group, but not in the 'non-responder' group, including NFA expressing SSTR5.
  • In addition, SRIF and pasireotide completely abrogated the promoting effects of VEGF on NFA cell viability.
  • Our data demonstrate that pasireotide can inhibit NFA cell viability by inhibiting VEGF secretion, and suggest that the multireceptor-SSTR agonist pasireotide might be useful in medical therapy of selected NFA.
  • [MeSH-major] Adenoma / secretion. Oligopeptides / pharmacology. Pituitary Neoplasms / secretion. Somatostatin / pharmacology. Vascular Endothelial Growth Factor A / secretion
  • [MeSH-minor] Adult. Aged. Cell Survival / drug effects. Female. Hormones / pharmacology. Humans. Ligands. Male. RNA, Messenger / metabolism. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism

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  • (PMID = 17395978.001).
  • [ISSN] 1351-0088
  • [Journal-full-title] Endocrine-related cancer
  • [ISO-abbreviation] Endocr. Relat. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hormones; 0 / Ligands; 0 / Oligopeptides; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / Vascular Endothelial Growth Factor A; 51110-01-1 / Somatostatin; 98H1T17066 / pasireotide
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6. Song H, Li C, Li R, Geng J: Prognostic significance of AEG-1 expression in colorectal carcinoma. Int J Colorectal Dis; 2010 Oct;25(10):1201-9
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  • BACKGROUND: Astrocyte elevated gene-1 (AEG-1), as an HIV-1 or TNF-alpha-inducible transcript, is associated with various aspects of tumor malignancy.
  • METHODS: By immunohistochemical and western blot analysis, we investigated AEG-1 expression in normal mucosa, adenomas, and carcinomas of colorectum.
  • RESULTS: We found that AEG-1 expression levels were gradually elevated in normal tissues, low-grade adenoma, high-grade adenoma, and colorectal carcinoma, respectively.
  • Though AEG-1 staining mainly emerged in the cytoplasm, we observed that nuclear staining of AEG-1 tends to become more common in lesions from patients with more advanced disease stages.
  • Furthermore, there was a similar trend for Ki67 expression (as a proliferative index) from normal mucous to adenoma and carcinoma.
  • In addition, AEG-1 expression in colorectal carcinoma may be associated with tumor progression, indicating that AEG-1 may be a potential preventive and chemotherapeutic target in the patients.
  • [MeSH-major] Cell Adhesion Molecules / analysis. Colorectal Neoplasms / diagnosis
  • [MeSH-minor] Blotting, Western. Disease Progression. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Ki-67 Antigen / analysis. Prognosis. Severity of Illness Index. Survival Rate

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  • (PMID = 20625905.001).
  • [ISSN] 1432-1262
  • [Journal-full-title] International journal of colorectal disease
  • [ISO-abbreviation] Int J Colorectal Dis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Ki-67 Antigen; 0 / MTDH protein, human
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7. Dourakis SP, Alexopoulou A, Georgousi KK, Delladetsima JK, Tolis G, Archimandritis AJ: Glucagonoma syndrome: survival 21 years with concurrent liver metastases. Am J Med Sci; 2007 Sep;334(3):225-7
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  • [Title] Glucagonoma syndrome: survival 21 years with concurrent liver metastases.
  • A patient who survived for 21 years since initial discovery of glucagonoma with concurrent liver metastases is described.
  • Psychiatric symptoms, weight loss, necrolytic migratory erythema, diarrhea, and diabetes mellitus developed gradually after diagnosis of the tumor.
  • The longevity of this patient may be related to the slow tumor growth expressed histologically by ischemic necrosis of the malignant cells and in imaging by extensive tumor calcifications, a very rare finding in this type of the tumor.
  • [MeSH-major] Glucagonoma / pathology. Liver Neoplasms / secondary. Pancreatic Neoplasms / pathology



8. Chaw L, Krop TM, Hood AF: What is your diagnosis? Necrolytic migratory erythema associated with a glucagonoma. Cutis; 2008 Jan;81(1):25, 30-2
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  • [Title] What is your diagnosis? Necrolytic migratory erythema associated with a glucagonoma.
  • [MeSH-major] Erythema / etiology. Glucagonoma / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / pathology. Skin / pathology. Skin Diseases / etiology
  • [MeSH-minor] Female. Glucagon / blood. Humans. Middle Aged

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  • (PMID = 18306843.001).
  • [ISSN] 0011-4162
  • [Journal-full-title] Cutis
  • [ISO-abbreviation] Cutis
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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9. Candolfi M, Jaita G, Pisera D, Ferrari L, Barcia C, Liu C, Yu J, Liu G, Castro MG, Seilicovich A: Adenoviral vectors encoding tumor necrosis factor-alpha and FasL induce apoptosis of normal and tumoral anterior pituitary cells. J Endocrinol; 2006 Jun;189(3):681-90
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  • [Title] Adenoviral vectors encoding tumor necrosis factor-alpha and FasL induce apoptosis of normal and tumoral anterior pituitary cells.
  • Our previous work showed that tumor necrosis factor (TNF)-alpha and FasL induce apoptosis of anterior pituitary cells.
  • To further analyze the effect of these proapoptotic factors, we infected primary cultures from rat anterior pituitary, GH3 and AtT20 cells with first-generation adenoviral vectors encoding TNF-alpha, FasL or, as a control, beta-galactosidase (beta-Gal), under the control of the human cytomegalovirus promoter.
  • Although we observed basal expression of TNF-alpha and FasL in control cultures of anterior pituitary cells, fluorescence-activated cell sorting (FACS) cell cycle analysis showed that the overexpression of TNF-alpha or FasL increases the percentage of hypodiploid lactotropes and somatotropes.
  • Nuclear morphology and TUNEL staining revealed that the cells undergo an apoptotic death process.
  • We detected strong immunoreactivity for TNFR1 and Fas in the somatolactotrope cell line GH3.
  • TNF-alpha, but not FasL, was expressed in control cultures of GH3 cells.
  • The infection of GH3 cells with adenovirus encoding TNF-alpha or FasL increased the percentages of hypodiploid and TUNEL-positive cells.
  • TNF-alpha or FasL immunoreactivity was not observed in the corticotrope cell line AtT20.
  • However, adenovirus encoding TNF-alpha or FasL efficiently transduced these cells and increased the percentages of hypodiploid and TUNEL-positive cells.
  • The expression of beta-Gal was detected in all these cultures but did not affect cell viability.
  • In conclusion, these results suggest that death signaling cascades triggered by TNF receptor 1 (TNFR1) and Fas are present in both normal and tumoral pituitary cells.
  • Therefore, overexpression of proapoptotic factors could be a useful tool in the therapy of pituitary adenomas.
  • [MeSH-major] Adenoviridae / genetics. Genetic Vectors / administration & dosage. Membrane Glycoproteins / genetics. Pituitary Gland, Anterior / cytology. Pituitary Neoplasms / pathology. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factors / genetics
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Fas Ligand Protein. Female. Flow Cytometry. Gene Expression. Immunohistochemistry / methods. Rats. Rats, Sprague-Dawley. Rats, Wistar

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  • (PMID = 16731798.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Grant] United States / FIC NIH HHS / TW / 1R03 TW006273-01; United States / NINDS NIH HHS / NS / 1R21 NS047298-01; United States / NINDS NIH HHS / NS / NS 42893-01; United States / NINDS NIH HHS / NS / U54 NS045309-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Tnfsf6 protein, rat; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Necrosis Factors
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10. Lee KS, Lee YS, Lee JM, Ito K, Cinghu S, Kim JH, Jang JW, Li YH, Goh YM, Chi XZ, Wee H, Lee HW, Hosoya A, Chung JH, Jang JJ, Kundu JK, Surh YJ, Kim WJ, Ito Y, Jung HS, Bae SC: Runx3 is required for the differentiation of lung epithelial cells and suppression of lung cancer. Oncogene; 2010 Jun 10;29(23):3349-61
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  • [Title] Runx3 is required for the differentiation of lung epithelial cells and suppression of lung cancer.
  • K-ras mutations are associated with the initiation of lung adenocarcinomas, but K-ras-independent mechanisms may also initiate lung tumors.
  • Here, we find that the runt-related transcription factor Runx3 is essential for normal murine lung development and is a tumor suppressor that prevents lung adenocarcinoma.
  • Importantly, Runx3-/- bronchioli exhibit impaired differentiation, as evidenced by the accumulation of epithelial cells containing specific markers for both alveolar (that is SP-B) and bronchiolar (that is CC10) lineages.
  • Runx3-/- epithelial cells also express Bmi1, which supports self-renewal of stem cells.
  • Lung adenomas spontaneously develop in aging Runx3+/- mice ( approximately 18 months after birth) and invariably exhibit reduced levels of Runx3.
  • As K-ras mutations are very rare in these adenomas, Runx3+/- mice provide an animal model for lung tumorigenesis that recapitulates the preneoplastic stage of human lung adenocarcinoma development, which is independent of K-Ras mutation.
  • We conclude that Runx3 is essential for lung epithelial cell differentiation, and that downregulation of Runx3 is causally linked to the preneoplastic stage of lung adenocarcinoma.
  • [MeSH-major] Core Binding Factor Alpha 3 Subunit / physiology. Lung / cytology. Lung Neoplasms / prevention & control
  • [MeSH-minor] Adenocarcinoma / etiology. Adenocarcinoma / pathology. Animals. Cell Differentiation. Cell Proliferation. Epithelial Cells / cytology. Humans. Mice. Mice, Inbred C57BL. Nuclear Proteins / analysis. Nuclear Proteins / physiology. Polycomb Repressive Complex 1. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins / physiology. Proto-Oncogene Proteins p21(ras) / genetics. Pulmonary Surfactant-Associated Protein B / analysis. Repressor Proteins / analysis. Repressor Proteins / physiology. Urethane / toxicity. Uteroglobin / analysis

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  • (PMID = 20228843.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bmi1 protein, mouse; 0 / Core Binding Factor Alpha 3 Subunit; 0 / Nuclear Proteins; 0 / Proto-Oncogene Proteins; 0 / Pulmonary Surfactant-Associated Protein B; 0 / Repressor Proteins; 0 / Runx3 protein, human; 0 / Runx3 protein, mouse; 0 / SCGB1A1 protein, human; 0 / Scgb1a1 protein, mouse; 3IN71E75Z5 / Urethane; 9060-09-7 / Uteroglobin; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); EC 6.3.2.19 / Polycomb Repressive Complex 1
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11. McGregor D: Ethyl tertiary-butyl ether: a toxicological review. Crit Rev Toxicol; 2007 May;37(4):287-312
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  • Increases in kidney weight were seen in both sexes, but protein droplet accumulation (with alpha(2u)-globulin involvement) and sustained increases in cell proliferation occurred only in males.
  • The proportion of liver cells engaged in S-phase DNA synthesis was increased in mice of both sexes exposed by inhalation.
  • In male rats only, TBA induced alpha(2u)-globulin nephropathy-related renal tubule adenomas.
  • In addition, increases in thyroid follicular cell adenoma incidence were associated with TBA treatment in female mice.

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  • (PMID = 17453936.001).
  • [ISSN] 1040-8444
  • [Journal-full-title] Critical reviews in toxicology
  • [ISO-abbreviation] Crit. Rev. Toxicol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Air Pollutants; 0 / Ethyl Ethers; 0 / Methyl Ethers; 29I4YB3S89 / methyl tert-butyl ether; 3R9B16WR19 / ethyl tert-butyl ether
  • [Number-of-references] 128
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12. Mełeń-Mucha G: [Molecular aspects of pituitary tumors]. Endokrynol Pol; 2005 May-Jun;56(3):333-8
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  • [Title] [Molecular aspects of pituitary tumors].
  • Pituitary adenomas are common benign neoplasms, accounting for approximately 15% of intracranial tumors.
  • In systematic autopsy, pituitary tumors are found in 25%, of the population, but only one-third of these tumors give rise to clinical manifestations.
  • The progress in the studies concerning pituitary tumorigenesis is rather slow and, due to several limitations, including the anatomic inaccessibility of human pituitary gland, the lack of functional human cell lines in culture and the discrepancies between human and animal pituitary oncogenesis (in rodents pituitary hyperplasia is a prerequisite for adenoma development).
  • In humans, the majority of pituitary tumors are monoclonal in origin and derived from single mutated pituicyte, rarely hyperplasia is a prerequisite for adenoma formation.
  • As in the case of other tumors, activating mutations in oncogenes (GNAS1, PTTG) and inactivating mutations in tumor suppressor genes (MEN1, CNC1) lead to pituitary tumors development.
  • However, mutations in classic oncogenes are very rarely associated with these tumors.
  • [MeSH-major] Pituitary Neoplasms / diagnosis. Pituitary Neoplasms / genetics
  • [MeSH-minor] Animals. Chromogranins. Cyclic AMP-Dependent Protein Kinase RIalpha Subunit. Cyclic AMP-Dependent Protein Kinases. GTP-Binding Protein alpha Subunits, Gs. Gene Expression Regulation, Neoplastic / genetics. Genes, Tumor Suppressor / physiology. Humans. Neoplasm Proteins. Proteins. Proto-Oncogene Proteins. Securin

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  • (PMID = 16350728.001).
  • [ISSN] 0423-104X
  • [Journal-full-title] Endokrynologia Polska
  • [ISO-abbreviation] Endokrynol Pol
  • [Language] pol
  • [Publication-type] Journal Article; Review
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Chromogranins; 0 / Cyclic AMP-Dependent Protein Kinase RIalpha Subunit; 0 / MEN1 protein, human; 0 / Neoplasm Proteins; 0 / PRKAR1A protein, human; 0 / Proteins; 0 / Proto-Oncogene Proteins; 0 / Securin; 0 / pituitary tumor-transforming protein 1, human; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.1.- / GNAS protein, human; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
  • [Number-of-references] 40
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13. Takashima K, Ito Y, Gonzalez FJ, Nakajima T: Different mechanisms of DEHP-induced hepatocellular adenoma tumorigenesis in wild-type and Ppar alpha-null mice. J Occup Health; 2008;50(2):169-80
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  • [Title] Different mechanisms of DEHP-induced hepatocellular adenoma tumorigenesis in wild-type and Ppar alpha-null mice.
  • Di (2-ethylhexyl) phthalate (DEHP) exposure is thought to lead to hepatocellular hypertrophy and hyperplasia in rodents mediated via peroxisome proliferator-activated receptor alpha (PPAR alpha).
  • A recent study revealed that long-term exposure to relatively low-dose DEHP (0.05%) caused liver tumors including hepatocellular carcinomas, hepatocellular adenomas, and chologiocellular carcinomas at a higher incidence in Ppar alpha-null mice (25.8%) than in wild-type mice (10.0%).
  • Using tissues with hepatocellular adenoma, microarray (Affymetrix MOE430A) as well as, in part, real-time quantitative PCR analysis was conducted to elucidate the mechanisms of the adenoma formation resulting from DEHP exposure in both genotyped mice.
  • The microarray profiles showed that the up- or down-regulated genes were quite different between hepatocellular adenoma tissues of wild-type and Ppar alpha-null mice exposed to DEHP.
  • The gene expressions of apoptotic peptidase activating factor 1 (Apaf1) and DNA-damage-inducible 45 alpha (Gadd45a) were increased in the hepatocellular adenoma tissues of wild-type mice exposed to DEHP, whereas they were unchanged in corresponding tissues of Ppar alpha-null mice.
  • On the other hand, the expressions of cyclin B2 and myeloid cell leukemia sequence 1 were increased only in the hepatocellular adenoma tissues of Ppar alpha-null mice.
  • Taken together, DEHP may induce hepatocellular adenomas, in part, via suppression of G2/M arrest regulated by Gadd45a and caspase 3-dependent apoptosis in Ppar alpha-null mice, but these genes may not be involved in tumorigenesis in the wild-type mice.
  • In contrast, the expression level of Met was notably increased in the liver adenoma tissue of wild-type mice, which may suggest the involvement of Met in DEHP-induced tumorigenesis in wild-type mice.
  • [MeSH-major] Diethylhexyl Phthalate / toxicity. Liver / drug effects. Liver Neoplasms, Experimental / chemically induced. Liver Neoplasms, Experimental / genetics. PPAR alpha / deficiency
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / physiology. Apoptotic Protease-Activating Factor 1 / antagonists & inhibitors. Apoptotic Protease-Activating Factor 1 / biosynthesis. Caspase 3 / metabolism. Cell Cycle Proteins / antagonists & inhibitors. Cell Cycle Proteins / biosynthesis. Cell Division / genetics. G2 Phase / genetics. Gene Expression Profiling. Hepatocytes / drug effects. Hyperplasia. Mice. Mice, Knockout. Microarray Analysis. Nuclear Proteins / antagonists & inhibitors. Nuclear Proteins / biosynthesis. Plasticizers / toxicity. Polymerase Chain Reaction. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 18403868.001).
  • [ISSN] 1348-9585
  • [Journal-full-title] Journal of occupational health
  • [ISO-abbreviation] J Occup Health
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Apaf1 protein, mouse; 0 / Apoptotic Protease-Activating Factor 1; 0 / Cell Cycle Proteins; 0 / Gadd45a protein, mouse; 0 / Nuclear Proteins; 0 / PPAR alpha; 0 / Plasticizers; 0 / RNA, Messenger; C42K0PH13C / Diethylhexyl Phthalate; EC 3.4.22.- / Caspase 3
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14. Letsas KP, Frangou-Lazaridis M, Skyrlas A, Tsatsoulis A, Malamou-Mitsi V: Transcription factor-mediated proliferation and apoptosis in benign and malignant thyroid lesions. Pathol Int; 2005 Nov;55(11):694-702
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  • Transcription factors play an essential role in regulating both cell proliferation and programmed cell death.
  • Proliferation and apoptosis-related transcription factor immunoexpression patterns were concomitantly investigated in tissue sections of normal thyroid, goiters, follicular adenomas and well-differentiated papillary and follicular carcinomas using antibodies against prothymosin alpha, E2F-1, p53, Bcl2, and Bax proteins.
  • Prothymosin alpha and E2F-1 immunoexpression levels were found to be significantly elevated in well-differentiated carcinomas compared to adenomas, goiters and normal tissues (P < 0.05).
  • Direct correlations were observed between prothymosin alpha and Bcl2 as well as between E2F-1 and Bax immunoexpression (P < 0.05).
  • These data demonstrate that prothymosin alpha and E2F-1 are strongly involved in the proliferation processes of thyroid neoplasias.
  • Furthermore, prothymosin alpha may promote cell survival through the Bcl2 anti-apoptotic pathway, while E2F-1-induced apoptosis via p53-independent pathways may be associated with transcriptional activation of bax pro-apoptotic gene.
  • [MeSH-major] Apoptosis. Cell Proliferation. Thyroid Diseases / pathology. Thyroid Gland / pathology. Thyroid Neoplasms / pathology. Transcription Factors / physiology
  • [MeSH-minor] Adenoma / pathology. Adenoma / physiopathology. Adolescent. Adult. Aged. Carcinoma, Papillary, Follicular / pathology. Carcinoma, Papillary, Follicular / physiopathology. DNA-Binding Proteins / analysis. DNA-Binding Proteins / immunology. DNA-Binding Proteins / physiology. E2F1 Transcription Factor / analysis. E2F1 Transcription Factor / immunology. E2F1 Transcription Factor / physiology. Female. Goiter / pathology. Goiter / physiopathology. Humans. Immunohistochemistry. Male. Middle Aged. Protein Precursors / analysis. Protein Precursors / immunology. Protein Precursors / physiology. Repressor Proteins / analysis. Repressor Proteins / immunology. Repressor Proteins / physiology. Thymosin / analogs & derivatives. Thymosin / analysis. Thymosin / immunology. Thymosin / physiology. Tumor Suppressor Protein p53 / analysis. Tumor Suppressor Protein p53 / immunology. Tumor Suppressor Protein p53 / physiology. Tumor Suppressor Proteins / analysis. Tumor Suppressor Proteins / immunology. Tumor Suppressor Proteins / physiology. bcl-2-Associated X Protein / analysis. bcl-2-Associated X Protein / immunology. bcl-2-Associated X Protein / physiology

