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1
alpha cell adenomas 2005:2010[pubdate] *count=100
294 results
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Items 1 to 100 of about 294
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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[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
MedlinePlus Health Information.
consumer health - Diagnostic Imaging
.
MedlinePlus Health Information.
consumer health - Pancreatic Cancer
.
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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
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).
MedlinePlus Health Information.
consumer health - Antioxidants
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
PROSTAGLANDIN F2ALPHA
.
Hazardous Substances Data Bank.
L-TYROSINE
.
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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
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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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.
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(PMID = 20182587.001).
[ISSN]
1943-8141
[Journal-full-title]
American journal of translational research
[ISO-abbreviation]
Am J Transl Res
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Other-IDs]
NLM/ PMC2826827
[Keywords]
NOTNLM ; CAP2 / HSP70 / Molecular genetics / glutamine synthetase / glypican 3 / hepatocellular carcinoma / liver cancer / β-catenin
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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[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
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
NCI CPTC Antibody Characterization Program.
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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
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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[
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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
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
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(PMID = 17873541.001).
[ISSN]
0002-9629
[Journal-full-title]
The American journal of the medical sciences
[ISO-abbreviation]
Am. J. Med. Sci.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
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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GLUCAGON
.
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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
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
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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ETHYL CARBAMATE
.
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.
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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
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.
Hazardous Substances Data Bank.
Methyl t-butyl ether
.
Hazardous Substances Data Bank.
Ethyl tert-butyl ether
.
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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
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
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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.
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(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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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
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
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
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
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[Copyright]
Copyright © 2010 Elsevier Inc. All rights reserved.
(PMID = 21167379.001).
[ISSN]
1532-8708
[Journal-full-title]
Seminars in oncology
[ISO-abbreviation]
Semin. Oncol.
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Biomarkers, Tumor
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
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
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
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
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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17ALPHA-HYDROXYPROGESTERONE
.
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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
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
MedlinePlus Health Information.
consumer health - Breast Cancer
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 19067857.001).
[ISSN]
1440-1827
[Journal-full-title]
Pathology international
[ISO-abbreviation]
Pathol. Int.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Australia
[Chemical-registry-number]
0 / Biomarkers, Tumor
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
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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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
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
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
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
The Lens.
Cited by Patents in
.
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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
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
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
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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.
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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
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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.
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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
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
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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.
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.
Hazardous Substances Data Bank.
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.
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.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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.
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Biochem J. 1992 Feb 15;282 ( Pt 1):197-202
[
1540135.001
]
(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
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
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
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
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
Hazardous Substances Data Bank.
ALPHA-METHYL STYRENE
.
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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
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
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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.
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.
Hazardous Substances Data Bank.
GLUCAGON
.
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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
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)
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
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
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
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(PMID = 15732554.001).
[ISSN]
0037-198X
[Journal-full-title]
Seminars in roentgenology
[ISO-abbreviation]
Semin Roentgenol
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
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
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(PMID = 19317246.001).
[ISSN]
1784-3286
[Journal-full-title]
Acta clinica Belgica
[ISO-abbreviation]
Acta Clin Belg
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Belgium
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
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
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
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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[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
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
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
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(PMID = 15757825.001).
[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
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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[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
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
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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[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
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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[Cites]
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Neurosurgery. 2003 Oct;53(4):880-5; discussion 885-6
[
14519220.001
]
(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
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
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
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[CommentIn]
Ugeskr Laeger. 2008 Dec 15;170(51):4241; author reply 4241
[
19160469.001
]
(PMID = 19014744.001).
[ISSN]
1603-6824
[Journal-full-title]
Ugeskrift for laeger
[ISO-abbreviation]
Ugeskr. Laeg.
[Language]
dan
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
Denmark
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
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(PMID = 19595004.001).
[ISSN]
0529-5815
[Journal-full-title]
Zhonghua wai ke za zhi [Chinese journal of surgery]
[ISO-abbreviation]
Zhonghua Wai Ke Za Zhi
[Language]
chi
[Publication-type]
English Abstract; Journal Article
[Publication-country]
China
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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[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
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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]
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]
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]
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Growth Horm IGF Res. 2004 Jun;14 Suppl A:S90-6
[
15135786.001
]
(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
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
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.
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(subscription/membership/fee required).
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Mouse Genome Informatics (MGI)
.
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.
NCI CPTC Antibody Characterization Program.
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.
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[ISSN]
0027-8424
[Journal-full-title]
Proceedings of the National Academy of Sciences of the United States of America
[ISO-abbreviation]
Proc. Natl. Acad. Sci. U.S.A.
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / R37 CA023226; United States / NCI NIH HHS / CA / R01 CA074131; United States / NCI NIH HHS / CA / CA-074131; United States / NCI NIH HHS / CA / CA-023226; United States / NCI NIH HHS / CA / R01 CA023226
[Publication-type]
Journal Article; Research Support, U.S. Gov't, P.H.S.
[Publication-country]
United States
[Chemical-registry-number]
0 / Lymphokines; 0 / Platelet-Derived Growth Factor; 0 / platelet-derived growth factor C
[Other-IDs]
NLM/ PMC552940
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
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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[Cites]
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89070.001
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Annu Rev Physiol. 1997;59:257-71
[
9074764.001
]
(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
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
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
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
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
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
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
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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[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
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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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
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
71.
Jabbour SA:
Skin manifestations of hormone-secreting tumors.
Dermatol Ther
; 2010 Nov-Dec;23(6):643-50
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[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
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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[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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[Cites]
Endocr Rev. 2004 Jun;25(3):458-511
[
15180952.001
]
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Aliment Pharmacol Ther. 2000 May;14(5):557-60
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[
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[
12490844.001
]
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]
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]
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Surg Clin North Am. 2001 Jun;81(3):511-25
[
11459268.001
]
[Cites]
Best Pract Res Clin Gastroenterol. 2005 Oct;19(5):753-81
[
16253899.001
]
(PMID = 17974529.001).
[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
[Publication-country]
Italy
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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[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
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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[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
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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[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
Genetics Home Reference.
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(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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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
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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[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
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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[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
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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Cell Oncol. 2007;29(3):229-40
[
17452775.001
]
(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
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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GLUCAGON
.
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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
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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.
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.
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.
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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
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
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
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
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
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.
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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
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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[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
Gene Ontology.
gene/protein/disease-specific - Gene Ontology annotations from this paper
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
SciCrunch.
OMIM: Data: Gene Annotation
.
SciCrunch.
Marmoset Gene list: Data: Gene Annotation
.
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