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1
adrenocorticotropin secreting adenoma of the pituitary 2005:2010[pubdate] *count=100
178 results
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Items 1 to 100 of about 178
1.
Keil MF, Stratakis CA:
Facial metrics in children with corticotrophin-producing pituitary adenomas suggest abnormalities in midface development.
J Pediatr Endocrinol Metab
; 2009 Jan;22(1):47-53
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[Title]
Facial metrics in children with corticotrophin-
producing
pituitary
adenomas
suggest abnormalities in midface development.
BACKGROUND: Tumors of the hypothalamic-
pituitary
unit have been linked to genetic syndromes that are associated with midfacial abnormalities.
AIM: We hypothesized that mutations of genes that affect the development of the face (and consequently of the anterior
pituitary
) may be present in children with
ACTH
-
producing
pituitary
adenomas
, and if this is true then facial measurements would be different from those predicted by parental features.
METHODS: We studied 20 children with
corticotropinomas
and a control group and their parents.
RESULTS: Significant differences were seen between the children with
pituitary
adenomas
and their parents for vertical facial height measures: nasal length (p < 0.001), lower facial height (p < 0.03) and overall facial height (p < 0.01).
CONCLUSION: We conclude that some of the indices of midline craniofacial development, in particular those affecting the vertical axis, are different in children with
corticotroph adenomas producing ACTH
.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ pathology.
Adenoma
/ pathology. Face / pathology. Maxillofacial Abnormalities / etiology. Maxillofacial Development / physiology
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[Cites]
J Craniofac Surg. 2003 Jan;14(1):13-28
[
12544216.001
]
[Cites]
Am J Med Genet. 2002 Sep 1;111(4):388-91
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12210297.001
]
[Cites]
Horm Res. 2003;60(4):168-73
[
14530604.001
]
[Cites]
Am J Phys Anthropol. 1974 Nov;41(3):423-9
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4473903.001
]
[Cites]
Am J Med Genet. 1980;7(1):47-74
[
7211952.001
]
[Cites]
Am J Med Genet. 1983 Mar;14(3):557-65
[
6859106.001
]
[Cites]
J Craniofac Genet Dev Biol. 1985;5(3):229-38
[
4044786.001
]
[Cites]
Clin Genet. 1993 Sep;44(3):129-38
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[Cites]
J Clin Endocrinol Metab. 1994 Nov;79(5):1498-502
[
7962349.001
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[Cites]
Am J Med Genet. 1998 Oct 2;79(4):294-304
[
9781911.001
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[Cites]
Am J Phys Anthropol. 1953 Mar;11(1):121-40
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13040508.001
]
[Cites]
Horm Metab Res. 2005 Jun;37(6):347-54
[
16001326.001
]
[Cites]
J Clin Endocrinol Metab. 2005 Sep;90(9):5134-40
[
15941871.001
]
[Cites]
J Clin Endocrinol Metab. 2006 Jan;91(1):221-4
[
16219718.001
]
[Cites]
Eur J Endocrinol. 2006 May;154(5):753-8
[
16645024.001
]
[Cites]
J Endocrinol Invest. 2006 Mar;29(3):208-13
[
16682832.001
]
[Cites]
J Clin Endocrinol Metab. 2006 Sep;91(9):3316-23
[
16787992.001
]
[Cites]
Genes Dev. 2006 Oct 15;20(20):2871-86
[
17043312.001
]
[Cites]
Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R73-9
[
17613551.001
]
[Cites]
Hum Mol Genet. 2007 Apr 15;16 Spec No 1:R80-7
[
17613552.001
]
[Cites]
Pediatrics. 2007 Sep;120(3):e575-86
[
17698579.001
]
[Cites]
J Clin Endocrinol Metab. 2000 Aug;85(8):2701-8
[
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]
[Cites]
J Clin Endocrinol Metab. 2000 Dec;85(12):4556-61
[
11134108.001
]
[Cites]
J Pediatr. 2001 Aug;139(2):215-9
[
11487746.001
]
[Cites]
J Neurooncol. 2001 Sep;54(2):95-110
[
11761437.001
]
[Cites]
Ann Med. 2002;34(3):179-91
[
12173688.001
]
[Cites]
Front Neuroendocrinol. 2003 Apr;24(2):94-127
[
12763000.001
]
(PMID = 19344074.001).
[ISSN]
0334-018X
[Journal-full-title]
Journal of pediatric endocrinology & metabolism : JPEM
[ISO-abbreviation]
J. Pediatr. Endocrinol. Metab.
[Language]
eng
[Databank-accession-numbers]
ClinicalTrials.gov/ NCT00001595
[Grant]
United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / / ZIA HD000642-13; United States / NICHD NIH HHS / HD / Z01-HD-000642-04
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
[Publication-country]
Germany
[Other-IDs]
NLM/ NIHMS310299; NLM/ PMC3143028
2.
Lad SP, Patil CG, Laws ER Jr, Katznelson L:
The role of inferior petrosal sinus sampling in the diagnostic localization of Cushing's disease.
Neurosurg Focus
; 2007;23(3):E2
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[Title]
The role of inferior petrosal sinus sampling in the diagnostic localization of
Cushing's disease
.
Cushing's
syndrome can present a complex problem of differential
diagnosis
.
Of cases in which hypercortisolemia results from an adrenocorticotropic hormone (
ACTH
)-dependent process, approximately 80% are due to a
pituitary adenoma
(
Cushing's disease
[CD]), 10% are due to adrenal lesions, and the remaining 10% are secondary to ectopic
ACTH
secretion.
For patients with CD, surgical removal of the
pituitary adenoma
is the treatment of choice.
Thus, localization of the source of
ACTH
secretion is critical in guiding timely treatment decisions.
Inferior petrosal sinus sampling (IPSS) is considered to be the gold standard for confirming the origin of
ACTH
secretion in patients with
Cushing's
syndrome.
A number of other techniques are discussed including sampling from the cavernous sinus, the jugular vein, and multiple sites to aid the
diagnosis
and lateralization of
ACTH
-
producing
pituitary
adenomas
.
[MeSH-major]
Petrosal Sinus Sampling / methods.
Pituitary
ACTH
Hypersecretion /
diagnosis
COS Scholar Universe.
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Hazardous Substances Data Bank.
Corticotropin
.
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(PMID = 17961020.001).
[ISSN]
1092-0684
[Journal-full-title]
Neurosurgical focus
[ISO-abbreviation]
Neurosurg Focus
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone
[Number-of-references]
46
3.
Giacomini D, Páez-Pereda M, Theodoropoulou M, Labeur M, Refojo D, Gerez J, Chervin A, Berner S, Losa M, Buchfelder M, Renner U, Stalla GK, Arzt E:
Bone morphogenetic protein-4 inhibits corticotroph tumor cells: involvement in the retinoic acid inhibitory action.
Endocrinology
; 2006 Jan;147(1):247-56
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[Title]
Bone morphogenetic protein-4 inhibits
corticotroph tumor
cells: involvement in the retinoic acid inhibitory action.
The molecular mechanisms governing the pathogenesis of
ACTH
-
secreting pituitary
adenomas
are still obscure.
In this study, we report that bone morphogenetic protein-4 (BMP-4) is expressed in the corticotrophs of human normal adenohypophysis and its expression is reduced in
corticotrophinomas
obtained from
Cushing's
patients compared with the normal
pituitary
.
BMP-4 treatment of AtT-20 mouse
corticotrophinoma
cells has an inhibitory effect on
ACTH
secretion and
cell
proliferation.
AtT-20 cells stably transfected with a dominant-negative form of the BMP-4 signal cotransducer Smad-4 or the BMP-4 inhibitor noggin have increased tumorigenicity in nude mice, showing that BMP-4 has an inhibitory role on
corticotroph
tumorigenesis in vivo.
Because the activation of the retinoic acid receptor has an inhibitory action on
Cushing's disease
progression, we analyzed the putative interaction of these two pathways.
Indeed, retinoic acid induces both BMP-4 transcription and expression and its antiproliferative action is blocked in Smad-4dn- and noggin-transfected Att-20 cells that do
not
respond to BMP-4.
This new mechanism is a potential target for therapeutic approaches for
Cushing's disease
.
[MeSH-major]
Adenoma
/ pathology. Bone Morphogenetic Proteins / pharmacology. Bone Morphogenetic Proteins / physiology. Cushing Syndrome / pathology.
Pituitary
Neoplasms / pathology. Tretinoin / pharmacology
[MeSH-minor]
Animals. Bone Morphogenetic Protein 4.
Cell
Division / drug effects.
Cell
Line,
Tumor
. Humans. Immunohistochemistry. Mice.
Pituitary
Gland
/ pathology.
Pituitary
Gland
/ physiology. Reference Values
MedlinePlus Health Information.
consumer health - Cushing's Syndrome
.
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
ALL-TRANS-RETINOIC ACID
.
KOMP Repository.
gene/protein/disease-specific - KOMP Repository
(subscription/membership/fee required).
Mouse Genome Informatics (MGI).
Mouse Genome Informatics (MGI)
.
The Lens.
Cited by Patents in
.
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(PMID = 16195406.001).
[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 / BMP4 protein, human; 0 / Bmp4 protein, mouse; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 5688UTC01R / Tretinoin
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4.
Pisarek H, Pawlikowski M, Kunert-Radek J, Radek M:
Expression of somatostatin receptor subtypes in human pituitary adenomas -- immunohistochemical studies.
Endokrynol Pol
; 2009 Jul-Aug;60(4):240-51
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[Title]
Expression of somatostatin receptor subtypes in human
pituitary
adenomas
-- immunohistochemical studies.
BACKGROUND: The highly variable expression of SSTR subtypes in
pituitary
adenomas
(PA) may partially explain why the subgroup of somatotropinomas or other
adenomas
do
not
respond to the therapeutic action of currently used long-acting somatostatin analogues like octreotide or lanreotide.
RESULTS: The pattern of SSTR immunostaining (estimated according to the percentage frequency of appearance) was in acromegaly: SSTR 5 > SSTR 1 > SSTR 2A = SSTR 3 > SSTR 2B, in prolactinomas: SSTR 2B = SSTR 3 = SSTR 5 > SSTR 1 = SSTR 2A, in gonadotropinomas: SSTR 3 > SSTR 2B > SSTR 1 = SSTR 2A > SSTR 5, in
corticotropinomas
: SSTR 2A > SSTR 1 = SSTR 3 > SSTR 5 > SSTR 2B.
In PA immunonegative for
pituitary
hormones, we noticed only a weak staining of all receptor subtypes including SSTR 4.
In plurihormonal
adenomas
with positive GH phenotype the staining pattern was: SSTR 5 > SSTR 1 = SSTR 2B and in plurihormonal PA with negative GH phenotype: SSTR 1 = SSTR 5 > SSTR 2A = SSTR 2B = SSTR 3.
In plurihormonal
adenoma
with
ACTH
immunopositivity, the staining pattern was: SSTR = SSTR 2A = SSTR 3 = SSTR 5.
SSTR 1 and SSTR 5 were the most frequent subtypes of somatostatin receptor in plurihormonal
adenomas
without
ACTH
expression.
Apart from applying SSTR 2 and SSTR 5-preferring octreotide and lanreotide - newly synthesized multiligand analogues, such as
SOM
230, KE 108, or other SST selective analogues, may represent a further useful approach for the treatment, especially in cases other than somatotropinoma or thyrotropinoma.
[MeSH-major]
Adenoma
/ metabolism.
Pituitary
Neoplasms / metabolism. Receptors, Somatostatin / metabolism
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
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(PMID = 19753537.001).
[ISSN]
0423-104X
[Journal-full-title]
Endokrynologia Polska
[ISO-abbreviation]
Endokrynol Pol
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Poland
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Peptides, Cyclic; 0 / Protein Isoforms; 0 / Receptors, Somatostatin; 0G3DE8943Y / lanreotide; 51110-01-1 / Somatostatin; RWM8CCW8GP / Octreotide
5.
Alzahrani AS, Farhat R, Al-Arifi A, Al-Kahtani N, Kanaan I, Abouzied M:
The diagnostic value of fused positron emission tomography/computed tomography in the localization of adrenocorticotropin-secreting pituitary adenoma in Cushing's disease.
Pituitary
; 2009;12(4):309-14
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[Title]
The diagnostic value of fused positron emission tomography/computed tomography in the localization
of adrenocorticotropin
-
secreting pituitary adenoma
in
Cushing's disease
.
Despite the high resolution of magnetic resonance imaging (MRI) of the
pituitary
gland
, up to 40% of cases of
Cushing's disease
(CD) have normal MRI.
Objective of this study is to explore the diagnostic potential of PET-CT for localization
of adrenocorticotropin
-
secreting pituitary
adenomas
in CD.
PET-CT was performed in 12 cases with
de
novo (7 cases) or persistent CD (5 cases) that were proven to have CD on biochemical, radiological and/or histopathological findings.
PET-CT was positive in 7 of the 12 cases of CD (58%) showing a focal area of uptake in
the pituitary
gland
.
If these findings are confirmed in larger studies, PET-CT might become an important diagnostic technique, especially when the more invasive and technically demanding procedure of IPSS is
not
available or inconclusive.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/
diagnosis
.
Pituitary
ACTH
Hypersecretion / pathology. Positron-Emission Tomography / methods. Tomography, X-Ray Computed / methods
[MeSH-minor]
Adult. Female. Humans. Magnetic Resonance Imaging / methods. Male. Middle Aged.
Pituitary
Gland
/ metabolism.
Pituitary
Gland
/ pathology
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[Cites]
Clin Nucl Med. 2002 Mar;27(3):176-8
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[ISSN]
1573-7403
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
6.
Choe JH, Lee KS, Jeun SS, Cho JH, Hong YK:
Endocrine outcome of endoscopic endonasal transsphenoidal surgery in functioning pituitary adenomas.
J Korean Neurosurg Soc
; 2008 Sep;44(3):151-5
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[Title]
Endocrine outcome of endoscopic endonasal transsphenoidal surgery in functioning
pituitary
adenomas
.
OBJECTIVE: Microscopic and endoscopic transsphenoidal approach (TSA) are major surgical techniques in the treatment
of pituitary adenoma
.
Endoscopic endonasal transsphenoidal approach (EETSA) has been increasingly used for
pituitary
adenomas
, however, its surgical outcome particularly in functioning
pituitary adenoma
has been debated.
Here, we investigated the endocrine outcome of the patients with growth hormone (GH) and adrenocorticotropic hormone (
ACTH
)
secreting pituitary adenoma
treated by EETSA.
METHODS: We treated 80 patients with
pituitary adenoma
by EETSA since 2004, of which 12 patients were affected by functioning
pituitary
adenomas
(9 GH, 3
ACTH
, 0 PRL; 9 macro, 3 micro).
Surgical outcome of those patients treated by EETSA was compared with that of the 11 functioning
pituitary adenoma
patients (8 GH, 3
ACTH
; 8 macro, 3 micro) who underwent sublabial microscopic TSA between 1997 and 2003.
CONCLUSION: EETSA appears to be an effective and safe method for the treatment of functioning
pituitary
adenomas
.
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[Cites]
Am J Rhinol. 2007 Jul-Aug;21(4):510-4
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17882925.001
]
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]
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]
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[
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]
[Cites]
Neurosurgery. 2005 Jun;56(6):1222-33; discussion 1233
[
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]
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[
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]
[Cites]
Surg Neurol. 1997 Mar;47(3):213-22; discussion 222-3
[
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]
[Cites]
Neurosurgery. 1996 Jul;39(1):189-92; discussion 192-3
[
8805160.001
]
[Cites]
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[
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]
[Cites]
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[
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]
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[
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Laryngoscope. 2007 Aug;117(8):1329-32
[
17597634.001
]
(PMID = 19096666.001).
[ISSN]
2005-3711
[Journal-full-title]
Journal of Korean Neurosurgical Society
[ISO-abbreviation]
J Korean Neurosurg Soc
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Korea (South)
[Other-IDs]
NLM/ PMC2588303
[Keywords]
NOTNLM ; ACTH-secreting pituitary adenoma / Endoscopy / GH-secreting pituitary adenoma / Transsphenoidal approach
7.
de Bruin C, Feelders RA, Waaijers AM, van Koetsveld PM, Sprij-Mooij DM, Lamberts SW, Hofland LJ:
Differential regulation of human dopamine D2 and somatostatin receptor subtype expression by glucocorticoids in vitro.
J Mol Endocrinol
; 2009 Jan;42(1):47-56
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Dopamine agonists (DA) and somatostatin (SS) analogues have been proposed in the treatment of
ACTH
-
producing
neuro-endocrine tumours that cause
Cushing's
syndrome.
In this study, we investigated the effects of the GC dexamethasone (DEX) on D(2) and sst expression in three human neuro-endocrine
cell
lines: BON (carcinoid) and TT (medullary thyroid carcinoma) versus DMS (small
cell
lung cancer), which is severely GC resistant.
In DMS, DEX did
not
cause significant changes in the expression of these receptor subtypes.
In conclusion, we show that GCs selectively down-regulate sst(2), but
not
D(2) and only to a minor degree sst(5) in human neuro-endocrine BON and TT cells.
This mechanism may also be responsible for the low expression of sst(2) in
corticotroph adenomas
and underwrite the current interest in sst(5) and D(2) as possible therapeutic targets for a medical treatment of
Cushing's disease
.
[MeSH-minor]
Animals. Antineoplastic Agents, Hormonal / metabolism.
Cell
Line.
Cell
Proliferation. DNA Fragmentation. Dexamethasone / metabolism. Dopamine / metabolism. Hormone Antagonists / metabolism. Humans. Mifepristone / metabolism. Octreotide / metabolism. RNA, Messenger / metabolism. Radioligand Assay. Somatostatin / metabolism
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DEXAMETHASONE
.
Hazardous Substances Data Bank.
DOPAMINE
.
Hazardous Substances Data Bank.
MIFEPRISTONE
.
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(PMID = 18852217.001).
[ISSN]
1479-6813
[Journal-full-title]
Journal of molecular endocrinology
[ISO-abbreviation]
J. Mol. Endocrinol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Glucocorticoids; 0 / Hormone Antagonists; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 320T6RNW1F / Mifepristone; 51110-01-1 / Somatostatin; 7S5I7G3JQL / Dexamethasone; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
8.
Giacomini D, Haedo M, Gerez J, Druker J, Páez-Pereda M, Labeur M, Stalla GK, Arzt E:
Differential gene expression in models of pituitary prolactin-producing tumoral cells.
Horm Res
; 2009 Apr;71 Suppl 2:88-94
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[Title]
Differential gene expression in models
of pituitary
prolactin-
producing
tumoral cells.
Although several genes and signalling pathways have been identified as important effectors in the development
of pituitary
tumours, our understanding
of pituitary
tumorigenesis remains incomplete and is the focus of much current research.
Use of the mRNA differential display technique in prolactinomas from D2-receptor knockout mice and in stable GH3
cell
line clones with enhanced tumorigenicity in vivo has led to the identification of two genes that are involved in the pathogenic process--BMP-4 and RSUME.
In contrast, BMP-4 has an inhibitory role in
corticotrophinomas
.
RSUME (RWD-containing sumoylation enhancer) was identified from a transformed lactosomatotrophic
cell
line that had increased tumorigenic and angiogenic potential.
The differential expression and action of BMP-4 in prolactinomas and
corticotrophinomas
highlights the importance of studying a gene with contrasting actions in two
cell
lineages of the same organ in order to understand
the pituitary
transformation process.