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  • (PMID = 16271081.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / BCLAF1 protein, human; 0 / DNA-Binding Proteins; 0 / E2F1 Transcription Factor; 0 / Protein Precursors; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / bcl-2-Associated X Protein; 0 / prothymosin alpha; 61512-21-8 / Thymosin
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15. Zucman-Rossi J, Jeannot E, Nhieu JT, Scoazec JY, Guettier C, Rebouissou S, Bacq Y, Leteurtre E, Paradis V, Michalak S, Wendum D, Chiche L, Fabre M, Mellottee L, Laurent C, Partensky C, Castaing D, Zafrani ES, Laurent-Puig P, Balabaud C, Bioulac-Sage P: Genotype-phenotype correlation in hepatocellular adenoma: new classification and relationship with HCC. Hepatology; 2006 Mar;43(3):515-24
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  • [Title] Genotype-phenotype correlation in hepatocellular adenoma: new classification and relationship with HCC.
  • Hepatocellular adenomas are benign tumors that can be difficult to diagnose.
  • A multicentric series of 96 liver tumors with a firm or possible diagnosis of hepatocellular adenoma was reviewed by liver pathologists.
  • No tumors were mutated in both HNF1alpha and beta-catenin enabling tumors to be classified into 3 groups, according to genotype.
  • Tumors with HNF1alpha mutations formed the most important group of adenomas (44 cases).
  • In contrast, the group of tumors defined by beta-catenin activation included 13 lesions with frequent cytological abnormalities and pseudo-glandular formation (P < 10(-5)).
  • The third group of tumors without mutation was divided into two subgroups based on the presence of inflammatory infiltrates.
  • The subgroup of tumors consisting of 17 inflammatory lesions, resembled telangiectatic focal nodular hyperplasias, with frequent cytological abnormalities (P = 10(-3)), ductular reaction (P < 10(-2)), and dystrophic vessels (P = .02).
  • In this classification, hepatocellular carcinoma associated with adenoma or borderline lesions between carcinoma and adenoma is found in 46% of the beta-catenin-mutated tumors whereas they are never observed in inflammatory lesions and are rarely found in HNF1alpha mutated tumors (P = .004).
  • In conclusion, the molecular and pathological classification of hepatocellular adenomas permits the identification of strong genotype-phenotype correlations and suggests that adenomas with beta-catenin activation have a higher risk of malignant transformation.
  • [MeSH-major] Adenoma, Liver Cell / genetics. Carcinoma, Hepatocellular / genetics. Hepatocyte Nuclear Factor 1-alpha / genetics. Liver Neoplasms / genetics. beta Catenin / genetics

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  • [CommentIn] Hepatology. 2006 Mar;43(3):401-4 [16496344.001]
  • [CommentIn] Histopathology. 2007 Dec;51(6):855-6 [17903198.001]
  • (PMID = 16496320.001).
  • [ISSN] 0270-9139
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin
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16. Oberg K: Pancreatic endocrine tumors. Semin Oncol; 2010 Dec;37(6):594-618
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  • [Title] Pancreatic endocrine tumors.
  • Pancreatic endocrine tumors have been steadily growing in incidence and prevalence during the last two decades, showing an incidence of 4-5/1,000,000 population.
  • They represent a heterogeneous group with very varying tumor biology and prognosis.
  • About half of the patients present clinical symptoms and syndromes related to substances released from the tumors (Zollinger-Ellison syndrome, insulinoma, glucagonoma, etc) and the other half are so-called nonfunctioning tumors mainly presenting with symptoms such as obstruction, jaundice, bleeding, and abdominal mass.
  • Ten percent to 15% of the pancreatic endocrine tumors are part of an inherited syndrome such as multiple endocrine neoplasia type 1 (MEN-1), von Hippel-Lindau (VHL), neurofibromatosis, or tuberousclerosis.
  • The diagnosis is based on histopathology demonstrating neuroendocrine features such as positive staining for chromogranin A and specific hormones such as gastrin, proinsulin, and glucagon.
  • Moreover, the biochemical diagnosis includes measurement of chromogranins A and B or specific hormones such as gastrin, insulin, glucagon, and vasoactive intestinal polypeptide (VIP) in the circulation.
  • Surgery is still one of the cornerstones in the management of pancreatic endocrine tumors, but curative surgery is rarely obtained in most cases because of metastatic disease.
  • Cytotoxic drugs, biological agents, such as somatostatin analogs, alpha interferons, mammalian target of rapamycin (mTOR) inhibitors and tyrosine kinase inhibitors are routinely used.
  • Tumor-targeted radioactive treatment is available in many centres in Europe and is effective in patients with tumors that express high content of somatostatin receptors type 2 and 5.
  • In the future, treatment will be based on tumor biology and molecular genetics with the aim of so-called personalized medicine.
  • [MeSH-major] Pancreatic Neoplasms
  • [MeSH-minor] Antineoplastic Agents / therapeutic use. Biological Therapy / methods. Biomarkers, Tumor. Humans. Neoplastic Syndromes, Hereditary / diagnosis. Neoplastic Syndromes, Hereditary / therapy. Pancreatectomy. Paraneoplastic Endocrine Syndromes / diagnosis. Paraneoplastic Endocrine Syndromes / therapy



17. Vitale G, Caraglia M, van Koetsveld PM, Maroni P, Marra M, Colao A, Lamberts SW, Cavagnini F, Hofland LJ: Potential role of type I interferons in the treatment of pituitary adenomas. Rev Endocr Metab Disord; 2009 Jun;10(2):125-33
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  • [Title] Potential role of type I interferons in the treatment of pituitary adenomas.
  • Treatment with type I IFNs of patients affected by chronic viral hepatitis, multiple sclerosis and tumors influences the secretion of pituitary hormones.
  • This article reviews the current knowledge about the effects of IFN-alpha and IFN-beta on hypothalamic-pituitary function and describes the potential role of type I IFNs in the treatment of pituitary adenomas.
  • [MeSH-minor] Humans. Hypothalamo-Hypophyseal System / drug effects. Pituitary-Adrenal System / drug effects. Receptor, Interferon alpha-beta / metabolism

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  • (PMID = 18604644.001).
  • [ISSN] 1573-2606
  • [Journal-full-title] Reviews in endocrine & metabolic disorders
  • [ISO-abbreviation] Rev Endocr Metab Disord
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Interferon Type I; 156986-95-7 / Receptor, Interferon alpha-beta
  • [Number-of-references] 72
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18. Huhtaniemi I, Rulli S, Ahtiainen P, Poutanen M: Multiple sites of tumorigenesis in transgenic mice overproducing hCG. Mol Cell Endocrinol; 2005 Apr 29;234(1-2):117-26
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  • We have produced transgenic (TG) mice expressing under the ubiquitin C promoter either the glycoprotein hormone common alpha-subunit (C(alpha)) or human chorionic gonadotropin (hCG) beta-subunit.
  • C(alpha) overexpression alone had no phenotypic effect, but the hCG(beta) expressing females, presenting with moderately elevated levels of bioactive LH/hCG, due to dimerization of the TG hCG(beta) with endogenous C(alpha), developed multiple gonadal and extragonadal neoplasias.
  • Crosses of the C(alpha) and hCG(beta) mice (hCG(alpha)beta) had >1000-fold elevated hCG levels, due to ubiquitous transgene expression, and presented with more aggressive tumour formation.
  • The ovaries displayed initially strong luteinisation of all somatic cell types, leading to formation of luteomas, and subsequently to germ cell tumours (teratomas).
  • In contrast to the females, similar high levels of hCG in male mice had only marginal effects in adulthood, with slight Leydig cell hyperplasia and atrophy in the seminiferous epithelium.
  • However, clear Leydig cell adenomas were observed in postnatal mice, apparently originating from fetal Leydig cells.
  • [MeSH-major] Chorionic Gonadotropin, beta Subunit, Human / genetics. Chorionic Gonadotropin, beta Subunit, Human / metabolism. Glycoprotein Hormones, alpha Subunit / genetics. Glycoprotein Hormones, alpha Subunit / metabolism. Neoplasms / etiology

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  • (PMID = 15836960.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human; 0 / Glycoprotein Hormones, alpha Subunit
  • [Number-of-references] 57
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19. Wang KL, Weinrach DM, Luan C, Han M, Lin F, Teh BT, Yang XJ: Renal papillary adenoma--a putative precursor of papillary renal cell carcinoma. Hum Pathol; 2007 Feb;38(2):239-46
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  • [Title] Renal papillary adenoma--a putative precursor of papillary renal cell carcinoma.
  • The precursor lesions of renal cell carcinoma (RCC) are unknown.
  • The purpose of this study is to determine the incidence, histomorphological features, and immunohistochemical features of papillary adenoma and elucidate its potential relationship to RCC.
  • Immunohistochemistry was carried out with antibodies specific for alpha-methyl-coenzyme A racemase (AMACR) and glutathione S-transferase alpha (clear-cell RCC marker).
  • Thirty-eight (7%) nephrectomy specimens showed histologic evidence of papillary adenoma.
  • Seven papillary adenomas (18%) occurred in the setting of acquired polycystic kidney disease (APKD), 6 in clear-cell RCCs, 3 in chromophobe RCCs, 2 in end-stage kidney disease, 1 in oncocytoma, 1 in angiomyolipoma, and 1 in renal schwannoma.
  • Furthermore, papillary adenomas were more commonly found in kidneys removed for PRCC (25%, 18/71) than in kidneys harboring clear-cell RCC (1.9%, 6/318).
  • Histomorphologically, papillary adenomas were characterized by varying proportions of papillae and tubules formed by cuboidal cells with scant basophilic cytoplasm similar to those in type 1 PRCC.
  • Adenomas associated with PRCC tend to be multiple in number (61% [11/18] of cases had >2 adenomas; mean, 5).
  • In contrast, 100% of papillary adenomas arising in other conditions had less than 2 adenomas.
  • Most of the adenomas (82%, 31/38) stained strongly for AMACR in a fashion similar to that of PRCC.
  • In this study of surgical specimens, the high coincidence, multifocality, and histologic and immunohistochemical similarities between papillary adenoma and PRCC suggest that the 2 are strongly associated and may represent a continuum of 1 biologic process.
  • In contrast, adenomas associated with APKD exhibit distinct morphological and immunohistochemical features and, therefore, may have an entirely different pathogenesis.
  • [MeSH-major] Carcinoma, Papillary / pathology. Carcinoma, Renal Cell / pathology. Kidney Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma, Clear Cell / enzymology. Adenocarcinoma, Clear Cell / pathology. Adenoma. Adenoma, Oxyphilic / enzymology. Adenoma, Oxyphilic / pathology. Adult. Aged. Aged, 80 and over. Angiomyolipoma / enzymology. Angiomyolipoma / pathology. Disease Progression. Female. Glutathione Transferase / analysis. Humans. Immunohistochemistry. Isoenzymes / analysis. Kidney / enzymology. Kidney / pathology. Kidney Failure, Chronic / enzymology. Kidney Failure, Chronic / pathology. Male. Middle Aged. Models, Biological. Polycystic Kidney Diseases / enzymology. Polycystic Kidney Diseases / pathology. Racemases and Epimerases / analysis

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  • (PMID = 17056094.001).
  • [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] 0 / Isoenzymes; EC 2.5.1.18 / Glutathione Transferase; EC 2.5.1.18 / glutathione S-transferase alpha; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
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20. Laumonier H, Bioulac-Sage P, Laurent C, Zucman-Rossi J, Balabaud C, Trillaud H: Hepatocellular adenomas: magnetic resonance imaging features as a function of molecular pathological classification. Hepatology; 2008 Sep;48(3):808-18
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  • [Title] Hepatocellular adenomas: magnetic resonance imaging features as a function of molecular pathological classification.
  • Hepatocellular adenomas (HCAs) are a group of benign tumors forming three molecular pathological subgroups:.
  • For the diagnosis of HNF-1alpha-inactivated HCA, the positive predictive value of homogeneous signal dropout on chemical shift images was 100%, the negative predictive value was 94.7%, the sensitivity was 86.7%, and the specificity was 100%.
  • Marked hypersignal on T2W sequences associated with delayed persistent enhancement had a positive predictive value of 88.5%, a negative predictive value of 84%, a sensitivity of 85.2%, and a specificity of 87.5% for the diagnosis of inflammatory HCA.
  • [MeSH-major] Adenoma, Liver Cell / classification. Adenoma, Liver Cell / pathology. Liver Neoplasms / classification. Liver Neoplasms / pathology. Magnetic Resonance Imaging
  • [MeSH-minor] Adult. Biomarkers, Tumor / metabolism. Fatty Liver / pathology. Female. Hepatocyte Nuclear Factor 1-alpha / metabolism. Humans. Inflammation / pathology. Liver / pathology. Male. Middle Aged. Predictive Value of Tests. Retrospective Studies. Sensitivity and Specificity. beta Catenin / metabolism

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  • [ErratumIn] Hepatology. 2008 Oct;48(4):1356
  • (PMID = 18688875.001).
  • [ISSN] 1527-3350
  • [Journal-full-title] Hepatology (Baltimore, Md.)
  • [ISO-abbreviation] Hepatology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / beta Catenin
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21. Barzon L, Maffei P, Sonino N, Pilon C, Baldazzi L, Balsamo A, Del Maschio O, Masi G, Trevisan M, Pacenti M, Fallo F: The role of 21-hydroxylase in the pathogenesis of adrenal masses: review of the literature and focus on our own experience. J Endocrinol Invest; 2007 Jul-Aug;30(7):615-23
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  • An exaggerated response of 17- hydroxyprogesterone (17-OHP) to exogenous ACTH stimulation has been found in 30 to 70% of patients with incidentally discovered adrenal tumors, supporting the concept that congenital 21- hydroxylase deficiency may be a predisposing factor for adrenocortical tumorigenesis.
  • Decreased expression of 21-hydroxylase gene has been observed in sporadic non-functioning adrenocortical adenomas and adrenocortical carcinomas, in agreement with the reduced steroidogenic activity found in these types of tumors.
  • Screening studies for the presence of mutations in CYP21A2 gene, encoding 21-hydroxylase, in patients with sporadic adrenocortical tumors yielded discordant results.
  • Overall, a higher frequency of germline 21-hydroxylase mutation carriers has been found among patients with adrenal tumors, including incidentalomas, than in the general population.
  • However, the presence of mutations did not correlate with endocrine test results and tumor mass features, suggesting that 21-hydroxylase deficiency does not represent a relevant mechanism in adrenal tumorigenesis.
  • [MeSH-minor] 17-alpha-Hydroxyprogesterone / metabolism. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Glucocorticoids / therapeutic use. Humans. Incidental Findings

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  • (PMID = 17848847.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Glucocorticoids; 68-96-2 / 17-alpha-Hydroxyprogesterone; EC 1.14.14.16 / Steroid 21-Hydroxylase
  • [Number-of-references] 64
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22. Terada T: Ductal adenoma of the breast: immunohistochemistry of two cases. Pathol Int; 2008 Dec;58(12):801-5
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  • [Title] Ductal adenoma of the breast: immunohistochemistry of two cases.
  • The author reports herein two cases of ductal adenoma of the breast with an emphasis on immunohistochemistry.
  • Histologically, both cases were ductal adenomas composed of ductal epithelial cells and myoepithelial cells.
  • Immunohistochemically, myoepithelial cells were noted in both cases; cytokeratin (CK) 14 and p63 were the most reliable myoepithelial markers, followed by CD10, alpha-smooth muscle actin and S100 protein.
  • The tumor cells expressed p53 protein (case 1, positive cell percentage 5%; case 2, 7%), c-erbB2 (HER2/neu, 76%, 64%), CEA (5%, 0%), estrogen receptor (33%, 84%), but were negative for progesterone receptor.
  • [MeSH-major] Adenoma / diagnosis. Breast Neoplasms / diagnosis. Papilloma, Intraductal / diagnosis
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Diagnosis, Differential. Epithelial Cells / chemistry. Epithelial Cells / pathology. Female. Humans. Immunohistochemistry. Middle Aged



23. Roeckel N, Woerner SM, Kloor M, Yuan YP, Patsos G, Gromes R, Kopitz J, Gebert J: High frequency of LMAN1 abnormalities in colorectal tumors with microsatellite instability. Cancer Res; 2009 Jan 1;69(1):292-9
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  • [Title] High frequency of LMAN1 abnormalities in colorectal tumors with microsatellite instability.
  • Glycosyl epitopes have been identified as tumor-specific markers in colorectal tumors and various lines of evidence indicate the significance of altered synthesis, transport, and secretion of glycoproteins in tumorigenesis.
  • However, aberrant glycosylation has been largely ignored in microsatellite unstable (MSI-H) colorectal tumors.
  • Therefore, we analyzed mutation frequencies of genes of the cellular glycosylation machinery in MSI-H tumors, focusing on frameshift mutations in coding MNRs (cMNRs).
  • Among 28 candidate genes, LMAN1/ERGIC53, a mannose-specific lectin mediating endoplasmatic reticulum (ER)-to-Golgi transit of glycosylated proteins, showed high mutation frequency in MSI-H colorectal cancer cell lines (52%; 12 of 23), carcinomas (45%; 72 of 161), and adenomas (40%; 8 of 20).
  • Biallelic mutations were observed in 17% (4 of 23) of MSI-H colorectal cancer cell lines.
  • LMAN1 was found to be transcribed but truncated protein remained undetectable in these LMAN1-mutant cell lines.
  • Immunohistochemical and molecular analysis of LMAN1-mutated carcinomas and adenomas revealed regional loss of LMAN1 expression due to biallelic LMAN1 cMNR frameshift mutations.
  • In LMAN1-deficient colorectal cancer cell lines, secretion of the LMAN1 client protein alpha-1-antitrypsin (A1AT), an inhibitor of angiogenesis and tumor growth, was significantly impaired but could be restored upon LMAN1 re-expression.
  • [MeSH-minor] Frameshift Mutation. Gene Expression. Humans. Microsatellite Instability. RNA, Messenger / genetics. alpha 1-Antitrypsin / secretion

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  • (PMID = 19118014.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LMAN1 protein, human; 0 / Mannose-Binding Lectins; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / alpha 1-Antitrypsin
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24. Zamora V, Cabanne A, Salanova R, Bestani C, Domenichini E, Marmissolle F, Giacomi N, O'Connor J, Méndez G, Roca E, Buenos Aires and La Plata Argentina Argentum Working Group: Immunohistochemical expression of somatostatin receptors in digestive endocrine tumours. Dig Liver Dis; 2010 Mar;42(3):220-5
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  • The somatostatin receptors types 1-5 expression in a series including 100 gastro-entero-pancreatic endocrine tumours were analysed.
  • METHODS: From a prospectively built database of patients with gastro-entero-pancreatic endocrine tumours referred from three institutions, 100 cases with clinical and pathological data were selected.
  • Somatostatin receptors expression by immunohistochemistry with somatostatin receptor types 1-5 antibodies in tissue paraffin sections were studied and correlated with the histological diagnosis according to the WHO classification, location and functional status.
  • RESULTS: Of the 100 cases, 67 were gastrointestinal tumours, 25 pancreatic and 8 liver metastasis of unknown origin.
  • Thirty-one of them were functioning tumours: 2 insulinomas, 5 gastrinomas, 1 glucagonoma and 23 carcinoids.
  • Somatostatin receptors expression was less frequent in pancreatic than in gastrointestinal tumours.
  • CONCLUSIONS: Immunohistochemistry revealed that somatostatin receptors were highly expressed in both primary and metastatic gastro-entero-pancreatic endocrine tumours with heterogeneous staining distribution.
  • It proved to be a reliable technique even in small tumour samples.

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  • [Copyright] 2009 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
  • [CommentIn] Dig Liver Dis. 2010 Mar;42(3):173-4 [20117969.001]
  • (PMID = 19819769.001).
  • [ISSN] 1878-3562
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Receptors, Somatostatin
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25. Kim K, Yoshida D, Teramoto A: Expression of hypoxia-inducible factor 1alpha and vascular endothelial growth factor in pituitary adenomas. Endocr Pathol; 2005;16(2):115-21
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  • [Title] Expression of hypoxia-inducible factor 1alpha and vascular endothelial growth factor in pituitary adenomas.
  • In malignant tumors, HIF-1alpha upregulates vascular endothelial growth factor (VEGF) expression to induce tumor angiogenesis.
  • Although VEGF and HIF-1alpha are expressed in pituitary adenomas, the relationships of these factors remain unclear.
  • Therefore, we examined the expression of HIF-1alpha and VEGF using real-time RT-PCR and immunohistochemistry to clarify the relationship of these factors in pituitary adenomas.
  • HIF-1alpha mRNA and VEGF mRNA levels in pituitary adenoma tissues from 25 operated patients were quantified using real-time RT-PCR.
  • HIF-1alpha mRNA and protein were expressed in all pituitary adenomas examined.
  • Their expression tended to be higher in GH-producing and lower in ACTH-producing tumors.
  • VEGF mRNA and protein were also expressed in all pituitary adenomas.
  • The mutual expression of HIF-1alpha and VEGF was of no significance; in only a few cells were HIF-1alpha and VEGF co-localized.
  • Our results suggest that in pituitary adenomas VEGF expression may not depend strongly on HIF-1alpha expression.
  • [MeSH-major] Adenoma / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Pituitary Neoplasms / metabolism. Vascular Endothelial Growth Factor A / biosynthesis

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  • (PMID = 16199896.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / RNA, Messenger; 0 / Vascular Endothelial Growth Factor A
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26. Mizuno T, Hiraoka H, Yoshioka C, Takeda Y, Matsukane Y, Shimoyama N, Morimoto M, Hayashi T, Okuda M: Superficial necrolytic dermatitis associated with extrapancreatic glucagonoma in a dog. Vet Dermatol; 2009 Feb;20(1):72-9
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  • [Title] Superficial necrolytic dermatitis associated with extrapancreatic glucagonoma in a dog.
  • Based on histopathological findings, blood examinations and necropsy findings, the condition was diagnosed as superficial necrolytic dermatitis associated with a glucagon-secreting extrapancreatic neuroendocrine tumour.
  • Gross necropsy revealed tumour invasion into the spleen, liver, adrenal glands and mesenteric lymph nodes.
  • Immunohistochemical analysis of the neoplastic cells revealed that the tumour was a glucagonoma, consistent with earlier findings of persistent glucagonaemia and hypoaminoacidaemia.
  • [MeSH-major] Dermatitis / veterinary. Dog Diseases / pathology. Glucagonoma / veterinary

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  • (PMID = 19152590.001).
  • [ISSN] 1365-3164
  • [Journal-full-title] Veterinary dermatology
  • [ISO-abbreviation] Vet. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
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27. Krause W: Skin diseases in consequence of endocrine alterations. Aging Male; 2006 Jun;9(2):81-95
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  • There, knowledge of skin alterations is important not only for dermatologists, but also for endocrinologists and other physicians, because a clinical diagnosis of the underlying disease is often possible.
  • These include acanthosis nigricans, diseases due to alterations of androgen metabolism, carcinoid syndrome, diseases due to alterations of corticosteroid metabolism, diseases in association with diabetes mellitus, diseases due to alterations of estrogen metabolism, genetic syndromes including dermatological and endocrine symptoms, the glucagonoma syndrome, diseases due to dysfunctions of growth hormone secretion, diseases in association with Merkel cells of the skin, diseases due to dysfunctions of the thyroid gland, diseases to alteration of vitamin D metabolism, and vitiligo and disorders of pigmentation.
  • [MeSH-minor] Androgens / deficiency. Androgens / secretion. Estrogens / deficiency. Estrogens / secretion. Glucagonoma / etiology. Malignant Carcinoid Syndrome / etiology. Thyroid Hormones / deficiency. Thyroid Hormones / secretion. Vitamin D / secretion. Vitiligo / etiology

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  • (PMID = 16916743.001).
  • [ISSN] 1368-5538
  • [Journal-full-title] The aging male : the official journal of the International Society for the Study of the Aging Male
  • [ISO-abbreviation] Aging Male
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Estrogens; 0 / Thyroid Hormones; 1406-16-2 / Vitamin D
  • [Number-of-references] 71
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28. Davies K, Conlon KC: Neuroendocrine tumors of the pancreas. Curr Gastroenterol Rep; 2009 Apr;11(2):119-27
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  • [Title] Neuroendocrine tumors of the pancreas.
  • Pancreatic endocrine tumors are rare neoplasms accounting for less than 5% of pancreatic malignancies.
  • They are broadly classified into either functioning tumors (insulinomas, gastrinomas, glucagonomas, VIPomas, and somatostatinomas) or nonfunctioning tumors.
  • The diagnosis of these tumors is difficult and requires a careful history and examination combined with laboratory tests and radiologic imaging.
  • Signs and symptoms are usually related to hormone hypersecretion in the case of functioning tumors and to tumor size or metastases with nonfunctioning tumors.
  • Surgical resection remains the treatment of choice even in the face of metastatic disease.
  • Further development of novel diagnostic and treatment modalities offers potential to greatly improve quality of life and prolong disease-free survival for patients with pancreatic endocrine tumors.
  • [MeSH-major] Adenoma, Islet Cell. Carcinoma, Islet Cell. Pancreatic Neoplasms
  • [MeSH-minor] Algorithms. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Catheter Ablation. Chemoembolization, Therapeutic / methods. Evidence-Based Medicine. Gastrins / secretion. Glucagon / secretion. Humans. Insulin / secretion. Quality of Life. Somatostatin / secretion. Survival Analysis. Treatment Outcome

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  • (PMID = 19281699.001).
  • [ISSN] 1534-312X
  • [Journal-full-title] Current gastroenterology reports
  • [ISO-abbreviation] Curr Gastroenterol Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Gastrins; 0 / Insulin; 51110-01-1 / Somatostatin; 9007-92-5 / Glucagon
  • [Number-of-references] 44
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29. Schmelz EM, Xu H, Sengupta R, Du J, Banerjee S, Sarkar FH, Rishi AK, Majumdar AP: Regression of early and intermediate stages of colon cancer by targeting multiple members of the EGFR family with EGFR-related protein. Cancer Res; 2007 Jun 1;67(11):5389-96
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  • In the present study, we evaluated the therapeutic effectiveness of ERRP on early and intermediate stages of colon cancer by examining regression of chemically induced aberrant crypt foci (ACF) in the colon of CF1 mice and intestinal adenomas in APC(Min+/-) (Min) mice.
  • After formation of ACF or adenomas, the mice were injected (i.p.) with ERRP (50 microg/mouse) for 10 consecutive days.
  • In Min mice, ERRP caused the regression of adenomas throughout the small intestine (P < 0.05) and reduced their size (P < 0.001).
  • [MeSH-minor] 1,2-Dimethylhydrazine. Adenoma / chemically induced. Adenoma / drug therapy. Adenoma / metabolism. Adenoma / pathology. Animals. Apoptosis / drug effects. Carcinogens. Cell Growth Processes / drug effects. Female. Intestinal Mucosa / drug effects. Intestinal Mucosa / metabolism. Male. Mice. Mice, Inbred C57BL. NF-kappa B / antagonists & inhibitors. NF-kappa B / metabolism. Neoplasm Staging. Precancerous Conditions / chemically induced. Precancerous Conditions / drug therapy. Precancerous Conditions / metabolism. Precancerous Conditions / pathology. Receptors, Estrogen / genetics. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / pharmacology. Transforming Growth Factor alpha / metabolism

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  • (PMID = 17545620.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG014343
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Drosophila Proteins; 0 / ERR protein, Drosophila; 0 / NF-kappa B; 0 / Receptors, Estrogen; 0 / Recombinant Fusion Proteins; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; IX068S9745 / 1,2-Dimethylhydrazine
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30. Hong J, Abudula R, Chen J, Jeppesen PB, Dyrskog SE, Xiao J, Colombo M, Hermansen K: The short-term effect of fatty acids on glucagon secretion is influenced by their chain length, spatial configuration, and degree of unsaturation: studies in vitro. Metabolism; 2005 Oct;54(10):1329-36
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  • [Title] The short-term effect of fatty acids on glucagon secretion is influenced by their chain length, spatial configuration, and degree of unsaturation: studies in vitro.
  • The influence of fatty acids on beta cell function has been well established whereas little is known about the role of fatty acids on alpha cell function.
  • The aim of our study was to investigate the short-term effects of chain length, spatial configuration, and degree of unsaturation of fatty acids on glucagon secretion from isolated mouse islets and alpha tumor cell 1 clone 6 cells (alpha TC1-6 cells).
  • Glucagon release was measured with different saturated and unsaturated fatty acids as well as cis and trans isomers of fatty acids at low and high glucose.
  • Palmitate (0.1-0.5 mmol/L) immediately stimulated glucagon release in a dose-dependent manner from both isolated islets and alpha TC 1-6 cells.
  • The longer chain length of saturated fatty acids, the higher glucagon responses were obtained.
  • The average fold increase in glucagon to saturated fatty acids (0.3 mmol/L) compared to control was octanoate 1.5, laurate 2.0, myristate 2.9, palmitate 5.4, and stearate 6.2, respectively.
  • Saturated fatty acids were more effective than unsaturated fatty acids in stimulating glucagon secretion.
  • Fatty acids immediately stimulate glucagon secretion from isolated mouse islets pancreatic alpha cells.
  • [MeSH-major] Fatty Acids / pharmacology. Glucagon / secretion

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  • (PMID = 16154432.001).
  • [ISSN] 0026-0495
  • [Journal-full-title] Metabolism: clinical and experimental
  • [ISO-abbreviation] Metab. Clin. Exp.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Fatty Acids; 0 / Insulin; 9007-92-5 / Glucagon
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31. Ho GY, Xue X, Cushman M, McKeown-Eyssen G, Sandler RS, Ahnen DJ, Barry EL, Saibil F, Bresalier RS, Rohan TE, Baron JA: Antagonistic effects of aspirin and folic acid on inflammation markers and subsequent risk of recurrent colorectal adenomas. J Natl Cancer Inst; 2009 Dec 02;101(23):1650-4
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  • [Title] Antagonistic effects of aspirin and folic acid on inflammation markers and subsequent risk of recurrent colorectal adenomas.
  • The Aspirin/Folate Polyp Prevention Trial found that aspirin, but not folic acid, reduced recurrence of colorectal adenomas.
  • There were 884 subjects who had colonoscopic evaluation for adenomas at year 3 and plasma levels of C-reactive protein (CRP), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), soluble TNF receptor type II (sTNF-R2), and IL-1 receptor antagonist (IL-1Ra) measured at baseline and year 3.
  • Changes in inflammation markers were not associated with adenoma recurrence.
  • Nevertheless, inflammation markers do not mediate the chemopreventive effect of aspirin on colorectal adenomas.
  • [MeSH-major] Adenoma / prevention & control. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Aspirin / pharmacology. C-Reactive Protein / metabolism. Colorectal Neoplasms / blood. Folic Acid / pharmacology. Inflammation / blood
  • [MeSH-minor] Aged. Biomarkers / blood. Drug Administration Schedule. Drug Antagonism. Female. Humans. Interleukin-6 / blood. Male. Middle Aged. Risk Assessment. Risk Factors. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 19822838.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA108841; United States / NCI NIH HHS / CA / U54 CA100971; United States / NCI NIH HHS / CA / U54-CA100971; United States / NCI NIH HHS / CA / R01 CA059005; United States / PHS HHS / / R01-108841; United States / NCI NIH HHS / CA / R01-CA059005
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Biomarkers; 0 / Interleukin-6; 0 / Tumor Necrosis Factor-alpha; 9007-41-4 / C-Reactive Protein; 935E97BOY8 / Folic Acid; R16CO5Y76E / Aspirin
  • [Other-IDs] NLM/ PMC2786916
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32. Jeske YW, So A, Kelemen L, Sukor N, Willys C, Bulmer B, Gordon RD, Duffy D, Stowasser M: Examination of chromosome 7p22 candidate genes RBaK, PMS2 and GNA12 in familial hyperaldosteronism type II. Clin Exp Pharmacol Physiol; 2008 Apr;35(4):380-5
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  • Adrenal hyperplasia and adenomas are features.
  • We subsequently reported finding no causative mutations in the retinoblastoma-associated Kruppel-associated box gene (RBaK), a candidate at 7p22 involved in tumorigenesis and cell cycle control.
  • 2. In the current study we investigated RBaK regulatory regions and two other candidate genes: postmeiotic segregation increased 2 (PMS2, involved in DNA mismatch repair and tumour predisposition) and guanine nucleotide-binding protein alpha-12 (GNA12, a transforming oncogene).
  • 4. The RBaK and PMS2 distal promoters were sequenced to -2150 bp from the transcription start site for RBaK and-2800 bp for PMS2.
  • [MeSH-minor] 5' Untranslated Regions / genetics. Adult. Aged. Female. Genetic Markers. Genetic Predisposition to Disease. Humans. Male. Middle Aged. Polymorphism, Single Nucleotide. Promoter Regions, Genetic / genetics. RNA Splice Sites / genetics

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  • (PMID = 18307725.001).
  • [ISSN] 1440-1681
  • [Journal-full-title] Clinical and experimental pharmacology & physiology
  • [ISO-abbreviation] Clin. Exp. Pharmacol. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / DNA-Binding Proteins; 0 / Genetic Markers; 0 / Intracellular Signaling Peptides and Proteins; 0 / RBaK protein, human; 0 / RNA Splice Sites; 0 / Repressor Proteins; 0 / URI1 protein, human; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / PMS2 protein, human; EC 6.5.1.- / DNA Repair Enzymes
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33. Bioulac-Sage P, Rebouissou S, Sa Cunha A, Jeannot E, Lepreux S, Blanc JF, Blanché H, Le Bail B, Saric J, Laurent-Puig P, Balabaud C, Zucman-Rossi J: Clinical, morphologic, and molecular features defining so-called telangiectatic focal nodular hyperplasias of the liver. Gastroenterology; 2005 May;128(5):1211-8
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  • [Title] Clinical, morphologic, and molecular features defining so-called telangiectatic focal nodular hyperplasias of the liver.
  • The aim of this study was to use molecular markers, in addition to morphologic features, to better characterize TFNH.
  • METHODS: Thirteen patients with TFNH were compared with 28 patients with FNH and 17 patients with hepatocellular adenoma.
  • Full clinical and morphologic data were analyzed.
  • RESULTS: No clinical differences were evident between patients with TFNH and adenoma; in particular, bleeding was observed in 77% and 53% of the cases, respectively.
  • Patients with TFNH were more likely to experience nodule recurrence and the presence of multiple nodules than those with either FNH or adenoma.
  • All TFNH and adenoma samples that were available for analysis were monoclonal, in contrast to 40% of the FNH samples.
  • Chromosome losses confirmed monoclonality and were significantly less frequent in TFNH and FNH (22% and 26%) than in adenoma (53%).
  • HNF1alpha mutations were found exclusively in half of the adenomas.
  • ANGPT2 was overexpressed in TFNH and down-regulated in adenoma (P < .01) and FNH (P < .0005).
  • CONCLUSIONS: TFNHs are monoclonal lesions frequently subject to bleeding that are similar to adenomas not carrying HNF1alpha mutations and require a similar type of treatment.
  • However, morphologic and molecular data support the hypothesis that TFNH is a separate entity.
  • [MeSH-minor] Adenoma, Liver Cell / blood supply. Adenoma, Liver Cell / genetics. Adenoma, Liver Cell / pathology. Adult. Angiopoietin-1 / genetics. Angiopoietins. Biomarkers. Blood Proteins / genetics. Chromosomes, Human, X. DNA-Binding Proteins / genetics. Female. Genome, Human. Hepatocyte Nuclear Factor 1. Hepatocyte Nuclear Factor 1-alpha. Humans. Intercellular Signaling Peptides and Proteins. Middle Aged. Mutation. Nuclear Proteins / genetics. RNA, Messenger / analysis. Transcription Factors / genetics