Both BMP-4 and RSUME may be interesting targets for inhibiting steps involved in
pituitary
tumorigenesis.
[MeSH-major]
Bone Morphogenetic Protein 4 / biosynthesis. Gene Expression Regulation, Neoplastic. Models, Biological.
Neoplasm
Proteins / biosynthesis. Prolactinoma / metabolism. Transcription Factors / biosynthesis
[MeSH-minor]
Animals.
Cell
Hypoxia / genetics.
Cell
Line,
Tumor
.
Cell
Transformation, Neoplastic / genetics.
Cell
Transformation, Neoplastic / metabolism. Gene Expression Profiling. Humans. Mice. Mice, Knockout. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Signal Transduction / genetics
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[Copyright]
Copyright 2009 S. Karger AG, Basel.
(PMID = 19407504.001).
[ISSN]
1423-0046
[Journal-full-title]
Hormone research
[ISO-abbreviation]
Horm. Res.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Neoplasm Proteins; 0 / RSUME protein, human; 0 / Receptors, Dopamine D2; 0 / Transcription Factors
[Number-of-references]
56
9.
Winczyk K, Pawlikowski M:
Immunohistochemical detection of PPARgamma receptors in the human pituitary adenomas: correlation with PCNA.
Folia Histochem Cytobiol
; 2005;43(3):137-41
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[Title]
Immunohistochemical detection of PPARgamma receptors in the human
pituitary
adenomas
: correlation with PCNA.
The occurrence of peroxisome proliferator-activated receptors gamma (PPARgamma) was investigated in 51 human
pituitary
adenomas
and in 6 non-tumoral human
pituitary
tissue samples.
The mean percentage of cells with positive nuclear reaction was 3-fold higher in
pituitary
adenomas
in comparison with non-tumoral
pituitary
tissues.
It was clearly stronger in
pituitary
adenomas
than in non-tumoral
pituitary
tissues.
A slight, statistically insignificant tendency towards negative correlation between PPARgamma and PCNA was found in somatotropinomas, prolactinomas,
corticotropinomas
and gonadotropinomas.
On the other hand, in null
cell adenomas
and "silent"
corticotropinomas
, a strong positve correlation between the expression of PPARgamma and PCNA was observed.
The strong expression of PPARgamma in human
pituitary
adenomas
and its possible involvement in control of
cell
proliferation in these tumors give a good reason for the attempts of their treatment with PPARgamma ligands.
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.
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(PMID = 16201313.001).
[ISSN]
0239-8508
[Journal-full-title]
Folia histochemica et cytobiologica
[ISO-abbreviation]
Folia Histochem. Cytobiol.
[Language]
ENG
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Poland
[Chemical-registry-number]
0 / PPAR gamma; 0 / Proliferating Cell Nuclear Antigen
10.
Vassiliadi D, Tsagarakis S:
Unusual causes of Cushing's syndrome.
Arq Bras Endocrinol Metabol
; 2007 Nov;51(8):1245-52
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[Title]
Unusual causes of
Cushing's
syndrome.
Although in the majority of the patients with
Cushing's
syndrome (CS), hypercortisolism is due to
ACTH
hypersecretion by a
pituitary
tumour or to ectopic
ACTH
secretion from an extrapituitary neoplastic lesion or to autonomous cortisol secretion by an adrenal tumour, in occasional patients a much rarer entity may be the cause of the syndrome.
The following unusual forms of CS were identified: (i)
ACTH
hyperesecretion due to ectopic
corticotroph adenomas
in the parasellar region or the neurohypophysis, or as part of double
adenomas
, or gangliocytomas;.
(ii)
ACTH
hypersecretion due to ectopic CRH or CRH-like peptide secretion by various neoplasms;.
(iii)
ACTH
-independent cortisol hypersecretion from ectopic or bilateral adrenal
adenomas
;.
Such unusual presentations of CS illustrate why
Cushing's
syndrome represents one of the most puzzling endocrine syndromes.
[MeSH-minor]
ACTH
Syndrome, Ectopic / complications. Adrenal
Gland
Neoplasms / complications. Female. Glucocorticoids / adverse effects. Humans. Liver Neoplasms / complications. Megestrol Acetate / adverse effects. Ovarian Neoplasms / complications.
Pituitary
Neoplasms / complications. Ritonavir / adverse effects
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(PMID = 18209862.001).
[ISSN]
0004-2730
[Journal-full-title]
Arquivos brasileiros de endocrinologia e metabologia
[ISO-abbreviation]
Arq Bras Endocrinol Metabol
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Brazil
[Chemical-registry-number]
0 / Glucocorticoids; O3J8G9O825 / Ritonavir; TJ2M0FR8ES / Megestrol Acetate
[Number-of-references]
58
11.
Matsuno A:
[Recent trends in the pathophysiology and treatment of pituitary adenomas].
Brain Nerve
; 2009 Aug;61(8):957-62
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[Title]
[Recent trends in the pathophysiology and treatment
of pituitary
adenomas
].
Recent molecular pathological investigations have elucidated the cytodifferentiation
of pituitary
cells and identified several transcriptional factors that regulate this cytodifferentiation
of pituitary
cells.
The patterns of cytodifferentiation are closely related to the pathogenesis
of pituitary
adenomas
.
Meanwhile, the role of hypothalamic hormones in the development
of pituitary
adenomas
has recently attracted the attention of investigators.
The expression of growth hormone-releasing hormone and corticotrophin releasing hormone in
corticotroph adenomas
have been demonstrated in somatotroph
adenomas
and
corticotropin adenomas
, respectively.
This
finding
indicates that the endogenous expression of hypothalamic hormones and their receptors in human
pituitary adenoma
cells has ample significance in the autocrine or paracrine regulation
of pituitary
hormone production and
tumor
extension induced by hypothalamic hormones produced by
adenoma
cells.
The recent progress in surgical techniques for treatment
of pituitary
adenomas
has provided several alternatives: transsphenoidal surgery vs. transcranial surgery, sublabial approach vs. endonasal approach, and microsurgery vs. endoscopic surgery.
There have also been developments in the medical treatment
of pituitary
adenomas
.
The frequently used dopamine agonist, cabergoline, is very effective for treating prolactin-
producing
adenoma
.
Long-acting octreotide and pegvisomant are now available for the treatment of growth hormone
producing
adenoma
.
Cabergoline is also used for growth hormone
producing
adenoma
.
Temozolomide has recently been used for atypical
adenomas
or
pituitary
carcinomas.
Adult growth hormone deficiency sometimes occurs in postoperative patients with
pituitary
adenomas
.
[MeSH-major]
Adenoma
/ etiology.
Adenoma
/ therapy.
Pituitary
Neoplasms / etiology.
Pituitary
Neoplasms / therapy
[MeSH-minor]
Antineoplastic Agents / therapeutic use.
Corticotropin
-Releasing Hormone. Dacarbazine / analogs & derivatives. Dacarbazine / therapeutic use. Ergolines / therapeutic use. Growth Hormone-Releasing Hormone. Human Growth Hormone / analogs & derivatives. Human Growth Hormone / therapeutic use. Humans. Hypothalamic Hormones. Incidental Findings. Neurosurgical Procedures / methods. Neurosurgical Procedures / trends. Octreotide / therapeutic use. Prolactinoma. Receptors, Neuropeptide. Receptors,
Pituitary
Hormone-Regulating Hormone
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(PMID = 19697885.001).
[ISSN]
1881-6096
[Journal-full-title]
Brain and nerve = Shinkei kenkyū no shinpo
[ISO-abbreviation]
Brain Nerve
[Language]
jpn
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Japan
[Chemical-registry-number]
0 / Antineoplastic Agents; 0 / Ergolines; 0 / Hypothalamic Hormones; 0 / Receptors, Neuropeptide; 0 / Receptors, Pituitary Hormone-Regulating Hormone; 0 / pegvisomant; 0 / somatotropin releasing hormone receptor; 12629-01-5 / Human Growth Hormone; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9015-71-8 / Corticotropin-Releasing Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide
[Number-of-references]
32
12.
Penezić Z, Zarković M, Vujović S, Ivović M, Beleslin B, Ciric J, Drezgić M:
[The value of corticotropin-releasing hormone (CRH) test for differential diagnosis of Cushing's syndrome].
Srp Arh Celok Lek
; 2007 Jan-Feb;135(1-2):31-7
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[Title]
[The value of
corticotropin
-releasing hormone (CRH) test for differential
diagnosis
of
Cushing's
syndrome].
INTRODUCTION:
Diagnosis
and differential
diagnosis
of
Cushing's
syndrome (CS) remain considerable challenge in endocrinology.
Following the CRH administration, the majority of patients with
ACTH
secreting pituitary adenoma
show a significant rise of plasma cortisol and
ACTH
, whereas those with ectopic
ACTH
secretion characteristically do
not
.
OBJECTIVE: The aim of our study was to assess the value of CRF test for differential
diagnosis
of CS using the ROC (receiver operating characteristic) curve method.
ACTH
secreting pituitary adenoma
was found in 18, ectopic
ACTH
secretion in 3 and cortisol
secreting
adrenal
adenoma
in 9 of all patients with CS.
Cortisol and
ACTH
were determined -15.0, 15, 30, 45, 60, 90 and 120 min. after i.v. administration of 100 microg of ovine CRH.
Cortisol and
ACTH
were determined by commercial RIA.
Due to small number, the patients with ectopic
ACTH
secretion were excluded from test evaluation by ROC curve method.
Consequently, basal
ACTH
was (100.9 +/- 85.0 vs. 138.0 +/- 123.7 vs. 4.8 +/- 4.3 pg/mL) and maximal stimulated
ACTH
(203.8 +/- 160.1 vs. 288.0 +/- 189.5 vs. 7.4 +/- 9.2 pg/mL).
For
ACTH
, determination area under ROC curve was 0.637 +/- 0.142 (CI 95% 0.359-0.916).
For
ACTH
increase cut-off level of 30%, test sensitivity was 70%, with specificity of 57%.
CONCLUSION: Determination of cortisol and
ACTH
levels in CRH test remains reliable tool in differential
diagnosis
of
Cushing's
syndrome.
[MeSH-major]
Corticotropin
-Releasing Hormone. Cushing Syndrome /
diagnosis
[MeSH-minor]
ACTH
Syndrome, Ectopic /
diagnosis
.
ACTH
-
Secreting Pituitary Adenoma
/
diagnosis
.
Adenoma
/
diagnosis
. Adrenocorticotropic Hormone / blood. Adult.
Diagnosis
, Differential. Female. Humans. Hydrocortisone / blood. Male. ROC Curve. Sensitivity and Specificity
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.
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.
Hazardous Substances Data Bank.
Corticotropin
.
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(PMID = 17503565.001).
[ISSN]
0370-8179
[Journal-full-title]
Srpski arhiv za celokupno lekarstvo
[ISO-abbreviation]
Srp Arh Celok Lek
[Language]
srp
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Serbia and Montenegro
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; WI4X0X7BPJ / Hydrocortisone
13.
Cho HY, Cho SW, Kim SW, Shin CS, Park KS, Kim SY:
Silent corticotroph adenomas have unique recurrence characteristics compared with other nonfunctioning pituitary adenomas.
Clin Endocrinol (Oxf)
; 2010 May;72(5):648-53
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[Title]
Silent
corticotroph adenomas
have unique recurrence characteristics compared with other nonfunctioning
pituitary
adenomas
.
OBJECTIVE: The prevalence of silent
corticotroph adenomas
(SCAs) is
not
rare among nonfunctioning
pituitary
adenomas
(NFPAs); however, it is unknown whether the clinical significance of SCAs differs from that of NFPAs without
ACTH
immunoreactivity (non-SCAs).
MEASUREMENTS: We analysed whether clinical manifestations at
diagnosis
, postoperative recurrence rate and recurrence characteristics differed between SCA and non-SCA patients.
The mean age at the time of
diagnosis
was 44 years (range, 13-67 years) in the SCA group and 50 years (18-79 years) in the non-SCA group (P = 0.026), with respective follow-up periods of 5.2 (range, 1.0-16.0 years) and 4.2 years (0.5-16.1 years) (P = 0.255).
[MeSH-major]
Adenoma
/ pathology. Adrenocorticotropic Hormone / analysis.
Neoplasm
Recurrence, Local.
Pituitary
Neoplasms / pathology
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Corticotropin
.
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(PMID = 19650787.001).
[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
England
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone
14.
van Aken MO, Feelders RA, van der Lely AJ, Romijn JA, Lamberts SW, de Herder WW:
[Cushing's syndrome. II. New forms of treatment].
Ned Tijdschr Geneeskd
; 2006 Oct 28;150(43):2365-9
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[Title]
[
Cushing's
syndrome. II. New forms of treatment].
Several new therapeutic options both medicinal and surgical, have emerged for the treatment of
Cushing's
syndrome.
In
Cushing's disease
caused by an
adrenocorticotropin
(
ACTH
)
secreting pituitary adenoma
, the introduction ofendoscopic
pituitary
surgery offers better visualization of the sella than does the traditional explorative surgery.
These agents may also be effective for the medicinal treatment of ectopic
ACTH
-secretion.
The primary treatment for
ACTH
-independent
Cushing's
syndrome is laparoscopic adrenalectomy.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ therapy.
Adenoma
/ therapy. Cushing Syndrome / therapy
[MeSH-minor]
Adrenalectomy. Adrenergic Antagonists / therapeutic use. Humans.
Pituitary
Gland
/ surgery. Treatment Outcome
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.
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.
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[CommentIn]
Ned Tijdschr Geneeskd. 2006 Oct 28;150(43):2345-9
[
17100122.001
]
[CommentIn]
Ned Tijdschr Geneeskd. 2007 Feb 3;151(5):330; author reply 331
[
17326480.001
]
(PMID = 17100127.001).
[ISSN]
0028-2162
[Journal-full-title]
Nederlands tijdschrift voor geneeskunde
[ISO-abbreviation]
Ned Tijdschr Geneeskd
[Language]
dut
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Netherlands
[Chemical-registry-number]
0 / Adrenergic Antagonists
[Number-of-references]
24
15.
van der Klaauw AA, Kienitz T, Strasburger CJ, Smit JW, Romijn JA:
Malignant pituitary corticotroph adenomas: report of two cases and a comprehensive review of the literature.
Pituitary
; 2009;12(1):57-69
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[Title]
Malignant
pituitary
corticotroph adenomas
: report of two cases and a comprehensive review of the literature.
Corticotroph
pituitary
carcinomas are tumors, defined by the presence of distant metastases that determine their poor prognosis.
The
diagnosis
and therapy of malignant
corticotroph adenomas
remains a clinical challenge.
The molecular mechanisms of malignant transformation
of pituitary
adenomas
are unclear, although they are believed to arise in an
adenoma
-to-carcinoma sequence.
We describe two cases of malignant
Cushing's disease
with metastases in liver and bone, respectively.
The primary
pituitary
tumors were treated by a combination of radiotherapy and transsphenoidal surgery, but recurred several times in both patients.
The time interval between the
diagnosis
of
Cushing's disease
and the discovery of metastases was 32 and 17 years, respectively.
In the first case the patient died within 6 months after
diagnosis
of metastasis, whereas the second patient is alive at a follow-up of 2 years after the discovery of the metastasis.
Furthermore, we reviewed all available cases of
corticotroph
pituitary
carcinomas reported in the literature and analyzed their clinical features and therapeutical management.
In conclusion, frequent relapses of
Cushing's disease
, aggressive growth of
macroadenoma
, Nelson's syndrome after adrenalectomy or persistently high
ACTH
levels should prompt the clinician to consider the possibility
of pituitary
corticotroph
carcinomas.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/
diagnosis
.
ACTH
-
Secreting Pituitary Adenoma
/ pathology.
Pituitary
ACTH
Hypersecretion / complications
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(PMID = 18176844.001).
[ISSN]
1573-7403
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
United States
[Number-of-references]
62
16.
De Menis E, Roncaroli F, Calvari V, Chiarini V, Pauletto P, Camerino G, Cremonini N:
Corticotroph adenoma of the pituitary in a patient with X-linked adrenal hypoplasia congenita due to a novel mutation of the DAX-1 gene.
Eur J Endocrinol
; 2005 Aug;153(2):211-5
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[Title]
Corticotroph
adenoma of the pituitary
in a patient with X-linked adrenal hypoplasia congenita due to a novel mutation of the DAX-1 gene.
We report the occurrence of an
ACTH
-
secreting adenoma
in a patient with X-linked congenital adrenal hypoplasia.
DESIGN AND METHODS: Detailed clinical, radiological and pathological investigation of the
pituitary adenoma
.
ACTH
was 24 980 pg/ml and nuclear magnetic resonance disclosed a huge
pituitary adenoma
.
Three transsphenoidal operations and radiotherapy were necessary to remove the
tumor
mass and control
ACTH
secretion.
Histologically,
the adenoma
was composed of chromophobic and
basophilic
neoplastic cells with positive immunostaining for
ACTH
.
CONCLUSIONS: This case suggests that in adrenal hypoplasia congenita the development of a
pituitary adenoma
should be considered when a sudden rise of
ACTH
occurs despite adequate steroid substitution.
[MeSH-major]
Adenoma
/ complications. Adrenal Insufficiency / complications. Adrenal Insufficiency / genetics. DNA-Binding Proteins / genetics.
Pituitary
Neoplasms / complications. Receptors, Retinoic Acid / genetics. Repressor Proteins / genetics
[MeSH-minor]
Adrenocorticotropic Hormone / metabolism. Adult. Chromosomes, Human, X. DAX-1 Orphan Nuclear Receptor. Family Health. Female. Frameshift Mutation. Humans. Magnetic Resonance Imaging. Male.
Pituitary
ACTH
Hypersecretion / complications.
Pituitary
ACTH
Hypersecretion / metabolism.
Pituitary
ACTH
Hypersecretion / pathology
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.
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.
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author profiles
.
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Corticotropin
.
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(PMID = 16061826.001).
[ISSN]
0804-4643
[Journal-full-title]
European journal of endocrinology
[ISO-abbreviation]
Eur. J. Endocrinol.
[Language]
eng
[Grant]
Italy / Telethon / / B.38
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / DAX-1 Orphan Nuclear Receptor; 0 / DNA-Binding Proteins; 0 / NR0B1 protein, human; 0 / Receptors, Retinoic Acid; 0 / Repressor Proteins; 9002-60-2 / Adrenocorticotropic Hormone
17.
Salgado LR, Machado MC, Cukiert A, Liberman B, Kanamura CT, Alves VA:
Cushing's disease arising from a clinically nonfunctioning pituitary adenoma.
Endocr Pathol
; 2006;17(2):191-9
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[Title]
Cushing's disease
arising from a clinically nonfunctioning
pituitary adenoma
.
A 49-yr-old woman with a large
pituitary
tumor
leading to visual loss and galactorrhea- amenorrhea was submitted to transcranial
pituitary
surgery, when a clinically nonfunctioning
pituitary adenoma
was partially removed.
Histopathology and immunohistochemistry confirmed the
diagnosis
of "non-
secreting
atypical
adenoma
."
Two years later, she presented high free urinary cortisol levels and a positive
ACTH
response to desmopressin testing on dexametasone 2 mg overnight.
A
pituitary
biopsy confirmed aggressive growth as well as positive immunoreactivity for
ACTH
, p53, Ki-67, and c-erb-B2.
The overall clinical, laboratory, and pathological data suggest a transition from a clinically nonfunctioning to a hypersecreting
ACTH
-
producing tumor
.
Putative mechanisms of
tumor
transformation and the possibility of a silent
corticotropinoma
evolving into clinical Cushing s syndrome are discussed.