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  • (PMID = 15887105.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ANGPT1 protein, human; 0 / ANGPTL2 protein, human; 0 / Angiopoietin-1; 0 / Angiopoietins; 0 / Biomarkers; 0 / Blood Proteins; 0 / DNA-Binding Proteins; 0 / HNF1A protein, human; 0 / Hepatocyte Nuclear Factor 1-alpha; 0 / Intercellular Signaling Peptides and Proteins; 0 / Nuclear Proteins; 0 / RNA, Messenger; 0 / Transcription Factors; 126548-29-6 / Hepatocyte Nuclear Factor 1
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34. Igaz P: MEN1 clinical background. Adv Exp Med Biol; 2009;668:1-15
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  • Multiple endocrine neoplasia Type 1 (MEN1) is a rare hereditary tumor syndrome predisposing to tumor development in several endocrine organs.
  • Its major manifestations include hyperparathyroidism, tumors of endocrine pancreas and pituitary.
  • Beside these three, several other endocrine (adrenocortical, foregut carcinoid) and nonendocrine (lipoma, angiofibroma, collagenoma, ependymoma, meningioma) tumors have been described to be associated with this syndrome.
  • Both familial and sporadic forms of the disease are known.
  • The diagnosis of MEN1 can be established if two of the three major manifestations are found in the same patient, whereas the diagnosis of familial MEN1 requires one MEN1 patient and a first degree relative with at least one MEN1 manifestation.
  • Both benign (parathyroid, anterior pituitary) and malignant (gastrinoma, glucagonoma) lesions may develop in MEN1 patients.
  • Regular surveillance of MEN1 gene mutation carriers is necessary to reveal disease manifestations.
  • Several diagnostic modalities can be used to screen for and to examine MEN1-related tumors.
  • The therapy of MEN1-associated tumors requires specific approach in some cases, as multiple tumors and recurrence is frequently observed.
  • [MeSH-minor] Adult. Child. Child, Preschool. Diagnosis, Differential. Genetic Predisposition to Disease. Genetic Testing. Humans. Middle Aged. Multiple Endocrine Neoplasia Type 2a / genetics. Multiple Endocrine Neoplasia Type 2a / pathology. Multiple Endocrine Neoplasia Type 2a / physiopathology. Mutation. Young Adult

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  • (PMID = 20175448.001).
  • [ISSN] 0065-2598
  • [Journal-full-title] Advances in experimental medicine and biology
  • [ISO-abbreviation] Adv. Exp. Med. Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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35. National Toxicology Program: Toxicology and carcinogenesis studies of alpha-methylstyrene (Cas No. 98-83-9) in F344/N rats and B6C3F1 mice (inhalation studies). Natl Toxicol Program Tech Rep Ser; 2007 Nov;(543):1-210
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  • [Title] Toxicology and carcinogenesis studies of alpha-methylstyrene (Cas No. 98-83-9) in F344/N rats and B6C3F1 mice (inhalation studies).
  • alpha-Methylstyrene is used in the production of acrylonitrile-butadiene-styrene resins and copolymers, which improve the impact and heat-resistant properties of polymers, specialty grades of plastics, rubber, and protective coatings. alpha-Methylstyrene also moderates polymerization rates and improves product clarity in coatings and resins.
  • Low molecular weight liquid polymers are used as plasticizers in paints, waxes, adhesives, and plastics. alpha-Methylstyrene was nominated by the U.S.
  • Male and female F344/N rats and B6C3F1 mice were exposed to alpha-methylstyrene (99.5% pure) by inhalation for 3 months or 2 years.
  • Genetic toxicology studies were conducted in Salmonella typhimurium, cultured Chinese hamster ovary cells, and mouse peripheral blood erythrocytes.
  • 3-MONTH STUDY IN RATS: Groups of 10 male and 10 female rats were exposed by whole-body inhalation to alpha-methylstyrene at concentrations of 0, 75, 150, 300, 600, or 1,000 ppm for 6 hours per day, 5 days per week for 14 weeks.
  • Consistent with the hyaline droplet accumulation, an exposure-related increase in alpha2μ-globulin was detected in the kidneys of males exposed to alpha-methylstyrene.
  • Morphologic changes were not detected in the liver.
  • 3-MONTH STUDY IN MICE: Groups of 10 male and 10 female mice were exposed by whole-body inhalation to alpha-methylstyrene at concentrations of 0, 75, 150, 300, 600, or 1,000 ppm for 6 hours per day, 5 days per week for 14 weeks.
  • Minimal to mild centrilobular hypertrophy was present in the livers of male and female mice exposed to 600 or 1,000 ppm alpha-methylstyrene.
  • 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats were exposed by whole body inhalation to alpha-methylstyrene at concentrations of 0, 100, 300, or 1,000 ppm for 6 hours per day, 5 days per week, except holidays, for 105 weeks.
  • Two 1,000 ppm males and one 300 ppm male had renal tubule carcinomas, and one 300 ppm male had a renal tubule adenoma.
  • Because of the neoplasms observed in 300 and 1,000 ppm males at the end of the 2-year study and the finding of alpha2μ-globulin accumulation in the kidneys at 3 months, which is often associated with kidney neoplasms, additional step sections of kidney were prepared; additional males with focal hyperplasia or adenoma were identified.
  • The incidences of renal tubule adenoma and carcinoma (combined) in the 1,000 ppm males were significantly greater than those in the chamber controls when the single and step sections were combined.
  • The incidence of mononuclear cell leukemia in 1,000 ppm males was significantly increased compared to the chamber controls.
  • In the nose, the incidences of basal cell hyperplasia were significantly increased in all exposed groups of males and females, and the incidences of degeneration of the olfactory epithelium were increased in 1,000 ppm males and females and 300 ppm females.
  • 2-YEAR STUDY IN MICE: Groups of 50 male and 50 female mice were exposed by whole body inhalation to alpha-methylstyrene at concentrations of 0, 100, 300, or 600 ppm for 6 hours per day, 5 days per week, except holidays, for 105 weeks.
  • The incidences of hepatocellular adenoma or carcinoma (combined) were significantly increased in the 100 and 600 ppm males and in all exposed groups of females.
  • The incidences of hepatocellular adenoma were significantly increased in all exposed groups of females, and the incidences in all exposed groups of males and females exceeded the historical range for chamber controls.
  • GENETIC TOXICOLOGY: alpha-Methylstyrene was not mutagenic in four strains of Salmonella typhimurium, with or without rat or hamster liver metabolic activation enzymes (S9).
  • alpha-Methylstyrene did not induce chromosomal aberrations in cultured Chinese hamster ovary cells, with or without S9 activation, but did significantly increase the frequency of sister chromatid exchanges in cultures exposed in the presence of S9.
  • CONCLUSIONS: Under the conditions of this 2-year inhalation study, there was some evidence of carcinogenic activity of alpha-methylstyrene in male F344/N rats based on increased incidences of renal tubule adenomas and carcinomas (combined).
  • The increased incidence of mononuclear cell leukemia in 1,000 ppm male F344/N rats may have been related to alpha-methylstyrene exposure.
  • There was no evidence of carcinogenic activity of alpha-methylstyrene in female F344/N rats exposed to 100, 300, or 1,000 ppm.
  • There was equivocal evidence of carcinogenic activity of alpha-methylstyrene in male B6C3F1 mice based on marginally increased incidences of hepatocellular adenoma or carcinoma (combined).
  • There was clear evidence of carcinogenic activity of alpha-methylstyrene in female B6C3F1 mice based on increased incidences of hepatocellular adenomas and carcinomas.
  • Exposure of rats to alpha-methylstyrene resulted in kidney toxicity, which in males exhibited some features of alpha2μ-globulin nephropathy.
  • Exposure to alpha-methylstyrene resulted in nonneoplastic lesions of the nose in male and female rats and mice and of the liver and kidney in female mice.
  • [MeSH-minor] Animals. Body Weight / drug effects. CHO Cells. Cricetinae. Cricetulus. DNA Damage. Female. Inhalation Exposure. Kidney / drug effects. Kidney / pathology. Kidney Neoplasms / chemically induced. Kidney Neoplasms / pathology. Leukemia, Myeloid / chemically induced. Leukemia, Myeloid / pathology. Liver Neoplasms / chemically induced. Liver Neoplasms / pathology. Male. Mice. Mice, Inbred Strains. Micronuclei, Chromosome-Defective / chemically induced. Nose Diseases / chemically induced. Rats. Rats, Inbred F344

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  • (PMID = 18685715.001).
  • [ISSN] 0888-8051
  • [Journal-full-title] National Toxicology Program technical report series
  • [ISO-abbreviation] Natl Toxicol Program Tech Rep Ser
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Air Pollutants, Occupational; 0 / Carcinogens; 0 / Mutagens; 0 / Styrenes; 98-83-9 / alpha-methylstyrol
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36. Ferru A, Fromont G, Gibelin H, Guilhot J, Savagner F, Tourani JM, Kraimps JL, Larsen CJ, Karayan-Tapon L: The status of CDKN2A alpha (p16INK4A) and beta (p14ARF) transcripts in thyroid tumour progression. Br J Cancer; 2006 Dec 18;95(12):1670-7
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  • [Title] The status of CDKN2A alpha (p16INK4A) and beta (p14ARF) transcripts in thyroid tumour progression.
  • CDKN2A locus on chromosome 9p21 encodes two tumour suppressor proteins pl6INK4A, which is a regulator of the retinoblastoma (RB) protein, and p14ARF, which is involved in the ARF-Mdm2-p53 pathway.
  • Overexpression of p14ARF and pl6INK4A was observed in follicular adenomas, follicular carcinomas and papillary carcinomas, while downregulation was found in oncocytic adenomas compared to nontumoral paired thyroid tissues.
  • These deregulations were statistically significant for pl6INK4a (P=0.006) in follicular adenomas and close to statistical significance for p14ARF in follicular adenomas (P=0.06) and in papillary carcinomas (P=0.05).
  • [MeSH-major] Cyclin-Dependent Kinase Inhibitor p16 / genetics. Thyroid Neoplasms / genetics. Transcription, Genetic / physiology. Tumor Suppressor Protein p14ARF / genetics
  • [MeSH-minor] Adenocarcinoma, Follicular / genetics. Adenocarcinoma, Follicular / metabolism. Adenocarcinoma, Follicular / pathology. Adult. Aged. Aged, 80 and over. Carcinoma, Papillary / genetics. Carcinoma, Papillary / metabolism. Carcinoma, Papillary / pathology. Cell Differentiation. Disease Progression. Humans. Immunoenzyme Techniques. Middle Aged. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Thyroid Gland / metabolism. Thyroid Gland / pathology

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  • (PMID = 17117177.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p14ARF
  • [Other-IDs] NLM/ PMC2360765
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37. Gin VC, Zacharias M: Glucagonoma: anaesthetic management. Anaesth Intensive Care; 2009 Mar;37(2):329-30
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  • [Title] Glucagonoma: anaesthetic management.
  • [MeSH-major] Anesthesia, General / methods. Glucagonoma / surgery. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Blood Glucose / analysis. Female. Glucagon / blood. Humans. Middle Aged

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  • (PMID = 19400510.001).
  • [ISSN] 0310-057X
  • [Journal-full-title] Anaesthesia and intensive care
  • [ISO-abbreviation] Anaesth Intensive Care
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Blood Glucose; 9007-92-5 / Glucagon
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38. Simonenko VB, Dulin PA, Beliaev LB, Makanin MA, Dem'ianenko AV, Zykova AA, Zhuravleva SI, Kolesnikova VN: [A case of pancreatic glucagonoma]. Klin Med (Mosk); 2007;85(8):67-70
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  • [Title] [A case of pancreatic glucagonoma].
  • Neuroendocrine tumor consisting of pancreatic alpha-cells -- glucagonoma -- is a very rare finding (one case per two million people a year).
  • This functionally active, usually malignant tumor has typical clinical manifestations.
  • Glucagonoma syndrome is a disease that has an original clinical picture that includes necrolytic migrating erythema with secondary bullous dermatitis, glucose tolerance disorder or diabetes mellitus, weight loss, anemia, hypoaminoacidemia, venous thrombosis, and alimentary and mental disturbances.
  • By the time diagnosis is made, 60 to 70% of glucagonomas already give metastases, and even small glucagonomas should be considered tumors with unknown malignant potential or malignant tumors.
  • Glucagonomas grow slowly, and patients live long (the survival median is approximately 15 years).
  • [MeSH-major] Glucagonoma / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 17926496.001).
  • [ISSN] 0023-2149
  • [Journal-full-title] Klinicheskaia meditsina
  • [ISO-abbreviation] Klin Med (Mosk)
  • [Language] rus
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Russia (Federation)
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39. Warner RR: Enteroendocrine tumors other than carcinoid: a review of clinically significant advances. Gastroenterology; 2005 May;128(6):1668-84
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  • [Title] Enteroendocrine tumors other than carcinoid: a review of clinically significant advances.
  • Only relatively recently has there been an increased clinical recognition and characterization of the heterogeneous group of rare gastroenteropancreatic neuroendocrine neoplasms.
  • This review summarizes the derivation of these tumors and the advances in their diagnosis and treatment over the past decade and a half.
  • They are varied in their biological behavior and clinical courses and, depending on their cell type, can produce different hormones causing distinct clinical endocrine syndromes (insulinoma [hypoglycemia], gastrinoma [Zollinger-Ellison syndrome (ZES)], vasoactive intestinal peptideoma [VIPoma], watery diarrhea, hypokalemia-achlorhydria [WDHA], glucagonoma [glucagonoma syndrome], and so forth).
  • In addition to surgery for cure or palliation (by excision and a variety of other cytoreductive techniques), they each are treated with anti-hormonal agents or drugs targeted to each tumor's specific product or its effects.
  • Because of their usual slow rate of growth it is recommended that, even when they are advanced and incurable, unlike in patients with common and more malignant cancers, patients with neuroendocrine tumors often can be palliated and appear to survive longer when managed with an active approach using sequential multimodality treatment.
  • [MeSH-major] Carcinoma, Neuroendocrine. Gastrointestinal Neoplasms
  • [MeSH-minor] Carcinoid Tumor. Humans

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  • (PMID = 15887158.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 222
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40. Tomita T: Lymphatic vessel endothelial hyaluronan receptor 1 immunocytochemical staining for pancreatic islets and pancreatic endocrine tumors. Pancreas; 2007 Nov;35(4):e18-22
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  • [Title] Lymphatic vessel endothelial hyaluronan receptor 1 immunocytochemical staining for pancreatic islets and pancreatic endocrine tumors.
  • OBJECTIVES: Immunocytochemical staining for lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) is able to recognize lymphatic vessel endothelium and pancreatic endocrine cells (PETs).
  • Pancreatic endocrine tumors were studied for LYVE-1 immunocytochemical staining compared with normal pancreatic islets to detect possible presence of LYVE-1 in PETs.
  • METHODS: Twenty-five cases of primary and metastatic PETs were immunocytochemically stained for LYVE-1, including insulinomas, glucagonomas, somatostatinoma, pancreatic polypeptidomas, gastrinomas, and nonfunctioning tumors.
  • RESULTS: All normal pancreatic islet cells were positive for LYVE-1, whereas 2 cases of 25 PETs, 1 each of gastrinoma and nonfunctioning tumor, were positive for LYVE-1, retaining immunocytochemical reactivity of islet cells.
  • CONCLUSIONS: Normal pancreatic islets were positive for LYVE-1, whereas only 2 of 25 PETs were positive, suggesting that most PETs lost LYVE-1 or contained below detectable levels of LYVE-1.
  • The presence of LYVE-1 in pancreatic islets and in some PETs may suggest structure-function relationship of LYVE-1/lymphatic vessel in hormone synthesis and secretion.
  • [MeSH-major] Gastrinoma / chemistry. Glucagonoma / chemistry. Immunohistochemistry. Insulinoma / chemistry. Islets of Langerhans / chemistry. Pancreatic Neoplasms / chemistry. Somatostatinoma / chemistry. Vesicular Transport Proteins / analysis

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  • (PMID = 18090227.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LYVE1 protein, human; 0 / Vesicular Transport Proteins
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41. Prout TM, Taylor AJ: Case of the season: glucagonoma syndrome. Semin Roentgenol; 2005 Jan;40(1):4-7
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  • [Title] Case of the season: glucagonoma syndrome.
  • [MeSH-major] Glucagonoma / radiography. Pancreatic Neoplasms / radiography
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged. Syndrome. Tomography, X-Ray Computed



42. Marogy G, De Man M, Verslype C: Necrolytic migratory erythaema and glucagonoma syndrome. Acta Clin Belg; 2009 Jan-Feb;64(1):70-1
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  • [Title] Necrolytic migratory erythaema and glucagonoma syndrome.
  • [MeSH-major] Erythema / etiology. Glucagonoma / pathology. Pancreatic Neoplasms / pathology
  • [MeSH-minor] Female. Humans. Middle Aged. Syndrome



43. Woods CG, Burns AM, Bradford BU, Ross PK, Kosyk O, Swenberg JA, Cunningham ML, Rusyn I: WY-14,643 induced cell proliferation and oxidative stress in mouse liver are independent of NADPH oxidase. Toxicol Sci; 2007 Aug;98(2):366-74
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  • [Title] WY-14,643 induced cell proliferation and oxidative stress in mouse liver are independent of NADPH oxidase.
  • Long-term exposure of rodents to peroxisome proliferators leads to increases in peroxisomes, hepatocellular proliferation, oxidative damage, suppressed apoptosis, and ultimately results in the development of hepatic adenomas and carcinomas.
  • Peroxisome proliferators-activated receptor (PPAR)alpha was shown to be required for these pleiotropic responses; however, Kupffer cells, resident liver macrophages, were also identified as playing a role in peroxisome proliferators-induced effects, independently of PPARalpha.
  • To determine if Kupffer cell oxidants are also involved in chronic effects, NADPH oxidase-deficient (p47(phox)-null) mice were fed 4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio acetic acid (WY-14,643)-containing diet (0.1% wt/wt) for 1 week, 5 weeks, or 5 months along with Pparalpha-null and wild type mice.
  • As expected, no change in liver size, cell replication rates, or other phenotypic effects of peroxisome proliferators were observed in Pparalpha-null mice.
  • Through 5 months of treatment, the p47(phox)-null and wild type mice exhibited peroxisome proliferators-induced adverse liver effects, along with increased oxidative DNA damage and increased cell proliferation, a response that is potentially mediated through nuclear factor kappa B (NFkB).
  • Collectively, these findings suggest that involvement of Kupffer cells in WY-14,643-induced parenchymal cell proliferation and oxidative stress in rodent liver is an acute phenomenon that is not relevant to long-term exposure, but they are still involved in chronic apoptotic responses.
  • [MeSH-major] Liver / drug effects. PPAR alpha / deficiency. Peroxisome Proliferators / toxicity. Pyrimidines / toxicity
  • [MeSH-minor] Acyl-CoA Oxidase / metabolism. Animals. Apoptosis / drug effects. Body Weight / drug effects. Caspase 8 / metabolism. Caspase 9 / metabolism. Cell Cycle Proteins / metabolism. Cell Proliferation / drug effects. DNA Damage. Male. Mice. Mice, Knockout. NADPH Oxidase / deficiency. NADPH Oxidase / genetics. Organ Size / drug effects. Oxidative Stress

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  • (PMID = 17483499.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / F32-ES13342; United States / NIEHS NIH HHS / ES / K22-ES11660; United States / NIEHS NIH HHS / ES / P30-ES10126; United States / NIEHS NIH HHS / ES / R01-ES12686; United States / NIEHS NIH HHS / ES / U19-ES11391
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / PPAR alpha; 0 / Peroxisome Proliferators; 0 / Pyrimidines; 86C4MRT55A / pirinixic acid; EC 1.3.3.6 / Acyl-CoA Oxidase; EC 1.6.3.1 / NADPH Oxidase; EC 1.6.3.1 / neutrophil cytosolic factor 1; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9
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44. Jeng YJ, Watson CS: Proliferative and anti-proliferative effects of dietary levels of phytoestrogens in rat pituitary GH3/B6/F10 cells - the involvement of rapidly activated kinases and caspases. BMC Cancer; 2009;9:334
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  • [Title] Proliferative and anti-proliferative effects of dietary levels of phytoestrogens in rat pituitary GH3/B6/F10 cells - the involvement of rapidly activated kinases and caspases.
  • Prolactin-secreting adenomas are the most prevalent form of pituitary tumors in humans and have been linked to estrogen exposures.
  • We examined the proliferative effects of phytoestrogens on a rat pituitary tumor cell line, GH3/B6/F10, originally subcloned from GH3 cells based on its ability to express high levels of the membrane estrogen receptor-alpha.
  • Except trans-resveratrol, all phytoestrogens increased GH3/B6/F10 cell proliferation at some concentration relevant to dietary levels.
  • CONCLUSION: Phytoestrogens can block physiological estrogen-induced tumor cell growth in vitro and can also stimulate growth at high dietary concentrations in the absence of endogenous estrogens; these actions are correlated with slightly different signaling response patterns.
  • Consumption of these compounds should be considered in strategies to control endocrine tumor cell growth, such as in the pituitary.
  • [MeSH-major] Caspases / metabolism. Cell Proliferation / drug effects. Mitogen-Activated Protein Kinases / metabolism. Phytoestrogens / pharmacology. Pituitary Neoplasms / enzymology
  • [MeSH-minor] Animals. Cell Line, Tumor. Enzyme Activation / drug effects. Humans. Phosphorylation / drug effects. Rats. Signal Transduction / drug effects

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  • (PMID = 19765307.001).
  • [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 / Phytoestrogens; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC2755011
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45. Jarufe NP, Coldham C, Orug T, Mayer AD, Mirza DF, Buckels JA, Bramhall SR: Neuroendocrine tumours of the pancreas: predictors of survival after surgical treatment. Dig Surg; 2005;22(3):157-62
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  • [Title] Neuroendocrine tumours of the pancreas: predictors of survival after surgical treatment.
  • AIMS: Neuroendocrine tumours of pancreatic and duodenal origin (NETP) are rare and we present a significant experience from a single centre.
  • RESULTS: Twenty-four patients had functioning tumours (16 insulinomas, 3 gastrinomas, 2 somatostatinomas, 1 vipoma, 1 glucagonoma and 1 carcinoid tumour).
  • [MeSH-major] Neuroendocrine Tumors / surgery. Pancreatic Neoplasms / surgery

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  • [Copyright] Copyright (c) 2005 S. Karger AG, Basel.
  • (PMID = 16043962.001).
  • [ISSN] 0253-4886
  • [Journal-full-title] Digestive surgery
  • [ISO-abbreviation] Dig Surg
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
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46. Al-Shraim M, Scheithauer BW, Horvath E, Kovacs K, Smyth H, Coire C, Lloyd RV, Jastania R, Al-Gahtany M: Plurihormonal gonadotroph cell pituitary adenoma: report of a unique case. Clin Neuropathol; 2009 May-Jun;28(3):182-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Plurihormonal gonadotroph cell pituitary adenoma: report of a unique case.
  • OBJECTIVE AND IMPORTANCE: Pituitary adenomas producing primarily FSH and to a lesser extent GH, LH, alpha-subunit, TSH and PRL without clinical or laboratory evidence of increased hormone release have not previously been reported.
  • Our aim was to obtain some insight into the possible cytogenesis of this unusual tumor.
  • The tumor was removed by the transsphenoidal approach.
  • RESULT: By light microscopy, the adenoma was chromophobic, weakly PAS-positive, and immunoreactive mainly for FSH (85%) and to a lesser extent for GH (30%), LH (15%), alpha-subunit (3%), TSH (2%), and PRL (1%).
  • Although double immunostaining showed hormone reactivities to be localized largely in separate distinct cells, the tumor was ultrastructurally monomorphous, i.e., consisted of a single-cell type, resembling gonadotrophs.
  • CONCLUSION: The cytogenesis of plurihormonal pituitary adenomas is not fully understood.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Gonadotrophs / metabolism. Gonadotrophs / pathology. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology

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  • [ErratumIn] Clin Neuropathol. 2011 May-Jun;30(3):157. Al-Sharim, M [corrected to Al-Shraim, M]
  • (PMID = 19537135.001).
  • [ISSN] 0722-5091
  • [Journal-full-title] Clinical neuropathology
  • [ISO-abbreviation] Clin. Neuropathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 9002-62-4 / Prolactin; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
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47. Kazanjian KK, Reber HA, Hines OJ: Resection of pancreatic neuroendocrine tumors: results of 70 cases. Arch Surg; 2006 Aug;141(8):765-9; discussion 769-70
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  • [Title] Resection of pancreatic neuroendocrine tumors: results of 70 cases.
  • HYPOTHESIS: Neuroendocrine tumors of the pancreas can be managed surgically with excellent outcomes.
  • PATIENTS: Seventy consecutive patients who underwent resection for pancreatic neuroendocrine tumors between January 1, 1990, and December 31, 2005.
  • RESULTS: Of the 70 patients, 50 (71.4%) had nonfunctional tumors.
  • Thirty-seven patients (52.9%) had neuroendocrine carcinomas and 13 (18.6%) had benign islet cell neoplasms.
  • Twenty patients had functional tumors.
  • Of these 20 patients, 16 had insulinomas, 2 had glucagonomas, and 2 had gastrinomas.
  • Patients undergoing enucleation as compared with those not undergoing enucleation were younger (mean age, 39 vs 51 years, respectively; P = .009) and had smaller tumors (mean tumor size, 2 vs 5 cm, respectively; P<.001).
  • With a median follow-up of 50 months, the 5-year actuarial survival for the patients with malignant neuroendocrine carcinomas (n = 37) was 77%, and all of the patients with functional tumors are alive.
  • CONCLUSIONS: This single-institutional case series demonstrates that pancreatic neuroendocrine tumors can be safely resected without mortality and with minimal morbidity.
  • The presence of lymphovascular invasion can be used to classify neuroendocrine tumors as malignant, and this appears to predict survival.
  • Patients with malignant tumors can expect long-term survival even in the setting of metastatic disease.
  • [MeSH-major] Neuroendocrine Tumors / surgery. Pancreatectomy / methods. Pancreatic Neoplasms / surgery. Pancreaticoduodenectomy / methods

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  • (PMID = 16924083.001).
  • [ISSN] 0004-0010
  • [Journal-full-title] Archives of surgery (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch Surg
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
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48. Technau K, Renkl A, Norgauer J, Ziemer M: Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma. Eur J Dermatol; 2005 Mar-Apr;15(2):110-2
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  • [Title] Necrolytic migratory erythema with myelodysplastic syndrome without glucagonoma.
  • Necrolytic migratory erythema is a cutaneous paraneoplastic manifestation, which is usually associated with a glucagon-secreting pancreatic tumor.
  • However, it also may occur in other circumstances in which serum glucagon is elevated, as in hepatic cirrhosis.
  • Rarely, necrolytic migratory erythema is reported in association with a jejunal and rectal adenocarcinoma or villous atrophy of the small intestine without any evidence for increased serum glucagon levels.
  • In this context we report the case of an 85-year-old male with myelodysplastic syndrome who developed typical necrolytic migratory erythema without glucagonoma syndrome or evidence for other pancreatic or liver disease.
  • We suggest that, in addition to the diseases listed, myelodysplastic syndrome might be able to cause necrolytic migratory erythema.
  • [MeSH-major] Erythema / complications. Glucagonoma / complications. Myelodysplastic Syndromes / complications. Pancreatic Neoplasms / complications. Paraneoplastic Syndromes / complications



49. Manoranjan B, Salehi F, Scheithauer BW, Rotondo F, Kovacs K, Cusimano MD: Estrogen receptors alpha and beta immunohistochemical expression: clinicopathological correlations in pituitary adenomas. Anticancer Res; 2010 Jul;30(7):2897-904
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Estrogen receptors alpha and beta immunohistochemical expression: clinicopathological correlations in pituitary adenomas.
  • AIM: We investigated the immunohistochemical expression of estrogen receptors alpha (ERalpha) and beta (ERbeta) in pituitary adenoma subtypes combined with clinicopathological factors.
  • MATERIALS AND METHODS: Pituitary adenomas (n=75) were immunostained for ERalpha and ERbeta using the streptavidin-biotin-peroxidase complex method with a monoclonal ERalpha antibody and polyclonal ERbeta antibody.
  • RESULTS: Nuclear immunoreactivity for both receptors was highest among PRL, FSH/LH, null cell, and GH adenomas.
  • ACTH, silent subtypes I and II corticotrophs, and subtype III adenomas were the least immunoreactive for both receptors.
  • ACTH adenomas expressed significantly less ERalpha than FSH-LH, GH, and null cell adenomas.
  • A significantly elevated ERalpha expression was observed in macroadenomas compared to microadenomas and non-invasive compared to invasive tumors.
  • CONCLUSION: ERalpha and ERbeta are differentially expressed in the various pituitary adenoma subtypes suggesting a cell-specific function for these receptors.
  • To elucidate the role of ERalpha in tumor size and invasiveness, additional studies are required.
  • [MeSH-major] Adenoma / metabolism. Adenoma / pathology. Estrogen Receptor alpha / biosynthesis. Estrogen Receptor beta / biosynthesis. Pituitary Neoplasms / metabolism. Pituitary Neoplasms / pathology
  • [MeSH-minor] Cell Nucleus / metabolism. Cytoplasm / metabolism. Female. Humans. Immunohistochemistry. Male. Neoplasm Invasiveness

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  • (PMID = 20683030.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta
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50. Krysiak R, Okopień B, Herman ZS: [Rare pancreatic endocrine tumors]. Przegl Lek; 2008;65(4):209-16
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  • [Title] [Rare pancreatic endocrine tumors].
  • [Transliterated title] Rzadkie guzy endokrynne trzustki.
  • Functional pancreatic endocrine tumors other than gastrinoma and insulinoma are quite rare.
  • Some of these tumors may be part of multiple endocrine neoplasia type one (MEN-1) syndrome or phakomatoses.
  • Depending on their cell type, functional pancreatic endocrine tumors may cause distinct clinical endocrine syndromes, such as the 'glucagonoma syndrome', Verner-Morrison syndrome and the 'somatostatinoma syndrome'.
  • Currently, the only curative treatment for islet cell tumors is complete surgical resection.
  • The medical treatment of endocrine pancreatic tumours consists of somatostatin analogues, chemotherapy, and interferon-alpha.
  • The purpose of this manuscript is to provide an overview of the contemporary etiopathogenesis, diagnosis and treatment of rare pancreatic endocrine tumors.
  • [MeSH-major] Glucagonoma / diagnosis. Glucagonoma / therapy. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / therapy. Somatostatinoma / diagnosis. Somatostatinoma / therapy. Vipoma / diagnosis. Vipoma / therapy
  • [MeSH-minor] Humans. Rare Diseases / diagnosis. Rare Diseases / therapy

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  • (PMID = 18724549.001).
  • [ISSN] 0033-2240
  • [Journal-full-title] Przegla̧d lekarski
  • [ISO-abbreviation] Prz. Lek.
  • [Language] pol
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Poland
  • [Number-of-references] 47
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51. Xue HD, Liu W, Sun H, Merges R, Wang X, Zhang XN, Wang Y, Zhao WM, Chen JH, Jin ZY: Spectrum of functioning islet cell tumor on multislice computed tomography: experience on 70 patients. Chin Med Sci J; 2008 Mar;23(1):1-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spectrum of functioning islet cell tumor on multislice computed tomography: experience on 70 patients.
  • OBJECTIVE: To review experience in preoperative detection of islet cell tumors using multislice computed tomography (MSCT) and summarize various imaging features of functioning islet cell tumors on enhanced MSCT.
  • METHODS: Seventy patients with clinical or pathological diagnosis of functioning pancreatic islet cell tumor between October 2003 and February 2007 were included in this retrospective study.
  • Surgery and pathology reports were used to confirm the diagnosis, localization, and size of tumors.
  • RESULTS: Totally, 73 functioning islet cell tumors including 65 benign insulinomas, 2 benign glucagonomas, 3 malignant insulinomas, and 3 malignant glucagonomas were pathologically diagnosed.
  • Tumors in only two cases were not found by MSCT.
  • In 67 benign lesions, 32 showed typical enhancement style, 21 showed prolonged enhancement in portal venous phase, 4 showed delayed enhancement, 4 had iso-dense enhancement with normal pancreatic parenchyma, 2 had no enhancement at all in arterial phase and portal venous phase, and 4 had inhomogeneous enhancement with necrosis or cyst-formation.
  • Patchy or spotty calcifications were found in 3 of the 67 tumors.
  • In 6 malignant islet cell tumors, vessel invasion (2/6) and bowel invasion (1/6) were seen.
  • CONCLUSIONS: Pancreatic islet cell tumor may display a wide spectrum of presentations in MSCT.
  • Tumors with unusual appearances often present as diagnostic challenges.
  • Non-contrast and post-contrast multiphase scans are recommended for the localization of functioning islet cell tumors.

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  • (PMID = 18437902.001).
  • [ISSN] 1001-9294
  • [Journal-full-title] Chinese medical sciences journal = Chung-kuo i hsueh k'o hsueh tsa chih
  • [ISO-abbreviation] Chin. Med. Sci. J.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] China
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52. Yoshida D, Kim K, Yamazaki M, Teramoto A: Expression of hypoxia-inducible factor 1alpha and cathepsin D in pituitary adenomas. Endocr Pathol; 2005;16(2):123-31
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  • [Title] Expression of hypoxia-inducible factor 1alpha and cathepsin D in pituitary adenomas.
  • Hypoxia-inducible factor (HIF)-1alpha is a crucial transcription factor involved in the adaptive response to hypoxia, whereas cathepsin D, which regulates angiostatin in several cancer cell lines, has been reported to be upregulated by HIF-1alpha.
  • In order to determine the involvement of angiogenesis in pituitary adenomas, we studied the expression of both HIF-1alpha and cathepsin D in tissues from 58 patients (39 women, 19 men, ranging in age from 20 to 78 yr), sorted by histological group, and assayed by double immunohistochemistry.
  • HIF-1alpha immunoreactivity, confined to the nucleoplasm, was present in both tumor and vascular endothelial cells.
  • ACTH-producing adenomas showed the lowest level of HIF-1alpha, whereas prolactin (PRL)-producing adenomas and HIF-1alpha-positive microvessels showed the highest (p < 0.001).
  • In contrast, the lowest expression of cathepsin D was observed in PRL-producing adenomas, whereas the highest expression was detected in ACTH-producing adenomas (p < 0.0001).
  • Imaging analysis with fluorescence double immunohistochemistry showed that HIF-1alpha-negative tumor cells did not express significantly higher levels of cathepsin D.
  • In these poorly vascularized tumors, the hypoxic marker HIF-1alpha may not downregulate cathepsin D.
  • The mechanisms of tumor angiogenesis and cell invasion in pituitary adenomas may differ from those in other tumor cells.
  • [MeSH-major] Adenoma / metabolism. Cathepsin D / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Pituitary Neoplasms / metabolism

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  • (PMID = 16199897.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 3.4.23.5 / Cathepsin D
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53. Goss JA, Seu P, Gao FQ, Wyllie S: Ischemia-reperfusion of rat liver modulates hepcidin in vivo expression. Liver Transpl; 2005 Jul;11(7):800-6
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  • Hepcidin has also been reported to be responsible for anemia associated with chronic inflammatory diseases, and in anemia in patients with hepatic adenomas.
  • Since Kupffer cells are known to be the primary contributor to early-phase ischemia-reperfusion injury in the liver and iron is known to modulate Kupffer cell production of proinflammatory cytokine and reactive oxygen species, we investigated hepcidin in vivo expression in the well-established rat partial-liver ischemia-reperfusion model.
  • Furthermore, currently proposed mediators of in vivo hepcidin expression, such as interleukin-6, signal transducers and activators of transcription-family transducers, and CCAAT/enhancing binding protein-alpha do not appear to modulate hepcidin expression in the liver ischemia-reperfusion acute inflammatory model.
  • [MeSH-minor] Animals. Aspartate Aminotransferases / blood. CCAAT-Enhancer-Binding Protein-alpha / metabolism. Hepcidins. Immunohistochemistry. Interleukin-6 / blood. Iron / blood. L-Lactate Dehydrogenase / blood. Male. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. STAT1 Transcription Factor / metabolism. STAT3 Transcription Factor / metabolism. Severity of Illness Index