[MeSH-major]
Adenoma
/ complications.
Adenoma
/ pathology.
Pituitary
ACTH
Hypersecretion / etiology.
Pituitary
Neoplasms / complications.
Pituitary
Neoplasms / pathology
MedlinePlus Health Information.
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.
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NCI CPTAC Assay Portal
.
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[
11141695.001
]
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(PMID = 17159252.001).
[ISSN]
1046-3976
[Journal-full-title]
Endocrine pathology
[ISO-abbreviation]
Endocr. Pathol.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
United States
18.
van der Hoek J, Lamberts SW, Hofland LJ:
The somatostatin receptor subtype 5 in neuroendocrine tumours.
Expert Opin Investig Drugs
; 2010 Mar;19(3):385-99
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AREAS COVERED IN THIS REVIEW: The scope of this review is primarily focused upon recent insights in sst(5)-receptor physiology, novel sst(5)-targeted treatment options predominantly directed towards
pituitary
adenomas
, and gastroenteropancreatic neuroendocrine tumours.
WHAT THE READER WILL GAIN: An understanding of the potential that novel sst(5)-targeted SRIF analogues might have in the medical treatment of
Cushing's disease
and acromegaly, as demonstrated by translational research, based on pathophysiological data combined with results from clinical trials.
Finally, absence of sst(5) in
corticotroph adenomas
could be related to tumour aggressiveness in
Cushing's disease
.
[MeSH-minor]
Adenoma
/ drug therapy.
Adenoma
/ physiopathology. Animals. Drug Design. Gastrointestinal Neoplasms / drug therapy. Gastrointestinal Neoplasms / physiopathology. Humans. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / physiopathology.
Pituitary
Neoplasms / drug therapy.
Pituitary
Neoplasms / physiopathology
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(PMID = 20151855.001).
[ISSN]
1744-7658
[Journal-full-title]
Expert opinion on investigational drugs
[ISO-abbreviation]
Expert Opin Investig Drugs
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Receptors, Somatostatin; 0 / somatostatin receptor 5
[Number-of-references]
101
19.
Machiavelli G, Cotignola J, Danilowicz K, Carbonara C, Paes de Lima A, Basso A, Bruno OD, Szijan I:
Expression of p16(INK4A) gene in human pituitary tumours.
Pituitary
; 2008;11(1):71-5
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[Title]
Expression of p16(INK4A) gene in human
pituitary
tumours.
Pituitary
adenomas
comprise 10-15% of primary
intracranial
tumours but the mechanisms leading to tumour development are yet to be clearly established.
The retinoblastoma pathway, which regulates the progression through the
cell
cycle, is often deregulated in different types of tumours.
We studied the cyclin-dependent kinase inhibitor p16(INK4A) gene expression at mRNA level in human
pituitary
adenomas
.
Forty-six tumour specimens of different subtypes, 21 clinically non-functioning, 12 growth hormone-
secreting
, 6 prolactin-
secreting
, 6
adrenocorticotropin
-
secreting
, and 1 thyrotropin-
secreting
tumours were studied.
All clinically non-functioning and most of the hormone-
secreting
tumours were macroadenomas (38/46).
The RT-PCR assay and electrophoresis of the PCR-products showed that p16(INK4A) mRNA was undetectable in: 62% of non-functioning, 8% of growth hormone-
secreting
, 17% of prolactin-
secreting
and 17%
of adrenocorticotropin
-
secreting
adenomas
.
Within the non-functioning
adenomas
63% were "null
cell
" and 37% were positive for some hormone, both subgroups showed similar percentage of cases with absence of p16(INK4A) mRNA.
Our results show that clinically non-functioning macroadenomas have impaired p16(INK4A) expression in a clearly higher proportion than any other
pituitary
tumour subtype investigated.
[MeSH-major]
Adenoma
/ genetics. Cyclin-Dependent Kinase Inhibitor p16 / genetics. Gene Expression Regulation, Neoplastic.
Pituitary
Neoplasms / genetics
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[Cites]
Cancer Res. 1996 Jun 1;56(11):2493-6
[
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(PMID = 18058237.001).
[ISSN]
1573-7403
[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 / Cyclin-Dependent Kinase Inhibitor p16; 0 / RNA, Messenger
20.
Chacko G, Chacko AG, Lombardero M, Mani S, Seshadri MS, Kovacs K, Scheithauer BW:
Clinicopathologic correlates of giant pituitary adenomas.
J Clin Neurosci
; 2009 May;16(5):660-5
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[Title]
Clinicopathologic correlates of giant
pituitary
adenomas
.
Giant
adenomas
comprise a clinical/therapeutic subset
of pituitary
adenomas
that pose a surgical challenge.
The study population consisted of 28 patients who had giant
pituitary
adenomas
, which are defined as tumors with a diameter greater than 5cm.
Clinically, five tumors (18%) were endocrinologically functional and 23 (82%) were
not
.
During surgery, one
tumor
was radically excised, four were subtotally excised, 12 were partially excised, and 11 were biopsied.
All of the tumors showed typical histological features
of pituitary adenoma
.
Of the 23 clinically non-functional
adenomas
, 18 were gonadotrophic tumors, four were null
cell adenomas
and one was a silent
corticotroph
adenoma
.
The present study found giant
adenomas
to be invasive but slow growing, histologically benign and often gonadotrophic in subtype.
[MeSH-major]
Adenoma
/ pathology.
Adenoma
/ therapy.
Pituitary
Neoplasms / pathology.
Pituitary
Neoplasms / therapy
[MeSH-minor]
Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Antigens, CD34 / metabolism. Female. Follow-Up Studies. Humans. Ki-67 Antigen / metabolism. Magnetic Resonance Imaging / methods. Male. Middle Aged.
Neoplasm
Invasiveness. Retrospective Studies. Treatment Outcome. Young Adult
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(PMID = 19285407.001).
[ISSN]
0967-5868
[Journal-full-title]
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
[ISO-abbreviation]
J Clin Neurosci
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
Scotland
[Chemical-registry-number]
0 / Antigens, CD34; 0 / Ki-67 Antigen; 9002-60-2 / Adrenocorticotropic Hormone
21.
Bademci G:
Pitfalls in the management of Cushing's disease.
J Clin Neurosci
; 2007 May;14(5):401-8; discussion 409
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[Title]
Pitfalls in the management of
Cushing's disease
.
Cushing's disease
is caused by functional
corticotroph adenomas
of the
pituitary
gland
, most commonly noninvasive microadenomas.
Transsphenoidal microsurgery is an effective means of control for patients with adrenocorticotrophic hormone-
producing
microadenomas.
The major causes of surgical failure in the treatment of
Cushing's disease
lies in inadequate preoperative evaluation, unsuccessful identification of the
adenoma
and inexperience of the surgeon.
For optimal results in this rare
disease
, endocrinological, radiological and surgical procedures should be co-ordinated in a specialized center.
[MeSH-major]
Pituitary
ACTH
Hypersecretion / therapy. Treatment Failure
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(PMID = 17386367.001).
[ISSN]
0967-5868
[Journal-full-title]
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
[ISO-abbreviation]
J Clin Neurosci
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
Scotland
[Number-of-references]
82
22.
Kreutzer J, Jeske I, Hofmann B, Blumcke I, Fahlbusch R, Buchfelder M, Buslei R:
No effect of the PPAR-gamma agonist rosiglitazone on ACTH or cortisol secretion in Nelson's syndrome and Cushing's disease in vitro and in vivo.
Clin Neuropathol
; 2009 Nov-Dec;28(6):430-9
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[Title]
No effect of the PPAR-gamma agonist rosiglitazone on
ACTH
or cortisol secretion in Nelson's syndrome and
Cushing's disease
in vitro and in vivo.
OBJECTIVE: Surgical
tumor
resection remains the primary treatment strategy in
ACTH
-
secreting pituitary
adenomas
, i.e.
Cushing's disease
(CD) and Nelson's syndrome (NS).
However, an effective long-term pharmacological regime is
not
available in patients with persistent
ACTH
-hypersecretion.
The nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-gamma) is abundantly expressed in most
pituitary
adenomas
.
First encouraging data reported that the PPAR-gamma ligand rosiglitazone antagonizes
ACTH
hypersecretion and exerts also antiproliferative effects in
pituitary
cell
lines.
Herein, we studied the potential therapeutical effects of rosiglitazone in patients with
ACTH
-
secreting pituitary
adenomas
in vitro and in vivo.
MATERIALS AND METHODS: Seven patients with persistent
ACTH
-hypersecretion (3 with NS, 4 with persistent CD) were treated 5 months with rosiglitazone (4 - 16 mg/day).
In vitro assays were performed in primary
cell
cultures obtained from eight additional patients with
ACTH
-
secreting pituitary
adenomas
applying 80 microM rosiglitazone repeatedly over a time period of 14 days.
RESULTS: Our long-term clinical trial with the PPAR-gamma activator rosiglitazone showed no amelioration of clinical symptoms nor an inhibiting effect on
ACTH
-secretion in vivo.
In vitro, rosiglitazone treatment led to a statistically significant decrease of
ACTH
levels in 2 out of 8 primary
cell
cultures after 14 days compared to untreated controls.
CONCLUSION: In contrast to the initially promising laboratory data gathered in
pituitary
cell
line experiments and nude mice models, our experimental data obtained in primary human
ACTH
-expressing
pituitary adenoma
cell
cultures as well as our clinical experience with a long-term rosiglitazone trial in approved antidiabetic doses support the recently reported disappointing reports on acute or short-term medical treatment of
ACTH
-hypersecretion with PPAR-gamma activators.
[MeSH-major]
Adrenocorticotropic Hormone / secretion. Hydrocortisone / secretion. Nelson Syndrome / blood. PPAR gamma / agonists.
Pituitary
ACTH
Hypersecretion / blood. Thiazolidinediones / pharmacology
[MeSH-minor]
Adenoma
/ pathology.
Adenoma
/ secretion. Adult. Female. Humans. In Vitro Techniques. Magnetic Resonance Imaging. Male. Middle Aged.
Pituitary
Neoplasms / pathology.
Pituitary
Neoplasms / secretion. Treatment Outcome.
Tumor
Cells, Cultured
Genetic Alliance.
consumer health - Cushing's Syndrome
.
Hazardous Substances Data Bank.
ROSIGLITAZONE
.
Hazardous Substances Data Bank.
HYDROCORTISONE
.
Hazardous Substances Data Bank.
Corticotropin
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 19919817.001).
[ISSN]
0722-5091
[Journal-full-title]
Clinical neuropathology
[ISO-abbreviation]
Clin. Neuropathol.
[Language]
eng
[Publication-type]
Clinical Trial; Journal Article
[Publication-country]
Germany
[Chemical-registry-number]
0 / PPAR gamma; 0 / Thiazolidinediones; 05V02F2KDG / rosiglitazone; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
23.
Pawlikowski M:
Immunohistochemical detection of dopamine D2 receptors in human pituitary adenomas.
Folia Histochem Cytobiol
; 2010 Sep 30;48(3):394-7
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[Title]
Immunohistochemical detection of dopamine D2 receptors in human
pituitary
adenomas
.
Thirty one
pituitary
adenomas
and 3 samples of peritumoral anterior
pituitary
tissue were immunostained with an antibody raised against dopamine D2 receptor protein.
The positive reactions were found in
cell
cytoplasm, a subpopulation of
cell
nuclei and the intratumoral blood vessels walls.
As expected, the positive immunostaining was shown in cytoplasm and/or
cell
nuclei of all examined prolactinomas (7/7).
In acromegaly the positive D2 staining occurred in 5/7 samples, in gonadotropinomas in 6/8 and in plurihormonal
adenomas
2/4.
The lowest expression was observed in
corticotropinomas
(1/5).
Moreover, the presence of D2 receptors in intratumoral blood vessels walls constitutes the possibility of the anti-angiogenic action of D2 agonists in
pituitary
adenomas
.
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.
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(PMID = 21071344.001).
[ISSN]
1897-5631
[Journal-full-title]
Folia histochemica et cytobiologica
[ISO-abbreviation]
Folia Histochem. Cytobiol.
[Language]
ENG
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Poland
[Chemical-registry-number]
0 / Receptors, Dopamine D2
24.
Mounier C, Pasquet F, Trouillas J, Perrin G, Jouanneau E, Borson-Chazot F, Colle B:
[Nelson's syndrome: course of aggressive pituitary corticotroph adenoma].
Ann Endocrinol (Paris)
; 2007 Feb;68(1):28-33
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[Title]
[Nelson's syndrome: course of aggressive
pituitary
corticotroph
adenoma
].
[Transliterated title]
Syndrome
de
Nelson: évolution d'un adénome
hypophysaire corticotrope
agressif.
Nelson's syndrome was defined in 1958 as the association of an expanding
pituitary
tumor
with high
ACTH
secretion after bilateral adrenalectomy for
Cushing's disease
.
Pituitary
MRI and
ACTH
measurements led to the definition of Nelson's syndrome as the proliferation of a corticotrophic microadenoma or an aggressive and highly proliferative
tumor
residue induced by the decreased glucocorticoid inhibition after bilateral adrenalectomy.
Now, the problem is
not
the definition of Nelson's syndrome but rather the identification of markers predictive of
tumor
growth.
Based on a typical case and a review of the literature, we point out some predictive markers of
tumor
growth after bilateral adrenalectomy: young age at
diagnosis
, presence of
tumor
residue on
pituitary
MRI before adrenalectomy, markers of
tumor
aggressiveness (Ki-67>3%, mitoses, nuclear PTTG) and increase of
ACTH
levels during the first months following adrenalectomy.
[MeSH-major]
Adenoma
/ physiopathology. Nelson Syndrome / physiopathology.
Pituitary
Neoplasms / physiopathology
[MeSH-minor]
Adrenocorticotropic Hormone / analysis. Adrenocorticotropic Hormone / secretion. Adult. Female. Humans. Magnetic Resonance Imaging.
Pituitary
Gland
/ pathology
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.
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(PMID = 17306208.001).
[ISSN]
0003-4266
[Journal-full-title]
Annales d'endocrinologie
[ISO-abbreviation]
Ann. Endocrinol. (Paris)
[Language]
fre
[Publication-type]
Case Reports; English Abstract; Journal Article
[Publication-country]
France
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone
25.
Tagliati F, Gentilin E, Buratto M, Molè D, degli Uberti EC, Zatelli MC:
Magmas, a gene newly identified as overexpressed in human and mouse ACTH-secreting pituitary adenomas, protects pituitary cells from apoptotic stimuli.
Endocrinology
; 2010 Oct;151(10):4635-42
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[Title]
Magmas, a gene newly identified as overexpressed in human and mouse
ACTH
-
secreting pituitary
adenomas
, protects
pituitary
cells from apoptotic stimuli.
Pituitary
tumors are mostly benign, being locally invasive in 5-35% of cases.
Deregulation of several genes has been suggested as a possible alteration underlying the development and progression
of pituitary
tumors.
We here report the identification of a cDNA, corresponding to Magmas gene (mitochondria-associated protein involved in granulocyte-macrophage colony-stimulating factor signal transduction), which is highly expressed in two different
ACTH
-
secreting
mouse
pituitary adenoma
cell
lines as compared with normal
pituitary
as well as in two thirds of 64 examined
pituitary
adenomas
as compared with human normal
pituitary
.
Tim 16, the mitochondrial protein encoded by Magmas, was indeed expressed in a mouse
ACTH
-
secreting pituitary adenoma
cell
line, AtT-20 D16v-F2 cells, in a subcellular compartment likely corresponding to mitochondria.
Our data demonstrate that Magmas is overexpressed in mouse and human
ACTH
-
secreting pituitary
adenomas
.
Moreover, our results show that Magmas protects
pituitary
cells from apoptosis, suggesting its possible involvement in neoplastic transformation.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ genetics.
Adenoma
/ genetics. Apoptosis / genetics. Mitochondrial Proteins / physiology
[MeSH-minor]
Animals.
Cell
Proliferation.
Cell
Transformation, Neoplastic / genetics.
Cell
Transformation, Neoplastic / pathology. Cells, Cultured. Cytoprotection / drug effects. Cytoprotection / genetics. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice.
Pituitary
Gland
/ metabolism. RNA, Small Interfering / pharmacology. Up-Regulation / drug effects
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)
.
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(PMID = 20719856.001).
[ISSN]
1945-7170
[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 / Mitochondrial Proteins; 0 / RNA, Small Interfering; 0 / magmas protein, human
26.
Xing B, Deng K, Ren ZY, Su CB, Wang RZ, Yang Y, Ma WB, Li YN:
Magnetic resonance imaging characteristics and surgical results of adrenocorticotropin-secreting pituitary adenomas.
Chin Med Sci J
; 2008 Mar;23(1):44-8
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[Title]
Magnetic resonance imaging characteristics and surgical results
of adrenocorticotropin
-
secreting pituitary
adenomas
.
OBJECTIVE: To evaluate magnetic resonance imaging (MRI) characteristics and surgical results
of adrenocorticotropin
(
ACTH
)-
secreting pituitary
adenomas
.
METHODS: MRI characteristics and relationship between MRI positive rate and surgical results of 266 patients with pathologically confirmed
Cushing's disease
were analyzed retrospectively.
All patients underwent thin-section sagittal and coronal scans of the
pituitary
gland
before and after administration of gadolinium-diethylene triamine pentaacetic acid (Gd-DTPA) on a 1.5 Tesla MRI scanner, and dynamic enhanced MRI was performed in 39 patients.
RESULTS: Preoperative MRI revealed normal results in 41 (15.4%) cases, microadenoma in 179 (67.3%),
macroadenoma
in 42 (15.8%), and huge
adenoma
in 4 (1.5%).
Pituitary
apoplexy was found in 13 (4.9%) cases.
Positive rate of
ACTH
-
secreting
adenomas
was 84.6% (225/266) on MRI scans, and that of small microadenomas was 87.2% (34/39) on dynamic enhanced MRI scans.
Preoperative endocrinological tests of 199 cases supported the
diagnosis
of typical
Cushing's disease
, while the other 67 cases had atypical endocrinological results.
CONCLUSIONS: Enhanced coronal
pituitary
MRI is helpful for preoperative localization of
ACTH
-
secreting pituitary
microadenoma.
MedlinePlus Health Information.
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Corticotropin
.
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(PMID = 18437910.001).
[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
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone
27.
Revill K, Dudley KJ, Clayton RN, McNicol AM, Farrell WE:
Loss of neuronatin expression is associated with promoter hypermethylation in pituitary adenoma.
Endocr Relat Cancer
; 2009 Jun;16(2):537-48
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[Title]
Loss of neuronatin expression is associated with promoter hypermethylation in
pituitary adenoma
.
The imprinted gene, neuronatin (NNAT), is one of the most abundant transcripts in
the pituitary
and is thought to be involved in the development and maturation of this
gland
.
In a recent whole-genome approach, exploiting a
pituitary
tumour
cell
line, we identified hypermethylation associated loss of NNAT.
In this report, we determined the expression pattern of NNAT in individual
cell
types of the normal
gland
and within each of the different
pituitary adenoma
subtypes.
Immunohistochemical (IHC) co-localization studies of normal pituitaries showed that each of the hormone
secreting
cells (GH, PRL,
ACTH
, FSH and TSH) expressed NNAT.
However, 33 out of 47
adenomas
comprising, 11 somatotrophinomas, 10 prolactinomas, 12
corticotrophinomas
and 14 non-functioning tumours, irrespective of subtype failed to express either NNAT transcript or protein as determined by quantitative real-time RT-PCR and IHC respectively.