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  • (PMID = 15973703.001).
  • [ISSN] 1527-6465
  • [Journal-full-title] Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
  • [ISO-abbreviation] Liver Transpl.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimicrobial Cationic Peptides; 0 / CCAAT-Enhancer-Binding Protein-alpha; 0 / Hamp protein, rat; 0 / Hepcidins; 0 / Interleukin-6; 0 / RNA, Messenger; 0 / STAT1 Transcription Factor; 0 / STAT3 Transcription Factor; 0 / Stat1 protein, rat; 0 / Stat3 protein, rat; E1UOL152H7 / Iron; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 2.6.1.1 / Aspartate Aminotransferases
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54. Mikkelsen CS, Mikkelsen DB, Vestergaard V, Clemmensen O, Nielsen HO, Bygum A: [Glucagonoma syndrome without diabetes mellitus]. Ugeskr Laeger; 2008 Nov 17;170(47):3876
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  • [Title] [Glucagonoma syndrome without diabetes mellitus].
  • Computerised tomography and endoscopic ultrasound showed a solid tumour of the pancreas.
  • A blood sample showed an increased level of glucagon without diabetes.
  • Glucagonoma syndrome is characterized by glucagon overproduction, diabetes, depression, deep venous thrombosis and necrolytic migrating erythema.
  • Glucagonoma is frequently diagnosed late which increases the risk of metastases.
  • It is important not to rule out glucagonoma in patients with a relevant clinical picture but without diabetes.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis



55. Yang J, Zhou GW, Chen X, Wei Y, Peng CH, Ning G, Li HW: [Diagnosis and treatment of multiple endocrine neoplasia type 1 related pancreatic endocrine tumors]. Zhonghua Wai Ke Za Zhi; 2009 Mar 1;47(5):329-32
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  • [Title] [Diagnosis and treatment of multiple endocrine neoplasia type 1 related pancreatic endocrine tumors].
  • OBJECTIVE: To summarize the experience on diagnosis and treatment of multiple endocrine neoplasia type 1 (MEN-1) related pancreatic endocrine tumors (PET).
  • The other patient was diagnosed as glucagonoma clinically.
  • [MeSH-major] Multiple Endocrine Neoplasia Type 1 / diagnosis. Multiple Endocrine Neoplasia Type 1 / surgery. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery



56. La Rosa S, Uccella S, Dainese L, Marchet S, Placidi C, Vigetti D, Capella C: Characterization of c-kit (CD117) expression in human normal pituitary cells and pituitary adenomas. Endocr Pathol; 2008;19(2):104-11
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  • [Title] Characterization of c-kit (CD117) expression in human normal pituitary cells and pituitary adenomas.
  • c-kit (CD117) is a tyrosine kinase receptor involved in the proliferation, differentiation, and secretory functions of various cells.
  • In experimental animal models, c-kit has been detected in the pars intermedia of the normal pituitary gland and in alpha-melanocyte-stimulating-hormone-positive adenomas and it has been suggested that it plays a role in regulating adrenocorticotropic hormone (ACTH) secretion.
  • To the best of our knowledge, the expression of c-kit in normal human pituitary cells and in pituitary adenomas has never been reported, so the possible biological role of this receptor in the control of pituitary hormone secretion remains unclear.
  • The aim of this study was to evaluate the immunohistochemical expression of c-kit in normal human pituitary glands and in a series of 62 well-characterized pituitary adenomas.
  • In normal adenohypophyses, several cells, mainly located in the central mucoid wedge, showed a c-kit immunoreactivity (IR).
  • Double label immunostaining procedures showed that the c-kit-IR cells corresponded to ACTH cells.
  • Out of 62 adenomas, 15 (24%) were c-kit-IR, including 7/16 (44%) ACTH cell, 3/7 (42%) null cell, 4/11 (36%) alpha-subunit cell, and 1/11 (10%) follicle-stimulating hormone-luteinizing hormone cell adenomas.
  • By contrast, all ten prolactin cell and seven growth hormone cell adenomas were c-kit negative.
  • [MeSH-major] Adenoma / metabolism. Pituitary Gland / metabolism. Pituitary Neoplasms / metabolism. Proto-Oncogene Proteins c-kit / biosynthesis
  • [MeSH-minor] ACTH-Secreting Pituitary Adenoma / metabolism. ACTH-Secreting Pituitary Adenoma / pathology. Adolescent. Adult. Aged. Blotting, Western. Child. Female. Follicle Stimulating Hormone / blood. Growth Hormone-Secreting Pituitary Adenoma / metabolism. Growth Hormone-Secreting Pituitary Adenoma / pathology. Humans. Immunohistochemistry. Luteinizing Hormone / blood. Male. Middle Aged. Paraffin Embedding. Prolactinoma / metabolism. Prolactinoma / pathology. Tissue Fixation

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  • (PMID = 18568298.001).
  • [ISSN] 1046-3976
  • [Journal-full-title] Endocrine pathology
  • [ISO-abbreviation] Endocr. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; EC 2.7.10.1 / Proto-Oncogene Proteins c-kit
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57. Raverot G, Arnous W, Calender A, Trouillas J, Sassolas G, Bournaud C, Pugeat M, Borson-Chazot F: Familial pituitary adenomas with a heterogeneous functional pattern: clinical and genetic features. J Endocrinol Invest; 2007 Oct;30(9):787-90
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  • [Title] Familial pituitary adenomas with a heterogeneous functional pattern: clinical and genetic features.
  • Familial pituitary adenoma is a rare syndrome which may present either as isolated lesions, or in association with other endocrine tumors, for example in the frame of multiple endocrine neoplasia (MEN-1) or Carney complex (CNC).
  • The most frequently described forms of familial isolated pituitary adenoma (FIPA) are familial somatotropinomas or prolactinomas.
  • The present report shows heterogeneous FIPA with 3 subtypes of tumor in 3 individuals of the same family: somatotropinoma in the proband, giant prolactinoma in a brother, and gonadotroph cell macroadenoma in the father.
  • A prospective survey also suggested the occurrence of a silent microadenoma in the proband's sister.
  • Genetic screening for germline mutation of the MEN-1, the gene encoding the protein kinase A (PKA) type 1 alpha regulatory subunit (R1 alpha) (PRKAR1alpha) and AIP gene was negative in 2 affected members.
  • In conclusion, these data suggest that familial pituitary adenomas can occur with a heterogeneous functional pattern that is distinguished from MEN-1 or CNC.
  • [MeSH-major] Adenoma / genetics. Adenoma / physiopathology. Pituitary Neoplasms / genetics. Pituitary Neoplasms / physiopathology
  • [MeSH-minor] Female. Genetic Predisposition to Disease / genetics. Genetic Testing. Humans. Male. Middle Aged. Pedigree. Polymorphism, Single Nucleotide / genetics. Proto-Oncogene Proteins / genetics. Receptors, Aryl Hydrocarbon / genetics

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  • (PMID = 17993773.001).
  • [ISSN] 1720-8386
  • [Journal-full-title] Journal of endocrinological investigation
  • [ISO-abbreviation] J. Endocrinol. Invest.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / MEN1 protein, human; 0 / Proto-Oncogene Proteins; 0 / Receptors, Aryl Hydrocarbon
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58. Tomita T, Masuzaki H, Noguchi M, Iwakura H, Fujikura J, Tanaka T, Ebihara K, Kawamura J, Komoto I, Kawaguchi Y, Fujimoto K, Doi R, Shimada Y, Hosoda K, Imamura M, Nakao K: GPR40 gene expression in human pancreas and insulinoma. Biochem Biophys Res Commun; 2005 Dec 30;338(4):1788-90
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  • [Title] GPR40 gene expression in human pancreas and insulinoma.
  • To assess gene expression of a membrane-bound G-protein-coupled fatty acid receptor, GPR40, in the human pancreas and islet cell tumors obtained at surgery were analyzed.
  • The mRNA level of the GPR40 gene in isolated pancreatic islets was approximately 20-fold higher than that in the pancreas, and the level was comparable to or rather higher than that of the sulfonylurea receptor 1 gene, which is known to be expressed abundantly in human pancreatic beta cells.
  • A large amount of GPR40 mRNA was detected in tissue extracts from two cases of insulinoma, whereas the expression was undetectable in glucagonoma or gastrinoma.
  • The present study demonstrates that GPR40 mRNA is expressed predominantly in pancreatic islets in humans and that GPR40 mRNA is expressed solely in human insulinoma among islet cell tumors.
  • These results indicate that GPR40 is probably expressed in pancreatic beta cells in the human pancreas.
  • [MeSH-major] Insulinoma / metabolism. Pancreas / metabolism. Pancreatic Neoplasms / metabolism. Receptors, G-Protein-Coupled / biosynthesis

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  • (PMID = 16289108.001).
  • [ISSN] 0006-291X
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / FFAR1 protein, human; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled
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59. Campbell JS, Hughes SD, Gilbertson DG, Palmer TE, Holdren MS, Haran AC, Odell MM, Bauer RL, Ren HP, Haugen HS, Yeh MM, Fausto N: Platelet-derived growth factor C induces liver fibrosis, steatosis, and hepatocellular carcinoma. Proc Natl Acad Sci U S A; 2005 Mar 1;102(9):3389-94
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  • Members of the platelet-derived growth factor (PDGF) ligand family are known to play important roles in wound healing and fibrotic disease.
  • We show that both transient and stable expression of PDGF-C results in the development of liver fibrosis consisting of the deposition of collagen in a pericellular and perivenular pattern that resembles human alcoholic and nonalcoholic fatty liver disease.
  • Fibrosis in PDGF-C transgenic mice, as demonstrated by staining and hydroxyproline content, is preceded by activation and proliferation of hepatic stellate cells, as shown by collagen, alpha-smooth muscle actin and glial fibrillary acidic protein staining and between 8 and 12 months of age is followed by the development of liver adenomas and hepatocellular carcinomas.
  • The hepatic expression of a number of known profibrotic genes, including type beta1 TGF, PDGF receptors alpha and beta, and tissue inhibitors of matrix metalloproteinases-1 and -2, increased by 4 weeks of age.
  • Increased PDGF receptor alpha and beta protein levels were associated with activation of extracellular regulated kinase-1 and -2 and protein kinase B.
  • At 9 months of age, PDGF-C transgenic mice had enlarged livers associated with increased fibrosis, steatosis, cell dysplasia, and hepatocellular carcinomas.



60. Ullah N, Qureshi K, Yordanova V, Hatfield J, Sochacki P, Lawson M, Tobi M: Differential labeling by monoclonal antibodies Adnab-9 and anti-alpha-defensin 5 based on the distribution and adenomatous tissue content of colonic polyps. Dig Dis Sci; 2005 Apr;50(4):708-13
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  • [Title] Differential labeling by monoclonal antibodies Adnab-9 and anti-alpha-defensin 5 based on the distribution and adenomatous tissue content of colonic polyps.
  • We sought a correlation between site and morphology of colonic polyps by labeling with neoplastic and general Paneth cell markers, monoclonal antibodies Adnab-9 and anti-alpha-defensin 5, respectively.
  • Proportions labeled by Adnab-9 and anti-alpha-defensin 5 were, respectively, 42 and 85% for adenomas, 39 and 63% for early tubular adenomas, 41 and 44% for serrated, 34 and 20% for mixed, and 11 versus 2.7% for hyperplastic polyps.
  • Compared with hyperplastic polyps, the proportion of other polyps labeled by Adnab-9 or anti-alpha-defensin 5 was higher but this difference was more significant for distal (P = 0.008 for Adnab-9 and P = 0.0001 for anti-alpha-defensin 5) than proximal (P = 0.645 and P = 0.154, respectively) polyps.
  • While increased labeling of all proximal polyps compared to distal ones mirrored the colonic distribution of Paneth cells, distal adenomas tended to have a higher proportion labeled by Adnab-9, suggesting that Adnab-9 labels Paneth cells associated with increased neoplastic potential.
  • [MeSH-major] Adenomatous Polyps / pathology. Antibodies, Monoclonal. Colonic Neoplasms / pathology. Colonic Polyps / pathology. alpha-Defensins / immunology
  • [MeSH-minor] Diagnosis, Differential. Humans. Immunohistochemistry / methods. Paneth Cells / pathology. Single-Blind Method. Staining and Labeling

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  • (PMID = 15844706.001).
  • [ISSN] 0163-2116
  • [Journal-full-title] Digestive diseases and sciences
  • [ISO-abbreviation] Dig. Dis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; 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 / Antibodies, Monoclonal; 0 / alpha-Defensins; 0 / alpha-defensin 5, human
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61. Vanderlan WB, Zhang Z, Abouljoud MS: Duodenal enteroglucagonoma revealed by differential comparison of serum and tissue glucagon reactivity with Siemens' Double Glucagon Antibody and DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon: a case report. J Med Case Rep; 2010;4:178
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  • [Title] Duodenal enteroglucagonoma revealed by differential comparison of serum and tissue glucagon reactivity with Siemens' Double Glucagon Antibody and DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon: a case report.
  • INTRODUCTION: This case report demonstrates that the differential immunohistochemical reactivities of Siemens' Double Antibody Glucagon compared to DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon allow for pathologic distinction of enteral versus pancreatic glucagonoma.
  • He had a low serum glucagon level using Siemens' Double Antibody Glucagon, a clinical syndrome consistent with glucagon hypersecretion.
  • A periampullary mass biopsy proved to be a neuroendocrine tumor, with positive immunohistochemical reactivity to DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon.
  • CONCLUSIONS: Differential comparison of the immunohistochemical reactivities of Siemens' Double Antibody Glucagon and DakoCytomation's Polyclonal Rabbit Anti-Human Glucagon discerns enteroglucagon from pancreatic glucagon.

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  • (PMID = 20550685.001).
  • [ISSN] 1752-1947
  • [Journal-full-title] Journal of medical case reports
  • [ISO-abbreviation] J Med Case Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2896376
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62. Iino K, Oki Y, Yamashita M, Matsushita F, Hayashi C, Yogo K, Nishizawa S, Yamada S, Maekawa M, Sasano H, Nakamura H: Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma. J Clin Endocrinol Metab; 2010 Aug;95(8):4003-11
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  • [Title] Possible relevance between prohormone convertase 2 expression and tumor growth in human adrenocorticotropin-producing pituitary adenoma.
  • CONTEXT: Methods for preoperative diagnosis of prohormone convertase 2 (PC2)-positive ACTH-producing pituitary adenomas (APPAs) have not been established.
  • OBJECTIVE: This study was designed to understand the meaning of plasma alphaMSH levels and the role of cell proliferation-signaling molecules in PC2-positive APPAs.
  • RESULTS: Nine adenomas (47.4%) were immunopositive for PC2 and were large and invasive in nature.
  • Eight adenomas (42.1%) were immunopositive for both PC2 and p-Akt, and seven others (36.8%) were immunonegative for both, suggesting significant coexpression of PC2 and p-Akt in tumors.
  • CONCLUSIONS: Our study suggests that PC2 expression and Akt phosphorylation are related at the molecular level, resulting in a change in cell cycle and an increase in pituitary adenoma size.
  • An elevation of plasma alphaMSH could conjecture the activation of the phosphatidylinositol 3/Akt cascade in PC2-positive APPAs and may become a valuable clinical marker of tumor growth in Cushing's disease.
  • [MeSH-major] ACTH-Secreting Pituitary Adenoma / metabolism. Adenoma / metabolism. Proprotein Convertase 2 / metabolism. alpha-MSH / blood

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  • (PMID = 20501680.001).
  • [ISSN] 1945-7197
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 581-05-5 / alpha-MSH; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.4.21.94 / Proprotein Convertase 2
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63. Muinelo-Romay L, Vázquez-Martín C, Villar-Portela S, Cuevas E, Gil-Martín E, Fernández-Briera A: Expression and enzyme activity of alpha(1,6)fucosyltransferase in human colorectal cancer. Int J Cancer; 2008 Aug 1;123(3):641-6
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  • [Title] Expression and enzyme activity of alpha(1,6)fucosyltransferase in human colorectal cancer.
  • Changes in enzyme activity and the expression levels of alpha(1,6)fucosyltransferase [alpha(1,6)FT] have been reported in certain types of malignant transformations.
  • To develop a better understanding of the role of alpha(1,6)FT in human colorectal carcinoma (CRC), we analysed the enzyme activity in healthy and tumour tissues. alpha(1,6)FT activity was considerably higher in tumour tissue than in healthy tissue and was related to gender, lymph node metastasis, type of growth and tumour stage.
  • We also observed a significant increase in the alpha(1,6)FT expression in tumour tissues as compared to healthy and transitional tissues, inflammatory lesions and adenomas.
  • The immunohistochemical expression in tumour tissues was correlated with the degree of infiltration through the intestinal wall.
  • All these findings demonstrate an alteration of alpha(1,6)FT activity and expression in CRC.
  • [MeSH-major] Adenocarcinoma / enzymology. Biomarkers, Tumor / metabolism. Colorectal Neoplasms / enzymology. Fucosyltransferases / metabolism
  • [MeSH-minor] Adenoma / enzymology. Aged. Blotting, Western. Cell Transformation, Neoplastic. Female. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male

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  • (PMID = 18491404.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; EC 2.4.1.- / Fucosyltransferases; EC 2.4.1.68 / Glycoprotein 6-alpha-L-fucosyltransferase
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64. Luo F, Brooks DG, Ye H, Hamoudi R, Poulogiannis G, Patek CE, Winton DJ, Arends MJ: Mutated K-ras(Asp12) promotes tumourigenesis in Apc(Min) mice more in the large than the small intestines, with synergistic effects between K-ras and Wnt pathways. Int J Exp Pathol; 2009 Oct;90(5):558-74
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  • Summary K-ras mutations are found in 40-50% of human colorectal adenomas and carcinomas, but their functional contribution remains incompletely understood.
  • Here, we show that a conditional mutant K-ras mouse model (K-ras(Asp12)/Cre), with transient intestinal Cre activation by beta-Naphthoflavone (beta-NF) treatment, displayed transgene recombination and K-ras(Asp12) expression in the murine intestines, but developed few intestinal adenomas over 2 years.
  • The numbers of adenomas in the small intestine and large intestine were significantly (P < 0.01) increased by 1.5-fold and 5.7-fold, respectively, in K-ras(Asp12)/Cre/Apc(Min/+) mice compared with Apc(Min/+) mice, with the more marked increase in adenoma prevalence in the large intestine.
  • K-ras(Asp12) increased activation of Mapk and Akt signalling pathway targets phospho-extracellular signal-regulated kinase (pErk) and pAkt, and increased relative expression levels of Wnt pathway targets vascular endothelial growth factor (VEGF), gastrin, cyclo-oxygenase 2 (Cox2) and T-cell lymphoma invasion and metastasis 1 (Tiam1) in K-ras(Asp12)/Cre/Apc(Min/+) adenomas compared with that of Apc(Min/+) adenomas, although other Wnt signalling pathway target genes such as Peroxisome proliferator-activated receptor delta (PPARd), matrix metalloproteinase 7 (MMP7), protein phosphatase 1 alpha (PP1A) and c-myc remained unchanged.
  • In conclusion, intestinal expression of K-ras(Asp12) promotes mutant Apc-initiated intestinal adenoma formation in vivo more in the large intestine than the small intestine, with evidence of synergistic co-operation between mutant K-ras and Apc involving increased expression of some Wnt-pathway target genes.