In normal pituitaries and
adenomas
that expressed NNAT the promoter-associated CpG island showed characteristics of an imprinted gene where approximately 50% of molecules were densely methylated.
However, in the majority of
adenomas
that showed loss or significantly reduced expression of NNAT, relative to normal pituitaries, the gene-associated CpG island showed significantly increased methylation.
Collectively, these findings point to an important role for NNAT in
the pituitary
and perhaps tumour development in this
gland
.
[MeSH-major]
DNA Methylation. Membrane Proteins / genetics. Nerve Tissue Proteins / genetics.
Pituitary
Gland
/ pathology.
Pituitary
Neoplasms / genetics. Promoter Regions, Genetic / genetics
[MeSH-minor]
Animals. CpG Islands. Gene Silencing. Humans. Immunoenzyme Techniques. Loss of Heterozygosity. Mice. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction.
Tumor
Cells, Cultured
MedlinePlus Health Information.
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.
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author profiles
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(PMID = 19218280.001).
[ISSN]
1351-0088
[Journal-full-title]
Endocrine-related cancer
[ISO-abbreviation]
Endocr. Relat. Cancer
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Membrane Proteins; 0 / NNAT protein, human; 0 / Nerve Tissue Proteins; 0 / RNA, Messenger
28.
Tateno T, Izumiyama H, Doi M, Yoshimoto T, Shichiri M, Inoshita N, Oyama K, Yamada S, Hirata Y:
Differential gene expression in ACTH -secreting and non-functioning pituitary tumors.
Eur J Endocrinol
; 2007 Dec;157(6):717-24
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[Title]
Differential gene expression in
ACTH
-
secreting
and non-functioning
pituitary
tumors.
OBJECTIVE: Differential expression of several genes between
ACTH
-
secreting pituitary
tumors causing Cushing'
disease
(CD), silent
corticotroph
adenoma
(SCA), and non-functioning
pituitary
tumors (NFT) was investigated.
DESIGN AND METHODS: We used tissue specimens from 35
pituitary
tumors (12 CD, 8 SCA, and 15 NFT).
Steady-state mRNA levels of the genes related to proopiomelanocortin (POMC) transcription, synthesis, processing, and secretion, such as neurogenic differentiation 1 (NeuroD1), T-box 19 (Tpit),
corticotropin
releasing hormone receptor (CRHR), vasopressin receptor 1b (V1bR), prohormone convertase (PC) 1/3 and PC2, 11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 1 and type 2, glucocorticoid receptor alpha (GRalpha), annexin A1, histone deacetylase 2 (HDAC2), and BRM/SWI2-related gene 1, were determined by real-time RT-PCR.
In conclusion, our study demonstrated that the genes related to transcription, synthesis, processing, and secretion of POMC are differentially regulated in
ACTH
-
secreting pituitary
tumors causing CD and SCA compared with those in NFT.
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The Lens.
Cited by Patents in
.
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(PMID = 18057378.001).
[ISSN]
1479-683X
[Journal-full-title]
European journal of endocrinology
[ISO-abbreviation]
Eur. J. Endocrinol.
[Language]
ENG
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Basic Helix-Loop-Helix Transcription Factors; 0 / CRF receptor type 1; 0 / Homeodomain Proteins; 0 / NEUROD1 protein, human; 0 / RNA, Messenger; 0 / Receptors, Corticotropin-Releasing Hormone; 0 / Receptors, Glucocorticoid; 0 / Receptors, Vasopressin; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / glucocorticoid receptor alpha; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 1.1.1.146 / 11-beta-Hydroxysteroid Dehydrogenases; EC 3.4.21.94 / Proprotein Convertase 2
29.
Wagenmakers MA, Netea-Maier RT, van Lindert EJ, Timmers HJ, Grotenhuis JA, Hermus AR:
Repeated transsphenoidal pituitary surgery (TS) via the endoscopic technique: a good therapeutic option for recurrent or persistent Cushing's disease (CD).
Clin Endocrinol (Oxf)
; 2009 Feb;70(2):274-80
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[Title]
Repeated transsphenoidal
pituitary
surgery (TS) via the endoscopic technique: a good therapeutic option for recurrent or persistent
Cushing's disease
(CD).
BACKGROUND: No data on results of repeated transsphenoidal surgery via the endoscopic technique for patients with persistent or recurrent
Cushing's disease
are available.
DESIGN AND PATIENTS: We retrospectively evaluated the remission rates and complications of repeated transsphenoidal surgery via the endoscopic technique in 14 patients with persistent (N = 6) or recurrent (N = 8)
Cushing's disease
treated in our centre between 1999 and 2007.
The success of repeated transsphenoidal surgery could
not
be predicted by visualization of an
adenoma
on MRI before first or second surgery, histopathological confirmation of an
ACTH
secreting adenoma
after first or second surgery, treatment with cortisol lowering agents before first or second surgery, the operation technique used during the first surgery, persistent vs. recurrent
disease
after the first surgery, age, gender and interval between the two surgeries.
CONCLUSION: Repeated transsphenoidal surgery via the endoscopic technique is a good treatment option for selected patients with recurrent or persistent
Cushing's disease
following primary
pituitary
surgery.
[MeSH-major]
Endoscopy / methods. Neurosurgical Procedures / methods.
Pituitary
ACTH
Hypersecretion / surgery.
Pituitary
Gland
/ surgery
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(PMID = 18616702.001).
[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
WI4X0X7BPJ / Hydrocortisone
30.
Batista D, Courkoutsakis NA, Oldfield EH, Griffin KJ, Keil M, Patronas NJ, Stratakis CA:
Detection of adrenocorticotropin-secreting pituitary adenomas by magnetic resonance imaging in children and adolescents with cushing disease.
J Clin Endocrinol Metab
; 2005 Sep;90(9):5134-40
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[Title]
Detection
of adrenocorticotropin
-
secreting pituitary
adenomas
by magnetic resonance imaging in children and adolescents with cushing
disease
.
CONTEXT: We recently showed that pre- and postcontrast spoiled gradient-recalled acquisition in the steady-state (SPGR) was superior to conventional pre- and postcontrast T-1 weighted spin echo (SE) acquisition magnetic resonance imaging (MRI) for the diagnostic evaluation
of pituitary
tumors in adult patients.
OBJECTIVE: The present investigation assessed the use of SPGR vs. SE-MRI in the diagnostic evaluation of
ACTH
-
secreting
tumors in children and adolescents with Cushing
disease
.
PATIENTS: Thirty children with Cushing
disease
(13 females and 17 males with a mean age of 12 +/- 3 yr) were studied.
Postcontrast SPGR-MRI identified the location of the
tumor
in 18 of 28 patients, whereas postcontrast SE-MRI identified the location and accurately estimated the size of the
tumor
in only five patients (P < 0.001).
CONCLUSIONS: We conclude that conventional MRI, even with contrast enhancement, mostly failed to identify
ACTH
-
secreting
microadenomas in children and adolescents with Cushing
disease
.
Postcontrast SPGR-MRI was superior to SE-MRI and should be used in addition to conventional SE-MRI in
the pituitary
evaluation of children and adolescents with suspected Cushing
disease
.
[MeSH-major]
Adenoma
/
diagnosis
.
Adenoma
/ secretion. Adrenocorticotropic Hormone / secretion. Cushing Syndrome /
diagnosis
. Magnetic Resonance Imaging.
Pituitary
Neoplasms /
diagnosis
.
Pituitary
Neoplasms / secretion
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(PMID = 15941871.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone
31.
Kawashima ST, Usui T, Sano T, Iogawa H, Hagiwara H, Tamanaha T, Tagami T, Naruse M, Hojo M, Takahashi JA, Shimatsu A:
P53 gene mutation in an atypical corticotroph adenoma with Cushing's disease.
Clin Endocrinol (Oxf)
; 2009 Apr;70(4):656-7
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[Title]
P53 gene mutation in an atypical
corticotroph
adenoma
with
Cushing's disease
.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ complications.
ACTH
-
Secreting Pituitary Adenoma
/ genetics.
Adenoma
/ genetics. Mutation / genetics.
Pituitary
ACTH
Hypersecretion / etiology.
Pituitary
Neoplasms / genetics.
Tumor
Suppressor Protein p53 / genetics
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(PMID = 18771563.001).
[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Case Reports; Letter
[Publication-country]
England
[Chemical-registry-number]
0 / Tumor Suppressor Protein p53
32.
Lodish MB, Sinaii N, Patronas N, Batista DL, Keil M, Samuel J, Moran J, Verma S, Popovic J, Stratakis CA:
Blood pressure in pediatric patients with Cushing syndrome.
J Clin Endocrinol Metab
; 2009 Jun;94(6):2002-8
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CONTEXT: Hypertension (HTN) has been reported in up to 60% of children with Cushing syndrome (CS), but its course, side effects, and potential differences among various causes of CS have
not
been adequately studied.
DESIGN: Data from 86 children with
corticotropinomas
[Cushing
disease
(CD)] and 27 children with
ACTH
-independent CS (AICS) were analyzed.
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(PMID = 19293264.001).
[ISSN]
1945-7197
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
ENG
[Grant]
United States / NICHD NIH HHS / HD / Z01 HD000642; United States / Intramural NIH HHS / /
[Publication-type]
Comparative Study; Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural
[Publication-country]
United States
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone
[Other-IDs]
NLM/ PMC2690429
33.
Guignat L, Assie G, Bertagna X, Bertherat J:
[Corticotroph adenoma].
Presse Med
; 2009 Jan;38(1):125-32
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[Title]
[
Corticotroph
adenoma
].
[Transliterated title]
Adénome
corticotrope
.
Corticotroph adenomas
cause
ACTH
oversecretion responsible for
Cushing's disease
.
This represents the most frequent cause of
Cushing's
syndrome, or chronic excess of endogenous glucocorticoids.
Ninety percent of
corticotroph adenomas
are microadenomas, sometime
not
visible on MRI.
Corticotroph
macroadenomas are rare, but can be responsible for an aggressive
tumor
.
Cushing's disease diagnosis
requires careful hormonal and imaging investigations, aiming first at the
diagnosis
of
Cushing's
syndrome and in a second step at the
diagnosis
of its
pituitary
origin.
The treatment of
corticotroph
adenoma
is mainly based on
pituitary
surgery.
In case of failure
of pituitary
surgery, or in patients in whom surgery is
not
appropriate as a first line treatment, medical therapy (mainly anticortisolic drugs),
pituitary
radiotherapy or surgical bilateral adrenalectomy can be discussed.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ complications.
Pituitary
ACTH
Hypersecretion / etiology.
Pituitary
Neoplasms / complications
[MeSH-minor]
Adrenalectomy. Adrenocorticotropic Hormone / analysis. Chemotherapy, Adjuvant.
Corticotropin
-Releasing Hormone / analysis. Cushing Syndrome /
diagnosis
. Cushing Syndrome / etiology. Cushing Syndrome / therapy.
Diagnosis
, Differential. Humans. Hydrocortisone / analysis. Hydrocortisone / antagonists & inhibitors. Magnetic Resonance Imaging. Neoadjuvant Therapy. Radiotherapy, Adjuvant
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(PMID = 19041214.001).
[ISSN]
2213-0276
[Journal-full-title]
Presse medicale (Paris, France : 1983)
[ISO-abbreviation]
Presse Med
[Language]
fre
[Publication-type]
English Abstract; Journal Article
[Publication-country]
France
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; WI4X0X7BPJ / Hydrocortisone
34.
Tateno T, Izumiyama H, Doi M, Akashi T, Ohno K, Hirata Y:
Defective expression of prohormone convertase 1/3 in silent corticotroph adenoma.
Endocr J
; 2007 Dec;54(5):777-82
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[Title]
Defective expression of prohormone convertase 1/3 in silent
corticotroph
adenoma
.
Silent
corticotroph
adenoma
(SCA) is defined as an
ACTH
-
producing
pituitary
tumor not
associated with clinical and endocrine feartures of
Cushing's
syndrome, but its underlying molecular mechanism(s) remains unknown thus far.
We tested the hypothesis that reduced expression of prohormone convertase (PC) 1/3 responsible for proteolytic processing of proopiomelanocortin (POMC) in SCA may lead to production of unprocessed, biologically inactive POMC and/or precursor of
ACTH
.
Among 30 non-functioning
pituitary
macroadenomas (NFA) examined, we found 6 SCAs by immunohistochemical study using anti-
ACTH
antibody.
Preoperative endocrine and diagnostic image tests did
not
reveal any differences between SCA and the remaining NFA except for the higher recurrence rate of SCA.
Our data suggest that defective PC1/3 expression may lead to preferential production of unprocessed, biologically inactive
ACTH
variants in SCA.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ genetics.
Adenoma
/ genetics. Proprotein Convertase 1 / genetics
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(PMID = 17917309.001).
[ISSN]
1348-4540
[Journal-full-title]
Endocrine journal
[ISO-abbreviation]
Endocr. J.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Protein Isoforms; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; EC 3.4.21.93 / Proprotein Convertase 1
35.
Giacomini D, Páez-Pereda M, Theodoropoulou M, Gerez J, Nagashima AC, Chervin A, Berner S, Labeur M, Refojo D, Renner U, Stalla GK, Arzt E:
Bone morphogenetic protein-4 control of pituitary pathophysiology.
Front Horm Res
; 2006;35:22-31
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[Title]
Bone morphogenetic protein-4 control
of pituitary
pathophysiology.
Bone morphogenetic protein-4 (BMP-4), a member of the transforming growth factor-Beta(TGF-Beta) family, is overexpressed in different prolactinoma models and induces the development of these lineage
adenomas
.
SMAD proteins activated by growth factors of the TGF-Beta and BMP family interact with estrogen receptors to stimulate the proliferation of prolactin and growth hormone-
secreting
cells.
Furthermore, BMP-4 presents differential expression in normal and adenomatous corticotropes and inhibitory action on
corticotropinoma cell
proliferation.
The present review highlights
not
only the crucial and opposite role of BMP-4 in the progression
of pituitary
adenomas
but also that BMP-4 and retinoic acid interaction might serve as a potential new mechanism target for therapeutic approaches for Cushing
disease
.
[MeSH-major]
Bone Morphogenetic Proteins / physiology.
Pituitary
Diseases / etiology
[MeSH-minor]
Adrenocorticotropic Hormone / secretion. Animals. Bone Morphogenetic Protein 4. Gene Expression. Humans. Models, Biological. Neurons / secretion.
Pituitary
Gland
/ cytology.
Pituitary
Gland
/ growth & development.
Pituitary
Gland
/ metabolism.
Pituitary
Gland
/ secretion. Receptors, Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / physiology. Tretinoin / pharmacology
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(PMID = 16809920.001).
[ISSN]
0301-3073
[Journal-full-title]
Frontiers of hormone research
[ISO-abbreviation]
Front Horm Res
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't; Review
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / BMP4 protein, human; 0 / Bone Morphogenetic Protein 4; 0 / Bone Morphogenetic Proteins; 0 / Receptors, Transforming Growth Factor beta; 0 / Transforming Growth Factor beta; 5688UTC01R / Tretinoin; 9002-60-2 / Adrenocorticotropic Hormone
[Number-of-references]
42
36.
Gallelli MF, Cabrera Blatter MF, Castillo V:
A comparative study by age and gender of the pituitary adenoma and ACTH and alpha-MSH secretion in dogs with pituitary-dependent hyperadrenocorticism.
Res Vet Sci
; 2010 Feb;88(1):33-40
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[Title]
A comparative study by age and gender of the
pituitary adenoma
and
ACTH
and alpha-MSH secretion in dogs with
pituitary
-dependent hyperadrenocorticism.
Pituitary
-dependent hyperadrenocorticism (PDH) is frequent in dogs.
Using magnetic resonance,
pituitary
tumours were intra-sellar (IS) in 30.8% and extra-sellar (ES) in 62.6% and the pars intermedia (PI) was affected in 6.5%.
ACTH
concentration was greater in the ES vs. IS (p<0.05).
alpha-MSH did
not
present significant differences according to tumour size, showing a negative correlation (r=-0.47; p<0.01) vs.
ACTH
.
Differences in
adenoma
size according to gender and their age-related frequency of apparition could be because of different origins of the
corticotrophinoma
.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ veterinary. Adrenocortical Hyperfunction / veterinary. Adrenocorticotropic Hormone / secretion. Dog Diseases / pathology.
Pituitary
Neoplasms / veterinary. alpha-MSH / secretion
[MeSH-minor]
Age Factors. Animals. Dogs. Female. Magnetic Resonance Imaging. Male.
Pituitary
Gland
/ pathology.
Pituitary
Gland
/ physiopathology.
Pituitary
Gland
/ secretion. Retrospective Studies. Sex Factors
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.
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.
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.
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.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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[Copyright]
Copyright 2009 Elsevier Ltd. All rights reserved.
(PMID = 19683322.001).
[ISSN]
1532-2661
[Journal-full-title]
Research in veterinary science
[ISO-abbreviation]
Res. Vet. Sci.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone
37.
Labeur M, Paez-Pereda M, Arzt E, Stalla GK:
Potential of retinoic acid derivatives for the treatment of corticotroph pituitary adenomas.
Rev Endocr Metab Disord
; 2009 Jun;10(2):103-9
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[Title]
Potential of retinoic acid derivatives for the treatment of
corticotroph
pituitary
adenomas
.
Cushing's disease
is a severe clinical condition caused by hypersecretion of corticosteroids due to excessive
ACTH
secretion from a
pituitary adenoma
.
This complex endocrine
disorder
still represents a major challenge for the physician in terms of efficient treatment.
In the last years there was only little progress in elucidating the molecular mechanisms responsible for the constitutive and autonomous
ACTH
secretion
of pituitary
corticotrophinomas
.
As a consequence, no effective drug therapy is currently available, particularly if surgical excision is
not
successful.
In the present article we examine recent studies that have investigated the therapeutic potential of retinoic acid receptors as nuclear receptor targets for the treatment of
Cushing's disease
.
Retinoic acid is an efficient drug used for the treatment of different types of cancers and it proved to
act
in animal models of
Cushing's disease
.
The efficiency of this treatment in patients with this
disorder
still needs to be tested in clinical trials.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ drug therapy. Antineoplastic Agents / therapeutic use.
Pituitary
Neoplasms / drug therapy. Tretinoin / therapeutic use
[MeSH-minor]
Animals. Humans.
Pituitary
ACTH
Hypersecretion / drug therapy.
Pituitary
ACTH
Hypersecretion / metabolism
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(PMID = 18604646.001).
[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; 5688UTC01R / Tretinoin
[Number-of-references]
62
38.
Thodou E, Argyrakos T, Kontogeorgos G:
Galectin-3 as a marker distinguishing functioning from silent corticotroph adenomas.
Hormones (Athens)
; 2007 Jul-Sep;6(3):227-32
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[Title]
Galectin-3 as a marker distinguishing functioning from silent
corticotroph adenomas
.
OBJECTIVE: Galectin-3 (Gal-3) belongs to the family of carbohydrate-binding proteins with high affinity for galactoside and is involved in many biological processes including
cell
growth and differentiation,
cell
adhesion,
tumor
progression, apoptosis and metastasis.
The aim of this study was to disclose differences in the expression of Gal-3 in silent and functioning
corticotroph
pituitary
adenomas
.
DESIGN: We examined 30
pituitary
adenomas
(19 functioning
corticotroph
, 11 silent
corticotroph adenomas
).