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  • (PMID = 19765110.001).
  • [ISSN] 1365-2613
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / DNA, Neoplasm; 0 / Neoplasm Proteins; 0 / Wnt Proteins; EC 3.6.5.2 / Kras2 protein, mouse; EC 3.6.5.2 / Oncogene Protein p21(ras); EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras)
  • [Other-IDs] NLM/ PMC2768154
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65. McGevna L, McFadden D, Ritvo J, Rabinowitz T: Glucagonoma-associated neuropsychiatric and affective symptoms: diagnostic dilemmas raised by paraneoplastic phenomena. Psychosomatics; 2009 Sep-Oct;50(5):548-50
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  • [Title] Glucagonoma-associated neuropsychiatric and affective symptoms: diagnostic dilemmas raised by paraneoplastic phenomena.
  • [MeSH-major] Glucagonoma / diagnosis. Pancreatic Neoplasms / diagnosis. Paraneoplastic Syndromes / diagnosis
  • [MeSH-minor] Bipolar Disorder / diagnosis. Diagnosis, Differential. Female. Humans. Lupus Erythematosus, Systemic / diagnosis. Middle Aged

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  • (PMID = 19855043.001).
  • [ISSN] 1545-7206
  • [Journal-full-title] Psychosomatics
  • [ISO-abbreviation] Psychosomatics
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
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66. O'Grady HL, Conlon KC: Pancreatic neuroendocrine tumours. Eur J Surg Oncol; 2008 Mar;34(3):324-32
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  • [Title] Pancreatic neuroendocrine tumours.
  • Pancreatic neuroendocrine tumours (PET) are rare neoplasms of the pancreas accounting for less than 5% of all primary pancreatic malignancies.
  • Included in this group are insulinomas, gastrinomas, glucagonoma and somatostatinomas.
  • Where a PET is not associated with a clinical syndrome due to hormone oversecretion, it is referred to as a non-functioning PET.
  • Non-functioning PETs are pancreatic tumours with endocrine differentiation but lack a clinical syndrome of hormone hypersecretion.
  • Presentation is related to the mass effect of the tumour with symptoms often non-specific.
  • [MeSH-major] Adenoma, Islet Cell. Carcinoma, Islet Cell. Pancreatic Neoplasms
  • [MeSH-minor] Algorithms. Biomarkers, Tumor. Diagnostic Imaging. Humans. Neoplasm Metastasis. Prognosis

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  • (PMID = 17967523.001).
  • [ISSN] 1532-2157
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  • [Number-of-references] 74
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67. Pomérance M, Quillard J, Chantoux F, Young J, Blondeau JP: High-level expression, activation, and subcellular localization of p38-MAP kinase in thyroid neoplasms. J Pathol; 2006 Jul;209(3):298-306
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  • The p38 family of MAP kinases (p38-MAPKs) is involved in regulating the proliferation, survival, and migration of various cancer cells.
  • The present study has investigated the expression, subcellular localization, phosphorylation, and activity of p38-MAPKs in normal and tumoural human thyroid tissues and in thyroid cell lines.
  • The expression and nucleo-cytosolic compartmentalization of the alpha-isoform of p38-MAPKs (p38alpha-MAPK) were studied by western blotting in the WRO and B-CPAP cell lines, which are derived from human follicular and papillary thyroid carcinomas, respectively, and in the non-transformed rat thyroid cell lines FRTL-5 and PCCL3.
  • Immunohistochemistry was used to study the expression and subcellular localization of p38alpha-MAPK, and of the phosphorylated forms of p38-MAPKs (P-p38-MAPKs) in human toxic adenomas (TAs), follicular adenomas (FAs), papillary thyroid carcinomas (PTCs), and follicular thyroid carcinomas (FTCs).
  • p38alpha-MAPK was expressed in all cell lines and this expression was restricted to the cytosolic compartment. p38 MAPK activity was involved in regulating DNA synthesis in B-CPAP cells. p38alpha-MAPK and P-p38-MAPKs were strongly expressed in PTC and FTC cells, although only in the cytoplasm, whereas they were only very weakly expressed in FA cells, and absent in adjacent normal tissues.
  • [MeSH-minor] Adenocarcinoma, Follicular / enzymology. Adenoma / enzymology. Animals. Carcinoma, Papillary / enzymology. Cell Nucleus / enzymology. Cytosol / enzymology. DNA, Neoplasm / biosynthesis. Enzyme Inhibitors / pharmacology. Humans. Imidazoles / pharmacology. Immunoenzyme Techniques. Phosphorylation. Pyridines / pharmacology. Rats. Thyroid Gland / enzymology. Tumor Cells, Cultured

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  • [Copyright] Copyright (c) 2006 Pathological Society of Great Britain and Ireland.
  • [CommentIn] J Pathol. 2006 Sep;210(1):133-4 [16826548.001]
  • (PMID = 16583356.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA, Neoplasm; 0 / Enzyme Inhibitors; 0 / Imidazoles; 0 / Pyridines; 0 / SB 203580; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases
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68. Shigematsu K, Nishida N, Sakai H, Igawa T, Toriyama K, Nakatani A, Takahara O, Kawai K: Synaptophysin immunoreactivity in adrenocortical adenomas: a correlation between synaptophysin and CYP17A1 expression. Eur J Endocrinol; 2009 Dec;161(6):939-45
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synaptophysin immunoreactivity in adrenocortical adenomas: a correlation between synaptophysin and CYP17A1 expression.
  • DESIGN AND METHODS: The adrenal cortex is not considered to be an intrinsic part of the diffuse neuroendocrine system, but adrenocortical neoplasms possess neuroendocrine properties.
  • In this study, we examined synaptophysin (SYP) and neural cell adhesion molecule (NCAM) expression in adrenocortical adenomas in relation to adrenal function.
  • RESULTS: Immunohistochemical analysis showed that 50.7 and 98.6% of the cortical adenomas showed SYP and NCAM immunoreactivities respectively.
  • There was no apparent difference in NCAM immunoreactivity among the adenomas.
  • However, the immunostaining for SYP was significantly stronger in cortisol-producing adenomas (CPA) than in aldosterone-producing adenomas (APA), nonfunctioning adenomas (NFA), showing no clinical or endocrinological abnormality, or adenomas associated with preclinical Cushing's syndrome (preCS).
  • It was unexpected that the ratio of positive cells for SYP in preCS was less than that in APA and NFA.
  • CONCLUSIONS: We propose that SYP expression in adrenocortical cells may be involved in some aspect of adrenal function such as transport or secretion of glucocorticoids.

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  • (PMID = 19755404.001).
  • [ISSN] 1479-683X
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neural Cell Adhesion Molecules; 0 / RNA, Messenger; 0 / Synaptophysin; EC 1.14.99.9 / CYP17A1 protein, human; EC 1.14.99.9 / Steroid 17-alpha-Hydroxylase
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69. Resmini E, Minuto F, Colao A, Ferone D: Secondary diabetes associated with principal endocrinopathies: the impact of new treatment modalities. Acta Diabetol; 2009 Jun;46(2):85-95
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Indeed, impaired glucose tolerance (IGT) and overt diabetes mellitus are frequently associated with acromegaly and hypercortisolism (Cushing syndrome).
  • The increased cardiovascular morbidity and mortality associated with acromegaly and Cushing syndrome may partly be a consequence of increased insulin resistance that normally accompanies hormone excess.
  • The prevalence of diabetes mellitus and that of IGT in acromegaly is reported to range 16-56%, whereas the degree of glucose tolerance seems correlated with circulating growth hormone (GH) levels, age, and disease duration.
  • Therapy with somatostatin analogues (SSAs) induce control of GH and IGF-I excess in the majority of patients, but their inhibitory effect on pancreatic insulin secretion might complicate the overall effect of this treatment on glucose tolerance.
  • Hypercortisolism produces visceral obesity, insulin resistance, and dyslipidemia that together with hypertension, hypercoagulability, and ventricular morphologic and functional abnormalities increase cardiovascular risk, and persist up to 5 years after resolution of hypercortisolism.
  • In Cushing syndrome the prevalence of diabetes varies between 20 and 50%, but probably this prevalence is underestimated, as not always an oral glucose tolerance test is performed in the presence of an apparently normal fasting glycaemia.
  • Again, disease duration, rather than hormone levels, seems to be the major determinant in the occurrence of systemic complications in Cushing syndrome.
  • Due to the impact they have on mortality and morbidity in both acromegaly and Cushing syndrome, these complications should be treated aggressively.
  • In patients with neuroendocrine tumours (NETs) the occurrence of altered glucose tolerance may be due to a decreased insulin secretion, like it happens in patients who underwent pancreatic surgery and in those with pheochromocytoma, or to an altered counterbalance between hormones, such as in patients with glucagonoma and somatostatinoma.
  • Moreover, SSAs represent a valid therapeutic choice in the symptomatic treatment of NETs, and also in this case the medical therapy of the primary disease, may have a significant impact on the prevalence of glucose metabolism imbalance.
  • [MeSH-minor] Cushing Syndrome / complications. Gluconeogenesis. Glucose Tolerance Test. Human Growth Hormone / physiology. Humans. Hypoglycemic Agents / therapeutic use. Insulin / therapeutic use. Insulin Resistance. Liver / physiology. Prevalence. Risk Factors

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  • (PMID = 19322513.001).
  • [ISSN] 1432-5233
  • [Journal-full-title] Acta diabetologica
  • [ISO-abbreviation] Acta Diabetol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / Insulin; 12629-01-5 / Human Growth Hormone
  • [Number-of-references] 73
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70. Obi N, Katabami T, Obi R, Odanaka M, Sasano K, Tanaka Y: Primary malignant hepatic glucagonoma: an autopsy case. Endocr J; 2009;56(5):715-9
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  • [Title] Primary malignant hepatic glucagonoma: an autopsy case.
  • She displayed the signs and symptoms of glucagonoma syndrome, including necrolytic migratory erythema (NME), low aminoacidemia, and a marked increase of the serum glucagon level (4,940 pg/ ml).
  • Thus, we suspected a glucagonoma causing secondary diabetes.
  • However, we could not detect any mass in the pancreas or the gastrointestinal tract, and only found a liver lesion resembling a hemangioma.
  • At autopsy, the only tumor detected was the liver mass.
  • This was a large solid tumor (8 x 6 x 5 cm) with a pattern of white and dark brown stripes located in the left lobe, while two white nodules were also found in the right lobe.
  • Based on the histopathological and immunohistochemical findings, the liver lesion was shown to be a malignant glucagonoma with intrahepatic metastases.
  • Since primary malignant hepatic glucagonoma has not been reported before, we present this extremely rare case of primary malignant glucagonoma of the liver.
  • [MeSH-major] Diabetes Mellitus, Type 2 / etiology. Glucagonoma / pathology. Liver Neoplasms / pathology

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  • (PMID = 19367016.001).
  • [ISSN] 1348-4540
  • [Journal-full-title] Endocrine journal
  • [ISO-abbreviation] Endocr. J.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Amino Acids
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71. Jabbour SA: Skin manifestations of hormone-secreting tumors. Dermatol Ther; 2010 Nov-Dec;23(6):643-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Skin manifestations of hormone-secreting tumors.
  • Dermatologists may see some of these skin lesions first, either before the endocrinologist, or even after the internist or specialist has missed the right diagnosis.
  • Because some skin lesions might reflect a life-threatening endocrine or metabolic disorder, identifying the underlying disorder is very important, so that patients can receive corrective rather than symptomatic treatment.
  • In this issue, we will review various hormone-secreting tumors, including pituitary disorders (Cushing's syndrome and acromegaly), hyperthyroidism, glucagonoma, carcinoid syndrome, mastocytosis, and hyperandrogenism.
  • We will focus on clinical manifestations, mainly cutaneous, followed by a brief discussion on how to make the diagnosis of each condition in addition to treatment options.
  • [MeSH-major] Hormones / secretion. Neoplasms / complications. Paraneoplastic Syndromes / etiology. Skin / pathology. Skin Diseases / etiology

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  • [Copyright] © 2010 Wiley Periodicals, Inc.
  • (PMID = 21054708.001).
  • [ISSN] 1529-8019
  • [Journal-full-title] Dermatologic therapy
  • [ISO-abbreviation] Dermatol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Hormones
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72. Gutiérrez V, Cobo M, Olea D, García J, Ramírez C, Bautista D, Alcalde J: Glucagonoma with two pancreatic masses and pulmonary metastases as debut of MEN-1. Clin Transl Oncol; 2007 Oct;9(10):674-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Glucagonoma with two pancreatic masses and pulmonary metastases as debut of MEN-1.
  • This is a rare case of a patient with type 1 multiple endocrine neoplasia (MEN-1) syndrome.
  • The case is further unusual in that the glucagonoma debuted with two synchronic pancreatic masses at the time of diagnosis and with pulmonary metastases as the primary site of metastasis and not the more usual site of the liver.
  • [MeSH-major] Glucagonoma / diagnostic imaging. Lung Neoplasms / diagnostic imaging. Multiple Endocrine Neoplasia Type 1 / diagnostic imaging. Pancreatic Neoplasms / diagnostic imaging

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  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
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73. Colombo E, Zuccoli R, Ugolini M, Dardano F, Leigheb G: Pancreatic glucagonoma presenting as necrolytic migratory erythema. J Clin Oncol; 2007 May 20;25(15):2135-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic glucagonoma presenting as necrolytic migratory erythema.
  • [MeSH-major] Erythema / complications. Glucagonoma / complications. Pancreatic Neoplasms / complications
  • [MeSH-minor] Cell Movement. Humans. Male. Middle Aged. Necrosis

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  • (PMID = 17513822.001).
  • [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
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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74. Akerström G, Hellman P: Surgery on neuroendocrine tumours. Best Pract Res Clin Endocrinol Metab; 2007 Mar;21(1):87-109
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Surgery on neuroendocrine tumours.
  • Neuroendocrine tumours of the gastrointestinal tract and pancreas present a major challenge to physicians in their recognition and treatment requirements, and surgical treatment of these tumours has become increasingly important for symptom palliation and survival.
  • For some carcinoid tumours the extent of surgery may depend on tumour size.
  • Midgut carcinoid is the most common cause of the carcinoid syndrome, requiring surgery for primary and mesenteric tumours to minimize the risk for abdominal complications but also for removal of liver metastases to palliate hormonal symptoms.
  • Among endocrine pancreatic tumours, insulinoma and gastrinoma often cause severe symptoms of hormone excess despite their inconspicuous size, but they can be successfully removed with improved pre- and intraoperative localization.
  • Other tumours--glucagonoma, VIPoma, and non-functioning endocrine pancreatic tumours--are often large or metastasizing, but generally require surgical debulking to alleviate hormonal symptoms and have favourable survival.
  • [MeSH-major] Neuroendocrine Tumors / surgery
  • [MeSH-minor] Algorithms. Carcinoid Tumor / pathology. Carcinoid Tumor / surgery. Gastrinoma / surgery. Glucagonoma / surgery. Humans. Insulinoma / surgery. Intestinal Neoplasms / surgery. Liver Neoplasms / secondary. Liver Neoplasms / surgery. Models, Biological. Multiple Endocrine Neoplasia Type 1 / complications. Multiple Endocrine Neoplasia Type 1 / surgery. Nesidioblastosis / surgery. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / pathology. Pancreatic Neoplasms / surgery. Stomach Neoplasms / surgery. Vipoma / surgery. Zollinger-Ellison Syndrome / surgery

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  • (PMID = 17382267.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 55
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75. Heliövaara E, Raitila A, Launonen V, Paetau A, Arola J, Lehtonen H, Sane T, Weil RJ, Vierimaa O, Salmela P, Tuppurainen K, Mäkinen M, Aaltonen LA, Karhu A: The expression of AIP-related molecules in elucidation of cellular pathways in pituitary adenomas. Am J Pathol; 2009 Dec;175(6):2501-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The expression of AIP-related molecules in elucidation of cellular pathways in pituitary adenomas.
  • Germline mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene predispose to the development of pituitary adenomas.
  • Here, we characterized AIP mutation positive (AIPmut+) and AIP mutation negative (AIPmut-) pituitary adenomas by immunohistochemistry.
  • The expressions of the AIP-related proteins aryl hydrocarbon receptor (AHR), AHR nuclear translocator (ARNT), cyclin-dependent kinase inhibitor 1B encoding p27(Kip1), and hypoxia-inducible factor 1-alpha were examined in 14 AIPmut+ and 53 AIPmut- pituitary adenomas to detect possible expression differences.
  • In addition, the expression of CD34, an endothelial and hematopoietic stem cell marker, was analyzed.
  • We found ARNT to be less frequently expressed in AIPmut+ pituitary adenomas (P = 0.001), suggesting that AIP regulates the ARNT levels.
  • AIP small interfering RNA-treated HeLa, HEK293, or Aip-null mouse embryonic fibroblast cells did not show lowered expression of ARNT.
  • Instead, in the pituitary adenoma cell line GH3, Aip silencing caused a partial reduction of Arnt and a clear increase in cell proliferation.
  • The expressions of p27(Kip1), hypoxia-inducible factor 1-alpha, or CD34 did not differ between tumor types.
  • The present study shows that the expression of ARNT protein is significantly reduced in AIPmut+ tumors.
  • [MeSH-minor] Animals. Antigens, CD34 / biosynthesis. Antigens, CD34 / genetics. Blotting, Western. Cyclin-Dependent Kinase Inhibitor p27. Down-Regulation. Gene Expression. Gene Expression Profiling. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis. Hypoxia-Inducible Factor 1, alpha Subunit / genetics. Immunohistochemistry. Mice. Mutation. RNA, Small Interfering. Receptors, Aryl Hydrocarbon / biosynthesis. Receptors, Aryl Hydrocarbon / genetics. Reverse Transcriptase Polymerase Chain Reaction. Transfection

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  • (PMID = 19850893.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ARNT protein, human; 0 / Antigens, CD34; 0 / CDKN1B protein, human; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering; 0 / Receptors, Aryl Hydrocarbon; 0 / aryl hydrocarbon receptor-interacting protein; 138391-32-9 / Aryl Hydrocarbon Receptor Nuclear Translocator; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27
  • [Other-IDs] NLM/ PMC2789606
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76. Chen HW, Chen HW, Su DH, Shun CT, Liu KL: Rare presentation of endocrine pancreatic tumor: a case of diffuse glucagonoma without metastasis and necrolytic migratory erythema. J Formos Med Assoc; 2005 May;104(5):363-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rare presentation of endocrine pancreatic tumor: a case of diffuse glucagonoma without metastasis and necrolytic migratory erythema.
  • Glucagonoma is a very rare endocrine pancreatic tumor.
  • At diagnosis, most glucagonomas are malignant and often metastatic.
  • Suspicion of glucagonoma is based on characteristic presentations known as "glucagonoma syndrome".
  • Glucagonoma is often found in the pancreatic body and/or tail and is usually large enough to be localized by computed tomography.
  • We report a case of diffuse glucagonoma necrolytic migratory erythema (NME) in a 45-year-old man with mild diabetes mellitus, mild anemia, and weight loss over 1.5 years.
  • Diffused enlarged pancreas was noted on abdominal ultrasonography incidentally during a routine health check-up.
  • No enlarged lymph node or extrapancreatic tumor mass was found by several imaging studies.
  • Total pancreatectomy was performed, and the pathology revealed glucagon-producing islet cells and intrapancreatic vascular emboli of tumor cells.
  • Presentation of diffuse malignant glucagonoma with tumor emboli but no metastasis or NME is unusual.