Two prolactinomas and 2 functioning somatotroph
adenomas
served as positive controls.
The independent variables t-test was used for comparison of the mean expression of Gal-3 in the two different
corticotroph
adenoma
subgroups.
RESULTS: Eighteen of the functioning
corticotroph adenomas
(94.73%) were positive for Gal-3 with a cytoplasmic and focally membranous distribution; two cases also exhibited nuclear expression, whereas 9 of the silent
corticotroph adenomas
(81.81%) had zero or<1% expression of Gal-3 (p=0.001).
CONCLUSIONS: Gal-3 is highly expressed in functioning
corticotroph adenomas
of the
pituitary
gland
, while silent
adenomas
exhibit very focal to null expression of Gal-3.
This observation can be used in the pathological
diagnosis
to separate functioning from silent
corticotroph adenomas
of the
pituitary
.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/
diagnosis
.
Adenoma
/
diagnosis
. Biomarkers,
Tumor
/ metabolism. Galectin 3 / metabolism
[MeSH-minor]
Humans. Immunohistochemistry.
Pituitary
Gland
/ metabolism
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(PMID = 17724007.001).
[ISSN]
1109-3099
[Journal-full-title]
Hormones (Athens, Greece)
[ISO-abbreviation]
Hormones (Athens)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Greece
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / Galectin 3
39.
Barber TM, Adams E, Ansorge O, Byrne JV, Karavitaki N, Wass JA:
Nelson's syndrome.
Eur J Endocrinol
; 2010 Oct;163(4):495-507
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Nelson's syndrome is a potentially life-threatening condition that does
not
infrequently develop following total bilateral adrenalectomy (TBA) for the treatment of
Cushing's disease
.
In this review article, we discuss some controversial aspects of Nelson's syndrome including
diagnosis
, predictive factors, aetiology, pathology and management based on data from the existing literature and the experience of our own tertiary centre.
We propose that Nelson's syndrome should be diagnosed in any patient with prior TBA for the treatment of
Cushing's disease
and with at least one of the following criteria: i) an expanding
pituitary
mass lesion compared with pre-TBA images;.
ii) an elevated 0800 h plasma level of
ACTH
(>500 ng/l) in addition to progressive elevations of
ACTH
(a rise of >30%) on at least three consecutive occasions.
Regarding predictive factors for the development of Nelson's syndrome post TBA, current evidence favours the presence of residual
pituitary
tumour on magnetic resonance imaging (MRI) post transsphenoidal surgery (TSS); an aggressive subtype of
corticotrophinoma
(based on MRI growth rapidity and histology of TSS samples); lack of prophylactic neoadjuvant
pituitary
radiotherapy at the time of TBA and a rapid rise of
ACTH
levels in year 1 post TBA.
Finally, more studies are needed to assess the efficacy of therapeutic strategies in Nelson's syndrome, including the alkylating agent, temozolomide, which holds promise as a novel and effective therapeutic agent in the treatment of associated aggressive
corticotroph
tumours.
Hazardous Substances Data Bank.
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.
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Corticotropin
.
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(PMID = 20668020.001).
[ISSN]
1479-683X
[Journal-full-title]
European journal of endocrinology
[ISO-abbreviation]
Eur. J. Endocrinol.
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
0 / Alkylating Agents; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide; 9002-60-2 / Adrenocorticotropic Hormone
[Number-of-references]
101
40.
Banasiak MJ, Malek AR:
Nelson syndrome: comprehensive review of pathophysiology, diagnosis, and management.
Neurosurg Focus
; 2007;23(3):E13
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[Title]
Nelson syndrome: comprehensive review of pathophysiology,
diagnosis
, and management.
Nelson syndrome (NS) is a rare clinical manifestation of an enlarging
pituitary adenoma
that can occur following bilateral adrenal
gland
removal performed for the treatment of Cushing
disease
.
It is characterized by excess adreno-
corticotropin
secretion and hyperpigmentation of the skin and mucus membranes.
The authors present a comprehensive review of the pathophysiology,
diagnosis
, and management of NS.
Corticotroph adenomas
in NS remain challenging tumors that can lead to significant rates of morbidity and mortality.
Although the primary treatment for each
tumor
type may vary, it is important to consider all of the available options and select the one that is most appropriate for the individual case, particularly in cases of lesions resistant to intervention.
Genetic Alliance.
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gene/protein/disease-specific - MalaCards for nelson syndrome
.
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(PMID = 17961028.001).
[ISSN]
1092-0684
[Journal-full-title]
Neurosurgical focus
[ISO-abbreviation]
Neurosurg Focus
[Language]
eng
[Publication-type]
Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
0 / Neurotransmitter Agents
[Number-of-references]
123
41.
Nandagopal R, Vortmeyer A, Oldfield EH, Keil MF, Stratakis CA:
Cushing's syndrome due to a pituitary corticotropinoma in a child with tuberous sclerosis: an association or a coincidence?
Clin Endocrinol (Oxf)
; 2007 Oct;67(4):639-41
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[Title]
Cushing's
syndrome due to a
pituitary
corticotropinoma
in a child with tuberous sclerosis: an association or a coincidence?
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ complications. Cushing Syndrome / etiology.
Pituitary
Neoplasms / complications. Tuberous Sclerosis / complications
Genetic Alliance.
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.
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.
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consumer health - Cushing's Syndrome
.
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
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consumer health - Tuberous Sclerosis
.
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(PMID = 17596199.001).
[ISSN]
0300-0664
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Grant]
United States / NICHD NIH HHS / HD / Z01-HD-000642-04; United States / Intramural NIH HHS / /
[Publication-type]
Case Reports; Letter; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
[Publication-country]
England
42.
Saveanu A, Gunz G, Guillen S, Dufour H, Culler MD, Jaquet P:
Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in pituitary adenomas.
Neuroendocrinology
; 2006;83(3-4):258-63
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[Title]
Somatostatin and dopamine-somatostatin multiple ligands directed towards somatostatin and dopamine receptors in
pituitary
adenomas
.
AIM: We report the comparative efficacy of octreotide, cabergoline and multiple ligands directed towards the different somatostatin subtypes (ssts), such as BIM-23A779 and
SOM
-230, and of chimeric analogs which bind both somatostatin and the dopamine D2 receptors (D2R), such as BIM-23A760 and BIM-23A781, in
cell
cultures from human growth hormone (GH)-
secreting pituitary
adenomas
.
PROCEDURES: RT-PCR analysis of the quantitative expression of the different ssts and D2R mRNAs was performed on
tumor
fragments of 22 GH-
secreting
adenomas
collected after surgery.
Pharmacological studies, using the different ligands, were performed on
cell
cultures of such tumors.
In each
tumor
tested, 3 patterns of response, in terms of GH suppression, were observed.
Among the compounds tested, the most potent inhibitors of GH secretion were the sst2, sst5, D2R chimeric compound BIM-23A760, followed by the sst universal ligand
SOM
-230.
The effect of multiple receptor activation on the functions of other
pituitary
tumor
types, such as prolactinomas and
corticotropinomas
, is
not
presently analyzed, and the efficacy of multireceptor ligands remains to be elucidated.
[MeSH-major]
Adenoma
/ drug therapy. Antineoplastic Agents, Hormonal / therapeutic use. Dopamine / analogs & derivatives.
Pituitary
Neoplasms / drug therapy. Somatostatin / analogs & derivatives
[MeSH-minor]
Adult. Drug Screening Assays, Antitumor. Ergolines / therapeutic use. Female. Human Growth Hormone / drug effects. Human Growth Hormone / metabolism. Humans. Ligands. Male. Octreotide / therapeutic use. RNA, Messenger / analysis. Receptors, Dopamine D2 / drug effects. Receptors, Dopamine D2 / genetics. Receptors, Dopamine D2 / metabolism. Receptors, Somatostatin / classification. Receptors, Somatostatin / drug effects. Receptors, Somatostatin / genetics. Receptors, Somatostatin / metabolism. Recombinant Fusion Proteins / therapeutic use.
Tumor
Cells, Cultured
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.
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DOPAMINE
.
The Lens.
Cited by Patents in
.
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(PMID = 17047391.001).
[ISSN]
0028-3835
[Journal-full-title]
Neuroendocrinology
[ISO-abbreviation]
Neuroendocrinology
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / BIM 23268; 0 / Ergolines; 0 / Ligands; 0 / RNA, Messenger; 0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / Recombinant Fusion Proteins; 12629-01-5 / Human Growth Hormone; 51110-01-1 / Somatostatin; LL60K9J05T / cabergoline; RWM8CCW8GP / Octreotide; VTD58H1Z2X / Dopamine
43.
Roelfsema F, Kok S, Kok P, Pereira AM, Biermasz NR, Smit JW, Frolich M, Keenan DM, Veldhuis JD, Romijn JA:
Pituitary-hormone secretion by thyrotropinomas.
Pituitary
; 2009;12(3):200-10
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[Title]
Pituitary
-hormone secretion by thyrotropinomas.
Hormone secretion by somatotropinomas,
corticotropinomas
and prolactinomas exhibits increased pulse frequency, basal and pulsatile secretion, accompanied by greater disorderliness.
Regulation of non-TSH
pituitary
hormones in this context is
not
well understood.
Cross-ApEn synchrony between TSH and GH did
not
differ between patients and controls, but TSH and PRL synchrony was reduced in patients.
We conclude that TSH secretion by thyrotropinomas shares many characteristics of other
pituitary
hormone-
secreting
adenomas
.
In addition, abnormalities in GH and PRL secretion exist ranging from decreased (joint) regularity to overt hypersecretion, although
not
always clinically obvious, suggesting tumoral transformation of thyrotrope lineage cells.
[MeSH-major]
Adenoma
/ physiopathology.
Pituitary
Hormones / blood.
Pituitary
Hormones / secretion.
Pituitary
Neoplasms / blood
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.
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(PMID = 19051037.001).
[ISSN]
1573-7403
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Grant]
United States / NCRR NIH HHS / RR / M01 RR000585
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Pituitary Hormones; 67763-96-6 / Insulin-Like Growth Factor I; 9002-62-4 / Prolactin; 9002-71-5 / Thyrotropin; 9002-72-6 / Growth Hormone
[Other-IDs]
NLM/ PMC2712623
44.
Castillo VA, Gómez NV, Lalia JC, Cabrera Blatter MF, García JD:
Cushing's disease in dogs: cabergoline treatment.
Res Vet Sci
; 2008 Aug;85(1):26-34
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[Title]
Cushing's disease
in dogs: cabergoline treatment.
The treatment
of pituitary
-dependent hyperadrenocorticism (PDH) in dogs has for a long time been focused on inhibiting the adrenal
gland
using drugs such as o-p'-DDD, Ketoconazole and Trilostane, without attacking the primary cause: the
corticotrophinoma
.
Corticotroph
cells can express the D2 dopaminergic receptor; therefore cabergoline (Cbg) could be effective as a treatment.
A year after the treatment, there was a significant decrease in
ACTH
(p<0.0001), alpha-MSH (p<0.01), urinary cortisol/creatinine ratio (p<0.001), and of the
tumor
size (p<0.0001) evaluated by nuclear magnetic resonance.
[MeSH-major]
Dog Diseases / drug therapy. Dopamine Agonists / therapeutic use. Ergolines / therapeutic use.
Pituitary
ACTH
Hypersecretion / veterinary
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(PMID = 17910968.001).
[ISSN]
0034-5288
[Journal-full-title]
Research in veterinary science
[ISO-abbreviation]
Res. Vet. Sci.
[Language]
eng
[Publication-type]
Controlled Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Dopamine Agonists; 0 / Ergolines; 581-05-5 / alpha-MSH; 9002-60-2 / Adrenocorticotropic Hormone; LL60K9J05T / cabergoline; R9400W927I / Ketoconazole
45.
Dam-Hieu P, Irthum B, Seizeur R, Roudaut N, Besson G:
Management of ACTH-secreting supradiaphragmatic adenomas.
Clin Neurol Neurosurg
; 2007 Oct;109(8):698-704
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[Title]
Management of
ACTH
-
secreting
supradiaphragmatic
adenomas
.
Supradiaphragmatic adrenocorticotropic hormone (
ACTH
)
secreting pituitary
adenomas
are exceptionally encountered (14 cases previously described) and raise issues concerning their nosology and management.
To illustrate this issue, we presented two cases of supradiaphragmatic
ACTH
secreting pituitary
adenomas
successfully excised via a subfrontal approach.
Both patients were female (20 and 41 years) and had a typical
Cushing's
syndrome.
MRI revealed, in both cases, a suprasellar mass in contact with the pars tuberalis of the
pituitary
.
One year later, the patient was operated on again via a subfrontal approach, allowing excision of a supradiaphragmatic
adenoma
and a complete cure of
Cushing's disease
.
In both cases, the diaphragma sellae was found to be intact and
the pituitary
stalk could be preserved.
Postoperative MRI demonstrated a clearly visible intact
pituitary
stalk in conjunction with normal aspect of the
pituitary
.
Supradiaphragmatic
pituitary
adenomas
are most likely
adenomas
of the
pituitary
stalk with extra-axial development.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ pathology.
ACTH
-
Secreting Pituitary Adenoma
/ surgery.
Adenoma
/ pathology.
Adenoma
/ surgery
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(PMID = 17532556.001).
[ISSN]
0303-8467
[Journal-full-title]
Clinical neurology and neurosurgery
[ISO-abbreviation]
Clin Neurol Neurosurg
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Netherlands
46.
Brito LP, Lerário AM, Bronstein MD, Soares IC, Mendonca BB, Fragoso MC:
Influence of the fibroblast growth factor receptor 4 expression and the G388R functional polymorphism on Cushing's disease outcome.
J Clin Endocrinol Metab
; 2010 Oct;95(10):E271-9
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[Title]
Influence of the fibroblast growth factor receptor 4 expression and the G388R functional polymorphism on
Cushing's disease
outcome.
CONTEXT: Abnormal FGFR4 expression has been detected in
pituitary
tumors, especially in larger and invasive
adenomas
.
Then, we hypothesized that FGFR4 expression and genotype could be markers of adverse outcome of
Cushing's disease
after transsphenoidal surgery.
OBJECTIVES: The objective was to investigate whether there is an association between the postoperative outcome of
Cushing's disease
(remission/recurrence) and the FGFR4 G388R genotype or the FGFR4 expression in
corticotrophinomas
.
FGFR4 expression was assessed by real-time PCR in 18
corticotrophinomas
.
MAIN OUTCOME MEASURES: The outcome measures included the FGFR4 G388R genotype and FGFR4 expression in postoperative remission and recurrence of
Cushing's disease
.
RESULTS: Homozygosis for FGFR4 glycine (Gly(388)) allele was associated with reduced
disease
-free survival, in the univariate analysis (hazard ratio of 6.91; 95% confidence interval of 1.14-11.26; P = 0.028).
Male gender (P = 0.036), lack of pathology confirmation (P = 0.009), and cortisol levels more than 2 μg/dl in the early postoperative period (P < 0.001) were also significant predictors of
Cushing's disease
recurrence in the univariate analysis.
FGFR4 overexpression was found in 44% of the
corticotrophinomas
, and it was associated with lower postoperative remission rate (P = 0.009).
CONCLUSIONS: Our data suggest that homozygosis for FGFR4 Gly(388) allele and FGFR4 overexpression are associated with higher frequency of postoperative recurrence and persistence of
Cushing's disease
, respectively.
[MeSH-major]
Pituitary
ACTH
Hypersecretion / genetics. Polymorphism, Single Nucleotide. Receptor, Fibroblast Growth Factor, Type 4 / genetics
[MeSH-minor]
ACTH
-
Secreting Pituitary Adenoma
/
diagnosis
.
ACTH
-
Secreting Pituitary Adenoma
/ genetics.
ACTH
-
Secreting Pituitary Adenoma
/ surgery. Adolescent. Adult. Amino Acid Substitution / genetics. Arginine / genetics. Child. Female. Gene Expression / physiology. Glycine / genetics. Humans. Hypophysectomy. Male. Middle Aged.
Pituitary
Neoplasms /
diagnosis
.
Pituitary
Neoplasms / genetics.
Pituitary
Neoplasms / surgery. Prognosis. Recurrence. Retrospective Studies. Treatment Outcome. Young Adult
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(PMID = 20660043.001).
[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; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
94ZLA3W45F / Arginine; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 4; TE7660XO1C / Glycine
47.
Gao C, Fu X, Pan Y, Li Q:
Surgical treatment of pancreatic neuroendocrine tumors: report of 112 cases.
Dig Surg
; 2010 Aug;27(3):197-204
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OBJECTIVES: To review the clinical data of a group of patients with pancreatic neuroendocrine tumors (pNETs) and to investigate the role of surgery in the treatment for pNETs by analyzing clinical manifestations and postoperative course of this rare
disease
.
Patients' data related to demographics and characteristics, diagnostic studies, surgical and
tumor
characteristics and survival were retrospectively reviewed.
RESULTS: Forty-six patients (41.1%) had a well-differentiated neuroendocrine
tumor
(WDT), 44 (48.2%) a well-differentiated neuroendocrine carcinoma (WD-Ca) and 12 (10.7%) a poorly differentiated neuroendocrine carcinoma (PD-Ca).
Nonfunctional tumors were seen in 65 (58.0%) patients, whereas functional tumors were found in 47 (42.0%) patients, including 26 insulinomas, 17 gastrinomas, 2 VIPomas, 1 glucagonoma, and 1
ACTHoma
.
Survival was significantly related to the type of neuroendocrine
tumor
(p = 0.001).
The 5-year survival rate differed significantly between patients with
tumor
node metastasis (TNM) stage I and II
disease
and those with stage III and IV tumors (p = 0.011).
Malignant cases should be treated with aggressive radical surgery to achieve complete
tumor
resection and potential for long-term survival.
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(PMID = 20571266.001).
[ISSN]
1421-9883
[Journal-full-title]
Digestive surgery
[ISO-abbreviation]
Dig Surg
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Switzerland
48.
Chowdhury IN, Sinaii N, Oldfield EH, Patronas N, Nieman LK:
A change in pituitary magnetic resonance imaging protocol detects ACTH-secreting tumours in patients with previously negative results.
Clin Endocrinol (Oxf)
; 2010 Apr;72(4):502-6
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[Title]
A change in
pituitary
magnetic resonance imaging protocol detects
ACTH
-
secreting
tumours in patients with previously negative results.
OBJECTIVE: While detection
of pituitary
tumours with magnetic resonance imaging (MRI) may reduce diagnostic costs and improve surgical outcomes for patients with
Cushing's disease
, the optimal T1-weighted spin-echo (SE) MRI protocol remains unknown.
We hypothesized that specific MR scanning parameters influence detection of
corticotropinomas
.
DESIGN AND PATIENTS: Between December 1997 and November 2004, 21 of 84 consecutive patients with
Cushing's disease
had a falsely negative initial
pituitary
MRI study and a lesion identified subsequently at the National Institutes of Health Clinical Center.
This study retrospectively reviewed and compared technical parameters used for the two
pituitary
T1-weighted SE MRIs in 18 patients with available scans.
Immunohistochemistry of tumours resected at transsphenoidal surgery confirmed all to be
corticotropinomas
.
CONCLUSIONS:
Not
all 'T1-weighted SE' scans are equally accurate.
We recommend that endocrinologists consider
pituitary
MRI parameters when interpreting the results.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/
diagnosis
. Magnetic Resonance Imaging / methods.
Pituitary
Neoplasms /
diagnosis
[MeSH-minor]
Adult. False Negative Reactions. Female. Humans. Male. Middle Aged.
Pituitary
ACTH
Hypersecretion / pathology.
Pituitary
Gland
/ pathology. Retrospective Studies
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[Cites]
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[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Grant]
United States / Intramural NIH HHS / / Z01 HD008833-01
[Publication-type]
Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural
[Publication-country]
England
[Other-IDs]
NLM/ NIHMS139974; NLM/ PMC2866063
49.
Gondim JA, Schops M, de Almeida JP, de Albuquerque LA, Gomes E, Ferraz T, Barroso FA:
Endoscopic endonasal transsphenoidal surgery: surgical results of 228 pituitary adenomas treated in a pituitary center.
Pituitary
; 2010;13(1):68-77
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[Title]
Endoscopic endonasal transsphenoidal surgery: surgical results of 228
pituitary
adenomas
treated in a
pituitary
center.
Pituitary
tumors are challenging tumors in the sellar region.
Surgical approaches to
the pituitary
have undergone numerous refinements over the last 100 years.
The introduction of the endoscope have revolutionized
pituitary
surgery.
The aim of this study is to report the results of a consecutive series of patients undergoing
pituitary
surgery using a pure endoscopic endonasal approach and to evaluate the efficacy and safety of this procedure.
We reviewed the data of 228 consecutive patients who underwent endonasal transsphenoidal
adenoma
removal over an 10-year period.
Tumor
removal rate, endocrinological outcomes, and complications were retrospectively assessed in 228 patients with
pituitary
adenomas
who underwent 251 procedures between December 1998 and December 2007.
There were 93 nonfunctioning
adenomas
, 58 growth hormone-
secreting
, 41 prolactin-
secreting
, 28
adrenocorticotropin
hormone
secreting
, 7 FSH-LH
secreting
and 1 thyroid-stimulating hormone-
secreting
adenomas
.
The remission results for patients with nonfunctioning
adenomas
was 83% and for functioning
adenomas
were 76.3% (70.6% for GH hormone-
secreting
, 85.3% for prolactin hormone-
secreting
, 71.4% for
ACTH
hormone-
secreting
, 85.7% for FSH-LH hormone-
secreting
and 100% for TSH hormone-
secreting
), with no recurrence at the time of the last follow-up.
The endoscopic endonasal approach for resection
of pituitary
adenomas
, provides acceptable results representing a safe alternative procedure to the microscopic approach.
This less invasive method, associated with a small number of complications, provides excellent
tumor
removal rates and represents an important tool for the achievement of good results in
the pituitary
surgery, mainly for the complete removal of large
adenomas
.
[MeSH-major]
Adenoma
/ surgery. Endoscopy / methods.
Pituitary
Neoplasms / surgery
[MeSH-minor]
Humans.
Pituitary
Hormones / blood. Postoperative Complications. Retrospective Studies
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.
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.
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.
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[ISSN]
1573-7403
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Publication-type]
Evaluation Studies; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Pituitary Hormones
50.
Karavitaki N, Scheithauer BW, Watt J, Ansorge O, Moschopoulos M, Llaguno AV, Wass JA:
Collision lesions of the sella: co-existence of craniopharyngioma with gonadotroph adenoma and of Rathke's cleft cyst with corticotroph adenoma.
Pituitary
; 2008;11(3):317-23
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[Title]
Collision lesions of the sella: co-existence of craniopharyngioma with gonadotroph
adenoma
and of Rathke's cleft cyst with
corticotroph
adenoma
.
Most contributions include a
pituitary adenoma
or a cyst/cystic
tumor
, particularly a Rathke cleft cyst.
The association of craniopharyngioma with an
adenoma
is particularly rare.
Among reported cases, some have included secondary prolactin
cell
hyperplasia due to
pituitary
stalk section effect.
Herein, we report two collision lesions, including a gonadotroph
adenoma
with adamantinomatous craniopharyngioma and a
corticotroph
adenoma
with Rathke's cleft cyst.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ complications.
Adenoma
/ complications. Central Nervous System Cysts / complications. Corticotrophs / pathology. Craniopharyngioma / complications. Gonadotrophs / pathology.
Pituitary
Neoplasms / complications. Sella Turcica / pathology
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[ISSN]
1386-341X
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Number-of-references]
65
51.
van der Hoek J, Waaijers M, van Koetsveld PM, Sprij-Mooij D, Feelders RA, Schmid HA, Schoeffter P, Hoyer D, Cervia D, Taylor JE, Culler MD, Lamberts SW, Hofland LJ:
Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of ACTH release by corticotroph tumor cells.
Am J Physiol Endocrinol Metab
; 2005 Aug;289(2):E278-87
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[Title]
Distinct functional properties of native somatostatin receptor subtype 5 compared with subtype 2 in the regulation of
ACTH
release by
corticotroph tumor
cells.
In a series of human
corticotroph adenomas
, we recently found predominant mRNA expression of somatostatin (SS) receptor subtype 5 (sst5).
After 72 h, the multiligand SS analog SOM230, which has a very high sst5 binding affinity, but
not
Octreotide (OCT), significantly inhibited basal
ACTH
release.
To further explore the role of sst5 in the regulation of
ACTH
release, we conducted additional studies with mouse AtT-20 cells.
SOM230 showed a 7-fold higher ligand binding affinity and a 19-fold higher potency in stimulating guanosine 5'-O-(3-thiotriphosphate) binding in AtT-20
cell
membranes compared with OCT.
SOM230 potently suppressed CRH-induced
ACTH
release, which was
not
affected by 48-h dexamethasone (DEX) pretreatment.
However, DEX attenuated the inhibitory effects of OCT on
ACTH
release, whereas it increased the inhibitory potency of BIM-23268, an sst5-specific analog, on
ACTH
release.
Quantitative PCR analysis showed that DEX lowered sst(2A+2B) mRNA expression significantly after 24 and 48 h, whereas sst5 mRNA levels were
not
significantly affected by DEX treatment.
Finally, after SS analog preincubation, compared with OCT both SOM230 and BIM-23268 showed a significantly higher inhibitory effect on CRH-induced
ACTH
release.
In conclusion, our data support the concept that the sst5 receptor might be a target for new therapeutic agents to treat
Cushing's disease
.
[MeSH-major]
Adrenocorticotropic Hormone / secretion.
Corticotropin
-Releasing Hormone / physiology.
Pituitary
Gland
/ secretion. Receptors, Somatostatin / physiology
[MeSH-minor]
Animals. Dose-Response Relationship, Drug. Down-Regulation. Glucocorticoids / physiology. Mice. Octreotide / pharmacology.
Pituitary
Neoplasms. RNA, Messenger / analysis. Somatostatin / analogs & derivatives. Somatostatin / pharmacology. Stimulation, Chemical.
Tumor
Cells, Cultured
Hazardous Substances Data Bank.
Corticotropin
.
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(PMID = 15769796.001).
[ISSN]
0193-1849
[Journal-full-title]
American journal of physiology. Endocrinology and metabolism
[ISO-abbreviation]
Am. J. Physiol. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / BIM 23268; 0 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
52.
Assie G, Louiset E, Sturm N, René-Corail F, Groussin L, Bertherat J, Thomas M, Lefebvre H, Feige JJ, Clauser E, Chabre O, Cherradi N:
Systematic analysis of G protein-coupled receptor gene expression in adrenocorticotropin-independent macronodular adrenocortical hyperplasia identifies novel targets for pharmacological control of adrenal Cushing's syndrome.
J Clin Endocrinol Metab
; 2010 Oct;95(10):E253-62
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[Title]
Systematic analysis of G protein-coupled receptor gene expression in
adrenocorticotropin
-independent macronodular adrenocortical hyperplasia identifies novel targets for pharmacological control of adrenal
Cushing's
syndrome.
CONTEXT: Stimulation of cortisol secretion through abnormally expressed G protein-coupled receptors (GPCRs) is a frequent feature of
ACTH
-independent macronodular adrenal hyperplasia (AIMAH).
This has opened a pharmacological strategy that targets GPCRs for the treatment of
Cushing's
syndrome in AIMAH.
OBJECTIVE: The objective of the study was to identify new GPCR targets for the pharmacological treatment of adrenal
Cushing's
syndrome.
DESIGN AND PATIENTS: We designed a cDNA chip containing 865 nucleotidic sequences of GPCRs. mRNAs were extracted from three normal adrenals, 18 AIMAHs, four adrenals from
Cushing's disease
patients, and 13 cortisol-
secreting
adenomas
.
RESULTS: The
ACTH
MC2 receptor showed a low expression in 15 of 18 AIMAHs samples, whereas several previously undescribed GPCR genes were found highly expressed in a subset of AIMAH, such as the receptors for motilin (MLNR; three of 18 AIMAHs) and γ-aminobutyric acid (GABBR1; five of 18 AIMAHs), and the α2A adrenergic receptor (ADRA2A; 13 of 18 AIMAHs), on which we focused our attention.
Western blot and immunochemistry analyses showed expression of ADRA2A protein in AIMAH but
not
in normal adrenal cortex.
CONCLUSION: ADRA2A is a potential target for pharmacological treatment of
Cushing's
syndrome linked to AIMAH.
[MeSH-minor]
ACTH
-
Secreting Pituitary Adenoma
/ genetics.
ACTH
-
Secreting Pituitary Adenoma
/ pathology. Adrenergic alpha-2 Receptor Agonists. Adrenocorticotropic Hormone / metabolism. Adrenocorticotropic Hormone / physiology. Antihypertensive Agents / administration & dosage. Antihypertensive Agents / pharmacology. Cells, Cultured. Clonidine / administration & dosage. Clonidine / pharmacology. Gene Expression. Gene Expression Profiling. Humans. Hyperplasia / genetics. Hyperplasia / metabolism. Oligonucleotide Array Sequence Analysis.
Pituitary
Neoplasms / genetics.
Pituitary
Neoplasms / pathology. Receptors, Adrenergic, alpha-2 / genetics. Receptors, Adrenergic, alpha-2 / metabolism. Receptors, Adrenergic, alpha-2 / physiology
Genetic Alliance.
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.
MedlinePlus Health Information.
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.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
Hazardous Substances Data Bank.
CLONIDINE
.
Hazardous Substances Data Bank.
Corticotropin
.
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(PMID = 20660048.001).
[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; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / ADRA2A protein, human; 0 / Adrenergic alpha-2 Receptor Agonists; 0 / Antihypertensive Agents; 0 / Receptors, Adrenergic, alpha-2; 0 / Receptors, G-Protein-Coupled; 9002-60-2 / Adrenocorticotropic Hormone; MN3L5RMN02 / Clonidine
53.
Gruszka A, Kunert-Radek J, Pawlikowski M, Stepien H:
Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with pituitary adenomas.
Pituitary
; 2005;8(2):163-8
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[Title]
Serum endostatin levels are elevated and correlate with serum vascular endothelial growth factor levels in patients with
pituitary
adenomas
.
The purpose of our study was to evaluate serum concentrations of endostatin in patients harbouring various
pituitary adenoma
types and to examine the relationship of serum endostatin levels to circulating vascular endothelial growth factor (VEGF) levels.
Preoperative serum endostatin and VEGF concentrations were measured using competitive enzyme immunoassays in 71 patients with
pituitary
adenomas
(20 somatotropinomas, 3
corticotropinomas
, 6 prolactinomas and 42 clinically nonfunctioning
pituitary
adenomas
- CNFPAs) and compared with levels from age-matched controls.
Serum endostatin concentrations were significantly higher in all
pituitary adenoma
types, except for prolactinomas (somatotropinomas: 124 +/- 16; p < 0.02,
corticotropinomas
: 157 +/- 42; p < 0.02, prolactinomas: 141 +/- 37; p > 0.05, CNFPAs: 169 +/- 11 ng/ml; p < 0.000005 vs 73 +/- 10 ng/ml in controls).
There was a significant positive correlation between endostatin and VEGF serum levels in patients with
pituitary
adenomas
(r = +0.322; p = 0.006).
The simultaneous elevation of endostatin and VEGF may attenuate the pro-angiogenic action of VEGF and be responsible for rather weak neovascularization
of pituitary
adenomas
.
Prospective studies are required to assess the usefulness of circulating endostatin and VEGF as markers of progression or recurrence
of pituitary
tumors.
[MeSH-major]
Adenoma
/ blood. Endostatins / blood.
Pituitary
Neoplasms / blood. Vascular Endothelial Growth Factor A / blood
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]
(PMID = 16379029.001).
[ISSN]
1386-341X
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Endostatins; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A
54.
Rosales C, Fierrard H, Bertagna X, Raffin-Sanson ML:
[Management of hypercortisolism].
Rev Med Interne
; 2008 Apr;29(4):337-46
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PURPOSE:
Cushing's
syndrome is a rare but frequently considered
disease
.
Its
diagnosis
can lead to some difficulties, including confirming the effective endogenous hypercortisolism and determining its cause.
The severity of this
disease
, the diversity of its complications and the multiple therapeutic options make its management challenging.
The aim of this review is to present the most recent data about management of
Cushing's
syndrome, especially diagnostic approaches and therapeutic options.
MAIN POINTS: We retained the following points: midnight salivary cortisol is a useful tool in the
diagnosis
of
Cushing's
syndrome; the desmopressin test can help to distinguish between
Cushing's
syndrome and "pseudoCushing's" due to alcohol consumption or psychiatric disorders; cavernous sinus and inferior petrosal sinus sampling is indicated in the evaluation of
ACTH
-dependent
Cushing's
syndromes when
pituitary
imaging is normal or equivocal or when dynamic tests are contradictory; multislice computed-tomography of the chest and the abdomen and somatostatin analogue scintigraphy, eventually combined, are the best imaging procedures in occult ectopic
ACTH
syndromes; patients with
Cushing's disease
should be referred to a neurosurgeon experienced in
corticotroph adenomas
surgery; metabolic consequences of
Cushing's
syndrome, such as cardiovascular risk factors and osteoporosis need an aggressive treatment.
PERSPECTIVES: The incidence of
Cushing's
syndrome is only 1/100000 per year.
Endocrinological management of the
disease
improves metabolic disorders in these patients.
If these results are confirmed, screening for
Cushing's
syndrome should be systematically performed in these populations.
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.
Hazardous Substances Data Bank.
MITOTANE
.
Hazardous Substances Data Bank.
KETOCONAZOLE
.
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(PMID = 18226430.001).
[ISSN]
0248-8663
[Journal-full-title]
La Revue de medecine interne
[ISO-abbreviation]
Rev Med Interne
[Language]
FRE
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
France
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 0 / Enzyme Inhibitors; 78E4J5IB5J / Mitotane; R9400W927I / Ketoconazole
[Number-of-references]
42
55.
Hashiba T, Saitoh Y, Asanuma N, Kouhara H, Maruo T, Fujinaka T, Kasayama S, Yoshimine T:
Reduction of a pancreatic tumor after total removal of an ACTH secreting pituitary tumor: differential diagnosis of Cushing's syndrome.
Endocr J
; 2006 Apr;53(2):203-8
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[Title]
Reduction of a pancreatic
tumor
after total removal of an
ACTH
secreting pituitary
tumor
: differential
diagnosis
of
Cushing's
syndrome.
Endocrinologic tests sometimes fail to distinguish adrenocorticotropic hormone (
ACTH
)-
secreting pituitary adenoma
from ectopic
ACTH
-
secreting
tumor
.
The authors experienced a case of
Cushing's disease
associated with a pancreatic
tumor
.
Venous sampling contributed to the final
diagnosis
of
Cushing's disease
in this complex case, while endocrinologic tests showed paradoxical results.
A 54-year-old woman presented with
Cushing's
syndrome and pancreatic
tumor
.
Magnetic resonance imaging (MRI) failed to reveal a
pituitary
tumor
, but a gadolinium-enhanced
tumor
with cystic components was seen in the pancreatic tail.
Results of conventional endocrinologic tests suggested ectopic
ACTH
syndrome, but venous sampling including cavernous sinus sampling indicated an
ACTH
-
secreting pituitary adenoma
.
Transsphenoidal surgery revealed a
pituitary
microadenoma, and total removal of the
tumor
was achieved.
Postoperative abdominal MRI revealed that the pancreatic
tumor
diminished gradually without treatment.
Selective cavernous sinus sampling was useful for distinguishing
ACTH
-
secreting pituitary adenoma
from ectopic
ACTH
syndrome in this complex case.
This was a rare case in which the pancreatic
tumor
diminished after total removal of the
ACTH
-
secreting pituitary adenoma
.
[MeSH-major]
Adrenocorticotropic Hormone / secretion. Cushing Syndrome /
diagnosis
. Pancreatic Neoplasms / complications.
Pituitary
Neoplasms / secretion
[MeSH-minor]
ACTH
Syndrome, Ectopic /
diagnosis
.
Adenoma
/ secretion.
Adenoma
/ surgery.
Diagnosis
, Differential. Female. Follow-Up Studies. Humans. Magnetic Resonance Imaging. Middle Aged.
Pituitary
ACTH
Hypersecretion /
diagnosis
. Positron-Emission Tomography
Genetic Alliance.
consumer health - Cushing's Syndrome
.
MedlinePlus Health Information.
consumer health - Cushing's Syndrome
.
MedlinePlus Health Information.
consumer health - Pancreatic Cancer
.
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
Hazardous Substances Data Bank.
Corticotropin
.
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(PMID = 16618978.001).
[ISSN]
0918-8959
[Journal-full-title]
Endocrine journal
[ISO-abbreviation]
Endocr. J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone
56.
Cavagnini F, Scacchi M, Pecori Giraldi F:
Hypopituitarism in Cushing's disease.
J Endocrinol Invest
; 2008 Sep;31(9 Suppl):44-7
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[Title]
Hypopituitarism in
Cushing's disease
.
Impaired GH secretion usually accompanies
Cushing's
syndrome and a variable proportion of patients reportedly fail to recover normal GH secretion after successful treatment.
We prospectively studied 34 patients (27 females and 7 males, age range 21- 68 yr) formerly affected by
Cushing's disease
.
All patients had undergone transsphenoidal surgery with the removal of an
ACTH
-
secreting adenoma
.
Our experience has demonstrated a GHD in a high percentage of patients with
Cushing's disease
even after long-term remission of hypercortisolism obtained by surgery alone.
This
finding
is significant as it highlights that even the most favorable therapeutical course, i.e. remission achieved by surgery, is often accompanied by impaired GH release.
Assessment of GH secretion is therefore recommended in all patients cured from
Cushing's disease
, even if
not
submitted to radiotherapy.
[MeSH-major]
Hypopituitarism / complications.
Pituitary
ACTH
Hypersecretion / complications
[MeSH-minor]
ACTH
-
Secreting Pituitary Adenoma
/ complications.
ACTH
-
Secreting Pituitary Adenoma
/ surgery.
Adenoma
/ complications.
Adenoma
/ surgery. Adult. Aged. Female. Follow-Up Studies. Growth Disorders / epidemiology. Growth Disorders / etiology. Human Growth Hormone / blood. Human Growth Hormone / secretion. Humans. Male. Middle Aged. Prevalence. Young Adult
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(PMID = 19020385.001).
[ISSN]
0391-4097
[Journal-full-title]
Journal of endocrinological investigation
[ISO-abbreviation]
J. Endocrinol. Invest.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone
57.
Fernandez A, Karavitaki N, Wass JA:
Prevalence of pituitary adenomas: a community-based, cross-sectional study in Banbury (Oxfordshire, UK).
Clin Endocrinol (Oxf)
; 2010 Mar;72(3):377-82
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[Title]
Prevalence
of pituitary
adenomas
: a community-based, cross-sectional study in Banbury (Oxfordshire, UK).