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  • (PMID = 15959605.001).
  • [ISSN] 0929-6646
  • [Journal-full-title] Journal of the Formosan Medical Association = Taiwan yi zhi
  • [ISO-abbreviation] J. Formos. Med. Assoc.
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Singapore
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77. Rotondo F, Oniya K, Kovacs K, Bell CD, Scheithauer BW: MAP-2 expression in the human adenohypophysis and in pituitary adenomas. An immunohistochemical study. Pituitary; 2005;8(2):75-9
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  • [Title] MAP-2 expression in the human adenohypophysis and in pituitary adenomas. An immunohistochemical study.
  • MAP-2, a well characterized member of the microtubule associated protein (MAP) family, binds to and stabilizes microtubules and is involved in cell proliferation as well as neuronal differentiation.
  • The aim of the present work was to study MAP-2 expression in human adenohypophyses and pituitary adenomas.
  • Nine non-tumorous adenohypophyses and 77 adenomas (GH-, PRL-, ACTH-, TSH-, FSH/LH- and/or alpha subunit- producing or immunonegative tumors) were investigated.
  • The results show that MAP-2 is expressed in the cytoplasm of non-tumorous adenohypophysial cells as well as of various pituitary adenoma types.
  • Thus MAP-2 expression cannot be used to estimate cell proliferation rate, growth potential, endocrine activity or biologic behaviour of an adenoma.
  • Immunopositivity appeared to be stronger in the cytoplasm of adenoma cells than in that of non-tumorous adenohypophysial cells, implying that the adenoma cells contain larger quantities of MAP-2.
  • It can be concluded that the functional activity of MAP-2 is not associated with the manufacture of any specific adenohypophysial hormone(s) and is not limited to one specific cell type.
  • [MeSH-major] Adenoma / metabolism. Microtubule-Associated Proteins / biosynthesis. Pituitary Gland, Anterior / metabolism. Pituitary Neoplasms / metabolism

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  • (PMID = 16195780.001).
  • [ISSN] 1386-341X
  • [Journal-full-title] Pituitary
  • [ISO-abbreviation] Pituitary
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MAP2 protein, human; 0 / Microtubule-Associated Proteins
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78. Greijer AE, Delis-van Diemen PM, Fijneman RJ, Giles RH, Voest EE, van Hinsbergh VW, Meijer GA: Presence of HIF-1 and related genes in normal mucosa, adenomas and carcinomas of the colorectum. Virchows Arch; 2008 May;452(5):535-44
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  • [Title] Presence of HIF-1 and related genes in normal mucosa, adenomas and carcinomas of the colorectum.
  • Expression of the transcription factor hypoxia-inducible factor 1 (HIF-1), which plays a key role in cellular adaptation to hypoxia, was investigated in normal colorectal mucosa (ten), adenomas (61), and carcinomas (23).
  • Tissue samples were analyzed for HIF-1 alpha, its upstream regulators, von Hippel-Lindau factor, AKT, and mammalian target of rapamycin (mTOR) and its downstream targets glucose transporter 1 (GLUT1), carbonic anhydrase IX, stromal-cell-derived factor 1 (SDF-1) by immunohistochemistry.
  • In normal colorectal mucosa, HIF-1 alpha was observed in almost all nuclei of surface epithelial cells, probably secondary to a gradient of oxygenation, as indicated by pimonidazole staining.
  • The same staining pattern was present in 87% of adenomas.
  • In carcinomas, HIF-1 alpha was present predominantly around areas of necrosis (78%).
  • Active AKT and mTOR, were present in all adenomas, carcinomas, and in normal colorectal mucosa.
  • GLUT1 and SDF-1 were present in the normal surface epithelium of all adenoma cases, whereas in the carcinoma GLUT1 was located around necrotic regions and SDF-1 was present in all epithelial cells.
  • In conclusion, HIF-1 alpha appears to be physiologically expressed in the upper part of the colorectal mucosa.
  • The present observations support that upregulation of HIF-1 alpha and its downstream targets GLUT1 and SDF-1 in colorectal adenomas and carcinomas may be due to hypoxia, in close interaction with an active phosphatidylinositol 3-kinases-AKT-mTOR pathway.
  • [MeSH-major] Adenoma / metabolism. Chemokine CXCL12 / metabolism. Colorectal Neoplasms / metabolism. Glucose Transporter Type 1 / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Intestinal Mucosa / metabolism

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  • (PMID = 18351386.001).
  • [ISSN] 0945-6317
  • [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 / Antigens, Neoplasm; 0 / Chemokine CXCL12; 0 / Glucose Transporter Type 1; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / SLC2A1 protein, human; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Oncogene Protein v-akt; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
  • [Other-IDs] NLM/ PMC2329727
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79. Yamamoto S, Tanaka H, Asai Y, Wakasa K, Takemura S, Hai S, Ichikawa T, Kodai S, Shinkawa H, Kubo S: A case of glucagonoma at the uncinate process of the pancreas successfully treated by pancreaticoduodenectomy. Pancreas; 2008 Jan;36(1):100-2
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  • [Title] A case of glucagonoma at the uncinate process of the pancreas successfully treated by pancreaticoduodenectomy.
  • [MeSH-major] Glucagonoma / diagnosis. Glucagonoma / surgery. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / surgery. Pancreaticoduodenectomy
  • [MeSH-minor] Aged. Glucagon / blood. Humans. Male. Tomography, X-Ray Computed

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  • (PMID = 18192893.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 9007-92-5 / Glucagon
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80. Kitamura Y, Sato M, Hatamochi A, Yamazaki S: Necrolytic migratory erythema without glucagonoma associated with hepatitis B. Eur J Dermatol; 2005 Jan-Feb;15(1):49-51
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  • [Title] Necrolytic migratory erythema without glucagonoma associated with hepatitis B.
  • We report a case of necrolytic migratory erythema (NME) without glucagonoma associated with hepatitis B.
  • Although the most common cause of NME is a glucagon-secreting alpha-islet cell tumor of the pancreas, a dermatitis clinically and histologicaly identical to NME has been described in patients without glucagonoma.
  • We added some discussion on the terminology of this disease.

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  • (PMID = 15701595.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] France
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81. Ilie M, Hofman V, Pedeutour F, Attias R, Santini J, Hofman P: Oncocytic lipoadenoma of the parotid gland: Immunohistochemical and cytogenetic analysis. Pathol Res Pract; 2010 Jan 15;206(1):66-72
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  • Salivary gland oncocytic lipoadenoma is an exceptional benign tumor composed of mature adipose tissue associated with a mixture of oncocytes.
  • A 64-year-old male developed a left parotid gland, well-encapsulated tumor measuring 3.5 x 3 cm(2), showing mature fat cells associated with oncocytic changes of epithelial components.
  • Immunohistochemistry showed a dual epithelial population with ductal (positivity for AE1/AE3, CK19, CK7 antibodies) and basal-cell (positivity for p63, CK14, CK5,6 antibodies) differentiation in oncocytic areas.
  • Moreover, oncocytic cells were stained with anti-alpha-1 antichymotrypsin antibody and phosphotungstic acid-hematoxylin staining.
  • Such alterations in HMGA2 have been described in both lipomas and pleomorphic adenomas of the salivary glands.
  • [MeSH-major] Adenoma / pathology. Parotid Neoplasms / pathology
  • [MeSH-minor] Disease-Free Survival. Humans. Immunohistochemistry. Lipoma / metabolism. Lipoma / pathology. Lipoma / surgery. Male. Middle Aged. Neoplasm Proteins / metabolism

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  • [Copyright] Copyright 2009 Elsevier GmbH. All rights reserved.
  • (PMID = 19346081.001).
  • [ISSN] 1618-0631
  • [Journal-full-title] Pathology, research and practice
  • [ISO-abbreviation] Pathol. Res. Pract.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Neoplasm Proteins
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82. Cruz-Bautista I, Lerman I, Perez-Enriquez B, Padilla LS, Torres CL, Lopez A, Cabrera T, Mehta RP, Gómez-Pérez FJ, Rull JA, Orozco-Topete R: Diagnostic challenge of glucagonoma: case report and literature review. Endocr Pract; 2006 Jul-Aug;12(4):422-6
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  • [Title] Diagnostic challenge of glucagonoma: case report and literature review.
  • OBJECTIVE: To report the diagnostic difficulties encountered in a case of glucagonoma.
  • METHODS: We provide a literature review and present the clinical findings, pertinent laboratory data, and results of related studies in a patient with a glucagonoma.
  • The patient was hospitalized, and because of the dermatologic findings suggestive of necrolytic migratory erythema, the presence of a glucagonoma was suspected.
  • Glucagon levels were found to be elevated, and imaging studies confirmed the presence of an enlarged mass in the pancreatic tail, without evidence of extension to surrounding structures.
  • After surgical removal of the tumor, the skin and oral mucosal lesions disappeared spontaneously.
  • The histologic appearance and immunohistochemical staining results confirmed the diagnosis of a glucagonoma.
  • Subsequently, all related symptoms resolved, and the glucagon levels normalized.
  • CONCLUSION: The diagnosis of glucagonoma is often delayed.
  • Clinicians should be aware of the unusual initial manifestations of this tumor and the potential for less than a full spectrum of the characteristic features of the glucagonoma syndrome.
  • [MeSH-major] Glucagonoma / diagnosis
  • [MeSH-minor] Erythema / etiology. Humans. Hyperpigmentation / etiology. Male. Middle Aged. Pancreatic Neoplasms / complications. Pancreatic Neoplasms / diagnosis. Pancreatic Neoplasms / ultrasonography. Pancreatic Neoplasms / ultrastructure. Regional Blood Flow. Tomography, X-Ray Computed. Wound Healing

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  • (PMID = 16901799.001).
  • [ISSN] 1530-891X
  • [Journal-full-title] Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
  • [ISO-abbreviation] Endocr Pract
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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83. Yamazumi K, Nakayama T, Kusaba T, Wen CY, Yoshizaki A, Yakata Y, Nagayasu T, Sekine I: Expression of interleukin-11 and interleukin-11 receptor alpha in human colorectal adenocarcinoma; immunohistochemical analyses and correlation with clinicopathological factors. World J Gastroenterol; 2006 Jan 14;12(2):317-21
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  • [Title] Expression of interleukin-11 and interleukin-11 receptor alpha in human colorectal adenocarcinoma; immunohistochemical analyses and correlation with clinicopathological factors.
  • AIM: There is strong evidence that interleukin-11 (IL-11) is involved in the regulation of tumor progression, cellular growth and differentiation.
  • Recently, interleukin-11 receptor (IL-11R) has been detected on some cancer cells.
  • METHODS: To elucidate the involvement of IL-11 and IL-11Ra in human intestinal adenocarcinomas, we examined 115 cases of surgically resected human colonic adenocarcinoma and 11 cases of adenoma by immunohistochemistry and Western blotting.
  • RESULTS: Among 115 cases of adenocarcinoma, 100 cases (87.0%) showed positive staining in the cytoplasm of carcinoma cells for the IL-11, and 87 cases (75.6%) were positive for the IL-11Ra.
  • Six cases (54.5%) and four cases (36.4%) of 11 adenomas were positive for IL-11 and IL-11Ra, respectively.
  • The expression of IL-11Ra correlated with the histological differentiation (P = 0.033503), the depth of tumor invasion (P = 0.006395), Dukes'classification (P = 0.015648) and lymphatic invasion (P = 0.003865).
  • In Western blot analysis, two human colorectal carcinoma cell lines and four tissues of surgically resected human carcinoma expressed both IL-11 and IL-11Ra proteins.
  • [MeSH-minor] Cell Line, Tumor. Humans. Immunohistochemistry. Interleukin-11 Receptor alpha Subunit. Receptors, Interleukin-11

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  • (PMID = 16482637.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / IL11RA protein, human; 0 / Interleukin-11; 0 / Interleukin-11 Receptor alpha Subunit; 0 / Receptors, Interleukin; 0 / Receptors, Interleukin-11
  • [Other-IDs] NLM/ PMC4066046
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84. Di Leo A, Barone M, Maiorano E, Tanzi S, Piscitelli D, Marangi S, Lofano K, Ierardi E, Principi M, Francavilla A: ER-beta expression in large bowel adenomas: implications in colon carcinogenesis. Dig Liver Dis; 2008 Apr;40(4):260-6
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  • [Title] ER-beta expression in large bowel adenomas: implications in colon carcinogenesis.
  • AIM: In the present study, we evaluated oestrogen receptor-beta expression and its possible correlation with proliferative activity and apoptosis in colorectal adenomas and normal colon tissue.
  • RESULTS: In adenomatous tissue, a significant reduction of oestrogen receptor-beta was observed compared to normal mucosa (10.1+/-5.5% vs. 44.2+/-13.7; p<0.03), while the expression of oestrogen receptor-alpha remained unvaried.
  • Cell proliferative activity significantly increased in adenomatous tissue compared to normal mucosa (59.3+/-7.1 vs. 18.5+/-8.8; p<0.0001), doubling the PCNA/apoptosis ratio.
  • An inverse correlation was found between oestrogen receptor-beta and PCNA expression in adenomas (r=-0.81), a datum confirmed by confocal microscopy evaluation.
  • [MeSH-major] Adenoma / metabolism. Estrogen Receptor beta / metabolism. Intestinal Neoplasms / metabolism

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  • (PMID = 18093886.001).
  • [ISSN] 1590-8658
  • [Journal-full-title] Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
  • [ISO-abbreviation] Dig Liver Dis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Estrogen Receptor beta
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85. Romano D, Magalon K, Pertuit M, Rasolonjanahary R, Barlier A, Enjalbert A, Gerard C: Conditional overexpression of the wild-type Gs alpha as the gsp oncogene initiates chronic extracellularly regulated kinase 1/2 activation and hormone hypersecretion in pituitary cell lines. Endocrinology; 2007 Jun;148(6):2973-83
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  • [Title] Conditional overexpression of the wild-type Gs alpha as the gsp oncogene initiates chronic extracellularly regulated kinase 1/2 activation and hormone hypersecretion in pituitary cell lines.
  • In pituitary cells, activation of the cAMP pathway by specific G protein-coupled receptors controls differentiative functions and proliferation.
  • Constitutively active forms of the alpha subunit of the heterotrimeric G(s) protein resulting from mutations at codon 201 or 227 (gsp oncogene) were first identified in 30-40% of human GH-secreting pituitary adenomas.
  • This rate of occurrence suggests that the gsp oncogene is not responsible for initiating the majority of these tumors.
  • Moreover, there is a large overlap between the clinical phenotypes observed in patients with tumors bearing the gsp oncogene and those devoid of this oncogene.
  • To explore the role of G(s)alpha in GH-secreting adenomas, we obtained somatolactotroph GH4C1 cell lines by performing doxycycline-dependent conditional overexpression of the wild-type G(s)alpha protein and expression of the gsp oncogene.
  • Although the resulting adenylyl cyclase and cAMP levels were 10-fold lower in the wild-type G(s)alpha-overexpressing cell line, a sustained MAPK ERK1/2 activation was observed in both cell lines.
  • Overexpression of the wild-type G(s)alpha protein as the gsp oncogene initiated chronic activation of endogenous prolactin synthesis and release, as well as chronic activation of ERK1/2-sensitive human prolactin and GH promoters.
  • [MeSH-major] GTP-Binding Protein alpha Subunits, Gs / genetics. Gene Expression Regulation, Enzymologic. Growth Hormone / secretion. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. Prolactin / secretion. Somatotrophs / metabolism
  • [MeSH-minor] Adenylyl Cyclases / metabolism. Animals. Cell Line. Cyclic AMP / metabolism. Doxycycline / pharmacology. Enzyme Activation. Oncogene Proteins / genetics. Rats. Time Factors. Transfection. Transgenes / drug effects

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
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  • (PMID = 17363453.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Oncogene Proteins; 9002-62-4 / Prolactin; 9002-72-6 / Growth Hormone; E0399OZS9N / Cyclic AMP; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 3.6.1.- / Gnas protein, rat; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs; EC 4.6.1.1 / Adenylyl Cyclases; N12000U13O / Doxycycline
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86. Shibata H, Takano H, Ito M, Shioya H, Hirota M, Matsumoto H, Kakudo Y, Ishioka C, Akiyama T, Kanegae Y, Saito I, Noda T: Alpha-catenin is essential in intestinal adenoma formation. Proc Natl Acad Sci U S A; 2007 Nov 13;104(46):18199-204
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alpha-catenin is essential in intestinal adenoma formation.
  • Although the molecular mechanism of tumor initiation is complex, several modifier genes have been identified using mouse models, including the ApcMin mouse.
  • Among the familial adenomatous polyposis mouse lines carrying a truncation mutation at codon 580 in Apc (Apc580D), one line (line19-Apc(580D/+)) showed a remarkably reduced incidence of intestinal adenomas (<5% compared with other lines).
  • Extensive genetic analysis identified a deletion in the alpha-catenin (Ctnna1) gene as the cause of this suppression.
  • In all adenomas generated in line19-Apc(580D/+), somatic recombination between the Apc and Ctnna1 loci retained the wild-type Ctnna1 allele.
  • These data strongly indicate that simultaneous inactivation of alpha-catenin and Apc during tumor initiation suppresses adenoma formation in line19-Apc(580D/+), suggesting that alpha-catenin plays an essential role in the initiation of intestinal adenomas.
  • Although accumulating evidence obtained from human colon tumors with invasive or metastatic potential has established a tumor-suppressive role for alpha-catenin in late-stage tumorigenesis, the role of alpha-catenin in the initiation of intestinal tumorigenesis is not well documented, especially compared with that of beta-catenin.
  • A mouse model used in this study focused on the early stage of tumor initiation and clearly indicated an essential role for alpha-catenin.
  • Thus, alpha-catenin has dual roles in intestinal tumorigenesis, a supporting role in tumor initiation, and a suppressive role in tumor progression.
  • [MeSH-major] Adenoma / pathology. Intestinal Neoplasms / pathology. alpha Catenin / physiology