BACKGROUND:
Pituitary
adenomas
(PAs) are associated with increased morbidity and mortality.
All cases of PAs were found following an exhaustive computer database search of agreed terms by the staff of each Practice and data on age, gender, presenting manifestations and their duration, imaging features at
diagnosis
, history of multiple endocrine neoplasia type 1 and family history of PA were collected.
RESULTS: A total of 63 patients with PA were identified amongst the study population of 81,149, with a prevalence of 77.6 PA cases/100,000 inhabitants (prolactinomas; PRLoma: 44.4, nonfunctioning PAs: 22.2, acromegaly; ACRO: 8.6,
corticotroph
adenoma
: 1.2 and unknown functional status; UFS: 1.2/100,000 inhabitants).
The distribution of each PA subtype was for PRLoma 57%, nonfunctioning PAs 28%, ACRO 11%,
corticotroph
adenoma
2% and UFS 2%.
The median age at
diagnosis
and the duration of symptoms until
diagnosis
(in years) were for PRLoma 32.0 and 1.5, nonfunctioning PAs 51.5 and 0.8, ACRO 47 and 4.5 and
corticotroph
adenoma
57 and 7, respectively.
Five patients (7.9%) presented with classical
pituitary
apoplexy, with a prevalence of 6.2 cases/100,000 inhabitants.
[MeSH-major]
Adenoma
/ epidemiology.
Pituitary
Neoplasms / epidemiology
[MeSH-minor]
Adolescent. Adult. Aged. Cross-Sectional Studies. Delayed
Diagnosis
. England / epidemiology. Female. Humans. Male. Middle Aged. Prevalence. Young Adult
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[CommentIn]
Clin Endocrinol (Oxf). 2010 Mar;72(3):290-1
[
19832856.001
]
(PMID = 19650784.001).
[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
58.
Pecori Giraldi F, Bucciarelli LG, Saccani A, Scacchi M, Pesce S, Losa M, Cavagnini F:
Ghrelin stimulates adrenocorticotrophic hormone (ACTH) secretion by human ACTH-secreting pituitary adenomas in vitro.
J Neuroendocrinol
; 2007 Mar;19(3):208-12
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[Title]
Ghrelin stimulates adrenocorticotrophic hormone (
ACTH
) secretion by human
ACTH
-
secreting pituitary
adenomas
in vitro.
Ghrelin is a
brain
-gut peptide with wide-ranging endocrine, metabolic, cardiovascular and neural effects.
Ghrelin, like its synthetic counterparts, the growth hormone (GH) secretagogues, has been shown to markedly stimulate adrenocorticotrophic hormone (
ACTH
) and cortisol secretion in humans and the
ACTH
-releasing effect of GH secretagogues is even greater in patients with
pituitary
ACTH
-
secreting
tumours.
The aim of the present study was to evaluate the effect of ghrelin on
ACTH
secretion by human
pituitary
corticotroph
tumours in vitro to test the functionality of this circuit.
Nine
ACTH
-
secreting pituitary
tumours (four microadenomas, five macroadenomas) were collected during surgery and incubated with 10-100 nM human ghrelin or with 10 nM human corticotrophin-releasing hormone (CRH).
Control experiments were performed in rat anterior
pituitary
primary cultures.
ACTH
secretion was assessed after 4 h and 24 h incubation by immunometric assay.
After 4 h of incubation with ghrelin, medium
ACTH
concentrations were two- to ten-fold higher compared to
ACTH
concentrations in unstimulated wells.
The
ACTH
-releasing effect of ghrelin was significantly less than the response elicited by 10 nM CRH (up to 40-fold) Similar results were obtained after 24 h of incubation and a superimposable response pattern was observed in rat anterior
pituitary
primary cultures.
The present study demonstrates that the endogenous GH secretagogue, ghrelin, stimulates
ACTH
secretion directly from human tumoural corticotrophs, as well as from normal rat
pituitary
, and indicates that the marked
ACTH
release elicited by ghrelin in patients with
Cushing's disease
in vivo is due, at least in part, to its action on
the pituitary
tumour.
Moreover, these data uphold the concept of a functional intratumoural ghrelin paracrine circuit in human
corticotroph adenomas
.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ secretion.
Adenoma
/ secretion. Adrenocorticotropic Hormone / secretion. Corticotrophs / secretion. Peptide Hormones / physiology
[MeSH-minor]
Adult. Animals.
Corticotropin
-Releasing Hormone / physiology. Female. Ghrelin. Humans. In Vitro Techniques. Male. Middle Aged.
Pituitary
ACTH
Hypersecretion / metabolism.
Pituitary
Gland
, Anterior / metabolism. Rats
Hazardous Substances Data Bank.
Corticotropin
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(PMID = 17280594.001).
[ISSN]
0953-8194
[Journal-full-title]
Journal of neuroendocrinology
[ISO-abbreviation]
J. Neuroendocrinol.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Ghrelin; 0 / Peptide Hormones; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
59.
Rudnik A, Zawadzki T, Gałuszka-Ignasiak B, Bazowski P, Duda I, Wojtacha M, Rudnik AI, Krawczyk I:
Endoscopic transsphenoidal treatment in recurrent and residual pituitary adenomas--first experience.
Minim Invasive Neurosurg
; 2006 Feb;49(1):10-4
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[Title]
Endoscopic transsphenoidal treatment in recurrent and residual
pituitary
adenomas
--first experience.
AIM OF THE STUDY: The aim of the study has been the assessment of the endoscopic method in the surgical management of recurrent and residual
pituitary
adenomas
, as concerns treatment efficiency, substantial complications, and its possible advantages for the operating surgeon and patient.
MATERIAL AND METHODS: In Department of Neurosurgery, Silesian University School of Medicine in Katowice, between October 2001 and June 2004, 125 patients underwent endoscopic surgery due to
pituitary adenoma
.
The analysis comprised 20 patients, who were operated on due to recurrent
adenomas
or residual tumour
not
completely removed during the first surgical procedure.
The analysed group had 14 non-functioning
adenomas
, 4 GH-
secreting
adenomas
, 1 PRL-
secreting adenoma
and 1
ACTH
-
secreting adenoma
.
11 of the 20
adenomas
infiltrated the cavernous sinuses.
In the group of 11 patients with
adenomas not
infiltrating the cavernous sinuses, recovery was reported for 8 of them, that is 73%.
CONCLUSIONS: The endoscopic method is a safe, hardly invasive and efficient surgical technique in the treatment of recurrent and residual
pituitary
adenomas
.
[MeSH-major]
Adenoma
/ surgery.
Neoplasm
Recurrence, Local / surgery. Neuroendoscopy.
Pituitary
Neoplasms / surgery. Sphenoid Sinus / surgery
[MeSH-minor]
Adult. Aged. Female. Follow-Up Studies. Humans. Male. Middle Aged.
Neoplasm
, Residual. Reoperation. Treatment Outcome
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(PMID = 16547875.001).
[ISSN]
0946-7211
[Journal-full-title]
Minimally invasive neurosurgery : MIN
[ISO-abbreviation]
Minim Invasive Neurosurg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Germany
60.
Andrioli M, Pecori Giraldi F, Losa M, Terreni M, Invitti C, Cavagnini F:
Cushing's disease due to double pituitary ACTH-secreting adenomas: the first case report.
Endocr J
; 2010;57(9):833-7
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[Title]
Cushing's disease
due to double
pituitary
ACTH
-
secreting
adenomas
: the first case report.
Double
pituitary
adenomas
are rare occurrences in autoptical, surgical and neuroradiological series and are mostly due to non-functioning
pituitary
adenomas
, GH-
secreting
and prolactin-
secreting
adenomas
.
ACTH
secreting
tumours are more rare and, to our knowledge, two distinct
ACTH
-
producing adenomas
within the same
pituitary
have never been reported.
We herewith describe a 56 year old woman with Cushing' s
disease
due to two clearly distinct
ACTH
-
secreting pituitary
adenomas
.
She presented with signs and symptoms of hypercortisolism and hormonal testing was indicative for
pituitary
-dependent Cushing' s syndrome.
Sellar MRI visualized an asymmetric
pituitary
gland
with suspect lesions in both the right and the left
pituitary
lobes.
Pathology confirmed the existence of two distinct
adenomas
located in different sites in the
gland
.
Both presented
ACTH
immunoreactivity but displayed distinct morphological features.
Our case indicates that double
ACTH
-
secreting pituitary
adenomas
may occur in patients with Cushing' s
disease
.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ pathology.
Adenoma
/ pathology. Neoplasms, Multiple Primary / pathology.
Pituitary
ACTH
Hypersecretion / etiology
[MeSH-minor]
Cushing Syndrome / etiology. Female. Humans. Middle Aged.
Pituitary
Neoplasms / pathology
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(PMID = 20595779.001).
[ISSN]
1348-4540
[Journal-full-title]
Endocrine journal
[ISO-abbreviation]
Endocr. J.
[Language]
eng
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
61.
Trapani F, Del Basso De Caro ML, Insabato L, Papparella S, Paciello O:
Type II muscle fibers atrophy associated with silent corticotroph adenoma in a dog.
Folia Histochem Cytobiol
; 2010 Sep 30;48(3):403-6
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[Title]
Type II muscle fibers atrophy associated with silent
corticotroph
adenoma
in a dog.
The Silent
Corticotroph
Adenoma
(SCA) is a
pituitary adenoma
variant characterized by the immunoreactivity for adrenocorticotropic hormone (
ACTH
) and related peptides, without the clinical signs of
Cushing's disease
.
SCA has been postulated to either secrete structurally abnormal
ACTH
that is inactive but detectable by immunohistochemistry or radioimmunoassay, or to secrete
ACTH
intermittently or at low levels continuously.
Excess of
ACTH
has been associated to type II muscle atrophy.
We describe a case of type II muscle fibers atrophy associated with silent
corticotroph
adenoma
in a dog.
The tumour showed a trabecular growth pattern and immunohistochemical analysis demonstrated the presence of cytoplasmic immunoreactivity for
ACTH
.
The muscle atrophy was considered to be related to an excess of inactive
ACTH
.
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(PMID = 21071346.001).
[ISSN]
1897-5631
[Journal-full-title]
Folia histochemica et cytobiologica
[ISO-abbreviation]
Folia Histochem. Cytobiol.
[Language]
ENG
[Publication-type]
Case Reports; Comparative Study; Journal Article
[Publication-country]
Poland
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.3.99.1 / Succinate Dehydrogenase; EC 1.6.- / NADH Tetrazolium Reductase
62.
Minniti G, Traish D, Ashley S, Gonsalves A, Brada M:
Fractionated stereotactic conformal radiotherapy for secreting and nonsecreting pituitary adenomas.
Clin Endocrinol (Oxf)
; 2006 May;64(5):542-8
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[Title]
Fractionated stereotactic conformal radiotherapy for
secreting
and nonsecreting
pituitary
adenomas
.
OBJECTIVE: To assess the medium-term outcome in a cohort of patients with residual or recurrent
pituitary adenoma
treated with fractionated stereotactic conformal radiotherapy (SCRT).
PATIENTS AND METHODS: Ninety-two patients (median age 50 years) with a residual or recurrent nonfunctioning (67) or a
secreting
(25)
pituitary adenoma
were treated between 1995 and 2003.
Eighteen patients had a GH-
secreting
, five PRL-
secreting
and two an
ACTH
-
secreting pituitary adenoma
.
In
secreting
adenomas
, hormone levels declined progressively, becoming normal in more than a third of patients with GH-
secreting
and PRL-
secreting pituitary
tumours.
Hypopituitarism was the most common long-term effect; 22% of patients had worsening
of pituitary
function.
CONCLUSION: SCRT as a high-precision technique of localized irradiation achieves tumour and hormone control
of pituitary
adenomas
comparable with previously published data on the efficacy of conventional radiotherapy.
Despite the potential advantage of reducing the volume of normal
brain
irradiated, the theoretical benefit over conventional radiotherapy in terms of the reduction in long-term morbidity has
not
yet been demonstrated and requires longer follow-up.
Potential effect on long-term cognitive function has
not
been tested.
[MeSH-major]
Adenoma
/ radiotherapy.
Pituitary
Neoplasms / radiotherapy. Radiotherapy, Conformal / methods
[MeSH-minor]
Adrenocorticotropic Hormone / secretion. Adult. Aged. Cohort Studies. Female. Growth Hormone / secretion. Humans. Magnetic Resonance Imaging. Male. Middle Aged.
Neoplasm
Recurrence, Local / pathology.
Neoplasm
Recurrence, Local / radiotherapy.
Neoplasm
, Residual / pathology.
Neoplasm
, Residual / radiotherapy. Prolactinoma / radiotherapy. Prolactinoma / secretion. Radiotherapy Dosage. Statistics, Nonparametric. Treatment Outcome
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.
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(PMID = 16649974.001).
[ISSN]
0300-0664
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
9002-60-2 / Adrenocorticotropic Hormone; 9002-72-6 / Growth Hormone
63.
Bucciarelli LG, Pecori Giraldi F, Cavagnini F:
No mutations in TPIT, a corticotroph-specific gene, in human tumoral pituitary ACTH-secreting cells.
J Endocrinol Invest
; 2005 Dec;28(11):1015-8
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[Title]
No mutations in TPIT, a
corticotroph
-specific gene, in human tumoral
pituitary
ACTH
-
secreting
cells.
BACKGROUND: TPIT is a recently identified transcription factor specific to proopiomelanocortin (POMC)-expressing cells within
the pituitary
and plays a pivotal role in the embryonal development of POMC lineage.
As with other transcription factors, TPIT could theoretically also be involved in
corticotroph
adenomatous transformation and
ACTH
hypersecretion and published data indicate that TPIT is present in normal and adenomatous human corticotrophs.
OBJECTIVE: The aim of the present study was to corroborate this
finding
and to seek evidence for mutations in the TPIT coding sequence in human tumoral corticotrophs.
DESIGN AND METHODS: Eight human
ACTH
-
secreting pituitary
adenomas
were collected during surgery, mRNA extracted from primary cultures and reverse transcribed.
RESULTS: TPIT mRNA was detected in all 8
ACTH
-
secreting pituitary
adenomas
without apparent mRNA variants.
Lastly, sequencing did
not
reveal differences in the nucleotide arrangement compared with the published sequence.
CONCLUSIONS: Aberrant TPIT is unlikely to play a role in
corticotroph
tumoral trasformation, ie,
Cushing's disease
, as the entire coding sequence is expressed without any mutation by human
pituitary
ACTH
-
secreting
adenomas
.
Conversely, the significance of this transcription factor in tumoral
ACTH
hypersecretion remains to be clarified.
[MeSH-major]
Adrenocorticotropic Hormone / secretion. Homeodomain Proteins / genetics. Mutation / genetics.
Pituitary
Neoplasms / genetics. Transcription Factors / genetics
[MeSH-minor]
Humans. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA,
Neoplasm
/ genetics. RNA,
Neoplasm
/ metabolism. Reverse Transcriptase Polymerase Chain Reaction. T-Box Domain Proteins.
Tumor
Cells, Cultured
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(PMID = 16483181.001).
[ISSN]
0391-4097
[Journal-full-title]
Journal of endocrinological investigation
[ISO-abbreviation]
J. Endocrinol. Invest.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Italy
[Chemical-registry-number]
0 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / T-Box Domain Proteins; 0 / TBX19 protein, human; 0 / Transcription Factors; 9002-60-2 / Adrenocorticotropic Hormone
64.
Nolan LA, Schmid HA, Levy A:
Octreotide and the novel multireceptor ligand somatostatin receptor agonist pasireotide (SOM230) block the adrenalectomy-induced increase in mitotic activity in male rat anterior pituitary.
Endocrinology
; 2007 Jun;148(6):2821-7
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[Title]
Octreotide and the novel multireceptor ligand somatostatin receptor agonist pasireotide (SOM230) block the adrenalectomy-induced increase in mitotic activity in male rat anterior
pituitary
.
Acting principally through the latter, it inhibits basal and CRH-stimulated
ACTH
secretion from the AtT20
corticotroph cell
line and
ACTH
release from a proportion of human
corticotroph adenomas
both in vitro and in vivo.
Data supporting an additional antiproliferative effect has led to pasireotide being explored as a potential therapy for patients with
Cushing's disease
.
We have compared the effects of pasireotide and octreotide on adrenalectomy-induced mitotic and apoptotic activity in the male rat anterior
pituitary
.
Pasireotide and octreotide had no effect on baseline
pituitary
cell
turnover and no measurable effects on apoptosis.
However, the wave of increased mitotic activity normally seen in
the pituitary
after adrenalectomy was completely abolished.
Nevertheless, pasireotide and octreotide did
not
diminish the increase in
ACTH
-immunopositive
cell
index after adrenalectomy, indicating that
cell
division and differentiation of hormonally null cells in
the pituitary
are under independent control.
In conclusion, basal
cell
turnover in
the pituitary
is
not
inhibited by pasireotide or octreotide.
Bilateral adrenalectomy stimulates differentiation of preexisting null cells into
ACTH
-positive cells.
Cell
division after bilateral adrenalectomy occurs in a specific subpopulation of hormonally null cells that are equally sensitive to the antiproliferative effects of pasireotide and octreotide, implicating SSTR2 receptors in this antimitotic response.
[MeSH-major]
Adrenalectomy. Mitosis / drug effects. Octreotide / pharmacology.
Pituitary
Gland
, Anterior / drug effects. Receptors, Somatostatin / agonists. Somatostatin / analogs & derivatives
Hazardous Substances Data Bank.
Corticotropin
.
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(PMID = 17347306.001).
[ISSN]
0013-7227
[Journal-full-title]
Endocrinology
[ISO-abbreviation]
Endocrinology
[Language]
eng
[Grant]
United Kingdom / Wellcome Trust / /
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Receptors, Somatostatin; 0 / Sstr2 protein, rat; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
65.
Taoda T, Hara Y, Takekoshi S, Itoh J, Teramoto A, Osamura RY, Tagawa M:
Effect of mitotane on pituitary corticotrophs in clinically normal dogs.
Am J Vet Res
; 2006 Aug;67(8):1385-94
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[Title]
Effect of mitotane on
pituitary
corticotrophs in clinically normal dogs.
OBJECTIVE: To evaluate the effects of mitotane administration on the function and morphology
of pituitary
corticotrophs in clinically normal dogs.
In both groups,
ACTH
stimulation testing and corticotrophin-releasing hormone (CRH) stimulation testing were performed.
Magnetic resonance imaging (MRI) of the
pituitary
gland
and
brain
was performed in mitotane treatment group dogs before and after administration of mitotane.
After CRH stimulation testing and MRI, dogs were euthanatized and
the pituitary
gland
and adrenal glands were excised for gross and histologic examination.
RESULTS:
ACTH
concentrations in mitotane treatment group dogs were significantly higher than in the control group dogs following CRH stimulation.
Magnetic resonance imaging revealed that
pituitary
glands were significantly larger in treatment group dogs after administration of mitotane, compared with before administration.
Immunohistochemistry revealed hypertrophy of corticotrophs in
pituitary
glands of mitotane treatment group dogs.
In instances of
corticotroph
adenoma
, hypertrophy of individual corticotrophs induced by mitotane may greatly facilitate enlargement of the
pituitary
gland
and increases in
ACTH
secretion.
[MeSH-major]
Adrenocorticotropic Hormone / metabolism.
Corticotropin
-Releasing Hormone / metabolism. Health. Mitotane / pharmacology.
Pituitary
Gland
/ drug effects.
Pituitary
Gland
/ metabolism
Hazardous Substances Data Bank.
MITOTANE
.
Hazardous Substances Data Bank.
Corticotropin
.
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(PMID = 16881851.001).
[ISSN]
0002-9645
[Journal-full-title]
American journal of veterinary research
[ISO-abbreviation]
Am. J. Vet. Res.
[Language]
eng
[Publication-type]
Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Antineoplastic Agents, Hormonal; 78E4J5IB5J / Mitotane; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
66.
Candrina R, Sleiman I, Zorzi F:
ACTH-secreting pituitary adenoma within an ovarian teratoma.
Eur J Intern Med
; 2005 Sep;16(5):359-60
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[Title]
ACTH
-
secreting pituitary adenoma
within an ovarian teratoma.
The differential
diagnosis
of
Cushing's
syndrome is one of the most difficult tasks in medicine, and it is especially problematic in cases with "occult" ectopic
ACTH
syndrome.
We describe the case of a 26-year-old woman who was found to suffer from ectopic
ACTH
syndrome due to
pituitary
microadenoma, localized within a mature ovarian teratoma.
Cushing's
syndrome caused by ovarian neoplasia is unusual, but when it occurs, it is most often due to excessive cortisol production by the ovary.
Only rarely has ectopic
ACTH
syndrome in association with an ovarian
tumor
been described.
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(PMID = 16137552.001).
[ISSN]
0953-6205
[Journal-full-title]
European journal of internal medicine
[ISO-abbreviation]
Eur. J. Intern. Med.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Netherlands
67.
Amaral FC, Torres N, Saggioro F, Neder L, Machado HR, Silva WA Jr, Moreira AC, Castro M:
MicroRNAs differentially expressed in ACTH-secreting pituitary tumors.
J Clin Endocrinol Metab
; 2009 Jan;94(1):320-3
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[Title]
MicroRNAs differentially expressed in
ACTH
-
secreting pituitary
tumors.
OBJECTIVE: The aim of the study was to analyze the differential expression of let-7a, miR-15a, miR-16, miR-21, miR-141, miR-143, miR-145, and miR-150 in
corticotropinomas
and normal
pituitary
tissue and verify whether their profile of expression correlates with
tumor
size or remission after treatment.
MATERIAL AND METHODS:
ACTH
-
secreting pituitary
tumor
samples were obtained during transphenoidal surgery from patients with Cushing
disease
and normal
pituitary
tissues from autopsies.
RESULTS: We found underexpression of miR-145 (2.0-fold; P = 0.04), miR-21 (2.4-fold; P = 0.004), miR-141 (2.6-fold; P = 0.02), let-7a (3.3-fold; P = 0.003), miR-150 (3.8-fold; P = 0.04), miR-15a (4.5-fold; P = 0.03), miR-16 (5.0-fold; P = 0.004), and miR-143 (6.4-fold; P = 0.004) in
ACTH
-
secreting pituitary
tumors when compared to normal
pituitary
tissues.
There were no differences between miRNA expression and
tumor
size as well as miRNA expression and ratio of remission after surgery, except in patients presenting lower miR-141 expression who showed a better chance of remission.
However, the lack of knowledge about miRNA target genes postpones full understanding of the biological functions of down-regulated or up-regulated miRNAs in
corticotropinomas
.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ genetics.
Adenoma
/ genetics. MicroRNAs / analysis
[MeSH-minor]
Adolescent. Adult. Female. Humans. Male. Middle Aged.
Pituitary
ACTH
Hypersecretion / genetics. Young Adult
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.
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(PMID = 18840638.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MicroRNAs
68.
Pollock BE, Brown PD, Nippoldt TB, Young WF Jr:
Pituitary tumor type affects the chance of biochemical remission after radiosurgery of hormone-secreting pituitary adenomas.
Neurosurgery
; 2008 Jun;62(6):1271-6; discussion 1276-8
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[Title]
Pituitary
tumor
type affects the chance of biochemical remission after radiosurgery of hormone-
secreting pituitary
adenomas
.
OBJECTIVE: Reported biochemical remission rates have ranged widely after stereotactic radiosurgery for patients with hormone-
secreting pituitary
adenomas
.
Confounding variables include histology, radiation dose, use
of pituitary
-suppressive medications, and length of follow-up.
METHODS: A retrospective review of 46 patients with
pituitary
adenomas
(growth hormone-
secreting
, n = 27; prolactin-
secreting
, n = 11;
adrenocorticotropin
-
secreting
, n = 8) undergoing radiosurgery between January 1990 and December 2003 was conducted.
All received a
tumor
margin dose of 18 Gy or more and were off
pituitary
-suppressive medications for at least 1 month before radiosurgery.
RESULTS: The 4-year remission rates were 87% for patients with
Cushing's disease
, 67% for patients with acromegaly, and 18% for patients with prolactinomas.
Patients with oversecretion
of adrenocorticotropin
or growth hormone were more likely to achieve remission after radiosurgery than patients with prolactinomas (hazard ratio, 4.4; 95% confidence interval, 1.1-18.2; P = 0.04).
Of 44 patients with normal or partial anterior
pituitary
function before radiosurgery, 16 (36%) developed one or more new anterior
pituitary
deficits.
The incidence of new anterior
pituitary
deficits was 26% at 4 years.
CONCLUSION: There seems to be a differential sensitivity after radiosurgery for hormone-
secreting pituitary
adenomas
.
Remission rates are greater for patients with
Cushing's disease
and acromegaly, whereas radiosurgery is less effective in achieving biochemical remission for patients with prolactinomas.
[MeSH-major]
Adenoma
/ metabolism.
Adenoma
/ surgery.
Pituitary
Hormones / metabolism.
Pituitary
Neoplasms / metabolism.
Pituitary
Neoplasms / surgery. Radiosurgery
MedlinePlus Health Information.
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.
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[CommentIn]
Neurosurgery. 2010 May;66(5):E1030; author reply E1030
[
20404679.001
]
(PMID = 18824993.001).
[ISSN]
1524-4040
[Journal-full-title]
Neurosurgery
[ISO-abbreviation]
Neurosurgery
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Pituitary Hormones
69.
Hanson JM, Mol JA, Leegwater PA, Bilodeau S, Drouin J, Meij BP:
Expression and mutation analysis of Tpit in the canine pituitary gland and corticotroph adenomas.
Domest Anim Endocrinol
; 2008 Apr;34(3):217-22
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[Title]
Expression and mutation analysis of Tpit in the canine
pituitary
gland
and
corticotroph adenomas
.
Pituitary
-dependent hyperadrenocorticism (PDH) in dogs is caused by a
pituitary
corticotroph
adenoma
.
Although PDH is a common
disorder
in dogs, little is known about the underlying pathogenesis.
In
the pituitary
glands of humans and mice, the pro-opiomelanocortin (POMC)-expressing
cell
lineages, the corticotrophs and melanotrophs, have a specific marker in common, the T-box transcription factor Tpit (Tbx19), which is obligate for POMC expression.
Tpit also regulates the late differentiation of the corticotrophs and melanotrophs, and therefore may contribute to the pathogenesis of the
corticotroph adenomas
.
The aim of this study was to perform an expression and mutation analysis of Tpit in the normal canine
pituitary
and in
corticotroph adenomas
.
The distribution of the Tpit protein in
the pituitary
gland
was studied with immunohistochemistry and the expression of the gene with RT-PCR.
Tpit was expressed in
corticotroph
and melanotroph cells of the normal and adenomatous canine
pituitary
, and remained present in non-adenomatous corticotrophs of pituitaries from PDH dogs.
No
tumor
-specific mutation in the Tpit cDNA from the
corticotroph adenomas
was found.
It is concluded that Tpit can be used as a reliable marker for the
corticotroph
and melanotroph cells in the canine
pituitary
tissue and that mutations in the Tpit gene are unlikely to play a major role in the pathogenesis of canine
corticotroph adenomas
.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ veterinary.
Adenoma
/ veterinary. Dog Diseases / genetics.
Pituitary
Gland
/ chemistry.
Pituitary
Neoplasms / veterinary. T-Box Domain Proteins / genetics
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
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(PMID = 17544240.001).
[ISSN]
0739-7240
[Journal-full-title]
Domestic animal endocrinology
[ISO-abbreviation]
Domest. Anim. Endocrinol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / T-Box Domain Proteins; 9007-49-2 / DNA
70.
Labeur M, Refojo D, Wölfel B, Stalla J, Vargas V, Theodoropoulou M, Buchfelder M, Paez-Pereda M, Arzt E, Stalla GK:
Interferon-gamma inhibits cellular proliferation and ACTH production in corticotroph tumor cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway.
J Endocrinol
; 2008 Nov;199(2):177-89
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[Title]
Interferon-gamma inhibits cellular proliferation and
ACTH
production in
corticotroph tumor
cells through a novel janus kinases-signal transducer and activator of transcription 1/nuclear factor-kappa B inhibitory signaling pathway.
Moreover, IFNG modulates normal
pituitary
hormone secretion, and was shown to inhibit the expression of the
ACTH
precursor POMC in murine
ACTH
-
secreting
AtT-2010/21/2008
tumor
cells.
We have studied the functional role of IFNG on
pituitary
tumor
cells, focusing on the involvement of IFNG in the molecular events leading to the control of POMC transcriptional repression.
Herein, it is shown that IFNG inhibits AtT-20
tumor cell
proliferation without inducing apoptosis.
In addition, 1 and 2 IFNG receptor immunoreactivity was detected in human
corticotropinoma
cells.
Interestingly, IFNG inhibits
ACTH
production from these cells in primary
cell
culture, without affecting basal
ACTH
biosynthesis in normal non-tumoral
pituitary
cells.
[MeSH-major]
Adrenocorticotropic Hormone / biosynthesis.
Cell
Proliferation / drug effects. Interferon-gamma / pharmacology. Janus Kinases / metabolism. NF-kappa B / metabolism.
Pituitary
Neoplasms / metabolism. STAT1 Transcription Factor / metabolism
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
COS Scholar Universe.
author profiles
.
Hazardous Substances Data Bank.
Corticotropin
.
NCI CPTAC Assay Portal.
NCI CPTAC Assay Portal
.
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(PMID = 18715881.001).
[ISSN]
1479-6805
[Journal-full-title]
The Journal of endocrinology
[ISO-abbreviation]
J. Endocrinol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / NF-kappa B; 0 / STAT1 Transcription Factor; 66796-54-1 / Pro-Opiomelanocortin; 82115-62-6 / Interferon-gamma; 9002-60-2 / Adrenocorticotropic Hormone; EC 2.7.10.2 / Janus Kinases
71.
Bondioni S, Mantovani G, Polentarutti N, Ambrosi B, Loli P, Peverelli E, Lania AG, Beck-Peccoz P, Spada A:
Evaluation of proopiomelanocortin mRNA in the peripheral blood from patients with Cushing's syndrome of different origin.
J Endocrinol Invest
; 2007 Nov;30(10):828-32
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[Title]
Evaluation of proopiomelanocortin mRNA in the peripheral blood from patients with
Cushing's
syndrome of different origin.
ACTH
-dependent
Cushing's
syndrome is due to
ACTH
overproduction originating from a
pituitary
corticotroph
adenoma
(
Cushing's disease
) or from ectopic tumors (ectopic
ACTH
syndrome).
Due to difficulties in the differential
diagnosis
between these two forms of hypercortisolism it would be important to have molecular tools able to discriminate the two conditions.
In order to analyse the presence of different POMC transcripts, we extracted total RNA from peripheral lymphocytes of 10 patients with
Cushing's disease
, 10 with ectopic Cushing syndrome, and 20 controls as well as from
pituitary
tissues (2
ACTH
-omas and a normal
pituitary
polyA+ sample).
Northern blot analysis correctly revealed a 1072 nt mRNA molecule in
pituitary
ACTH
-oma and in the normal
pituitary
polyA+ RNA samples, whereas neither this molecule nor other alternative transcripts were detected in blood samples from patients and controls.
This study further underlines the need for alternative approaches in the
diagnosis
of
ACTH
-dependent
Cushing's
syndrome.
[MeSH-major]
ACTH
Syndrome, Ectopic /
diagnosis
.
ACTH
-
Secreting Pituitary Adenoma
/
diagnosis
.
Adenoma
/
diagnosis
. Biomarkers,
Tumor
/ genetics. Cushing Syndrome /
diagnosis
. Pro-Opiomelanocortin / genetics
[MeSH-minor]
Blotting, Northern.
Diagnosis
, Differential. Humans. RNA, Messenger / blood. Reverse Transcriptase Polymerase Chain Reaction
Genetic Alliance.
consumer health - Cushing's Syndrome
.
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consumer health - Cushing's Syndrome
.
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(PMID = 18075284.001).
[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
[Publication-country]
Italy
[Chemical-registry-number]
0 / Biomarkers, Tumor; 0 / RNA, Messenger; 66796-54-1 / Pro-Opiomelanocortin
72.
Hosoyama T, Nishijo K, Garcia MM, Schaffer BS, Ohshima-Hosoyama S, Prajapati SI, Davis MD, Grant WF, Scheithauer BW, Marks DL, Rubin BP, Keller C:
A Postnatal Pax7 Progenitor Gives Rise to Pituitary Adenomas.
Genes Cancer
; 2010 Apr 1;1(4):388-402
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[Title]
A Postnatal Pax7 Progenitor Gives Rise to
Pituitary
Adenomas
.
Pituitary
adenomas
are classified into functioning and nonfunctioning (silent) tumors on the basis of hormone secretion.
However, the mechanism of tumorigenesis and the
cell
of origin for
pituitary adenoma
subtypes remain to be elucidated.
Employing a tamoxifen-inducible mouse model, we demonstrate that a novel postnatal Pax7(+) progenitor
cell
population in
the pituitary
gland
gives rise to silent
corticotroph
macro-
adenomas
when the retinoblastoma
tumor
suppressor is conditionally deleted.
While Pax transcriptional factors are critical for embryonic patterning as well as postnatal stem
cell
renewal for many organs, we have discovered that Pax7 marks a restricted
cell
population in the postnatal
pituitary
intermediate lobe.
This Pax7(+) early progenitor
cell
population is overlapping but ontologically downstream of the Nestin(+)
pituitary
stem
cell
population, yet upstream of another newly discovered Myf6(+) late progenitor
cell
population.
Interestingly, the Pax7(+) progenitor
cell
population is evolutionarily conserved in primates and humans, and Pax7 expression is maintained
not
only in murine tumors but also in human functioning and silent
corticotropinomas
.
Taken together, our results strongly suggest that human silent
corticotroph adenomas
may in fact arise from a Pax7 lineage of the intermediate lobe, a region of the human
pituitary
bearing closer scientific interest as a reservoir
of pituitary
progenitor cells.
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(PMID = 20811506.001).
[ISSN]
1947-6019
[Journal-full-title]
Genes & cancer
[ISO-abbreviation]
Genes Cancer
[Language]
ENG
[Grant]
United States / NCI NIH HHS / CA / CA133229-03; United States / NCRR NIH HHS / RR / P41 RR012553; United States / NCI NIH HHS / CA / R01 CA133229
[Publication-type]
JOURNAL ARTICLE
[Publication-country]
United States
73.
Tateno T, Kato M, Tani Y, Oyama K, Yamada S, Hirata Y:
Differential expression of somatostatin and dopamine receptor subtype genes in adrenocorticotropin (ACTH)-secreting pituitary tumors and silent corticotroph adenomas.
Endocr J
; 2009;56(4):579-84
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[Title]
Differential expression of somatostatin and dopamine receptor subtype genes in
adrenocorticotropin
(
ACTH
)-
secreting pituitary
tumors and silent
corticotroph adenomas
.
Somatostatin analogs and dopamine agonists are clinically used for medical therapy of functioning
pituitary
tumors, such as growth hormone- and prolactin-
secreting
tumors, however, their effects on
ACTH
-
secreting
tumors are controversial.
This study was aimed to determine whether somatostatin receptor (SSTR) subtype (1-5) and dopamine receptor type 2 (D2R) are differentially expressed in
pituitary
tumors causing
Cushing's disease
(CD), silent
corticotroph
adenoma
(SCA), and non-functioning
pituitary
tumor
(NFT).
Tissue specimens were obtained from 35
pituitary
tumors during transsphenoidal surgery.
Both SSTR1 and 2 mRNA levels in SCA were greater than CD, while SSTR1 mRNA levels, but
not
SSTR2, in SCA were also greater than NFT.
SSTR5 mRNA levels in CD were greater than SCA, but did
not
differ between NFT and SCA.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ genetics.
Adenoma
/ genetics.
Pituitary
ACTH
Hypersecretion / metabolism.
Pituitary
Neoplasms / genetics. Receptors, Dopamine D2 / genetics. Receptors, Somatostatin / physiology
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
Hazardous Substances Data Bank.
Corticotropin
.
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(PMID = 19318729.001).
[ISSN]
1348-4540
[Journal-full-title]
Endocrine journal
[ISO-abbreviation]
Endocr. J.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Japan
[Chemical-registry-number]
0 / Receptors, Dopamine D2; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 2; 0 / somatostatin receptor 5; 0 / somatostatin receptor type 1; 9002-60-2 / Adrenocorticotropic Hormone
74.
Martínez-Fuentes AJ, Moreno-Fernández J, Vázquez-Martínez R, Durán-Prado M, de la Riva A, Tena-Sempere M, Diéguez C, Jiménez-Reina L, Webb SM, Pumar A, Leal-Cerro A, Benito-López P, Malagón MM, Castaño JP:
Ghrelin is produced by and directly activates corticotrope cells from adrenocorticotropin-secreting adenomas.
J Clin Endocrinol Metab
; 2006 Jun;91(6):2225-31
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[Title]
Ghrelin is produced by and directly activates
corticotrope
cells from
adrenocorticotropin
-
secreting
adenomas
.
CONTEXT: In
Cushing's disease
,
ACTH
hypersecretion by
pituitary
corticotrope
adenoma
cells and resulting hypercortisolism is accompanied by a severely blunted GH secretory response.
Interestingly, in
Cushing's disease
, ghrelin markedly increases plasma
ACTH
, whereas its stimulatory action on GH secretion is reduced.
Although the reported expression of ghrelin receptors (GHS-R) in
corticotrope
tumors offers a potential mechanism for ghrelin-induced
ACTH
hypersecretion, studies on the direct effects of synthetic GH secretagogues on
corticotropinoma
cells offered contradictory results.
OBJECTIVE AND DESIGN: To evaluate the direct action of ghrelin on
corticotropinoma
cells from two patients with
Cushing's disease
, we measured its effect on free cytosolic calcium concentration ([Ca(2+)](i)).
Additionally, expression of GHS-R and its ligand ghrelin was examined in these cells and in five additional
corticotropinomas
.
RESULTS: Ghrelin (10(-6) m) induced a marked [Ca(2+)](i) increase in 89.5% (case 1; n = 19 cells) and 85% (case 2; n = 13 cells) of
corticotropinoma
cells.
Moreover, RT-PCR showed that expression of GHS-R isoforms is accompanied by that of ghrelin in all seven
corticotrope adenomas
examined.
Importantly, double immunogold electron microscopy revealed that ghrelin is costored within
ACTH
secretory vesicles in densely granulated adenomatous corticotropes.
CONCLUSIONS: These results constitute the first demonstration that ghrelin acts directly on
corticotrope tumor
cells derived from patients with
Cushing's disease
.
The presence of ghrelin and GHS-R suggests that
pituitary
ghrelin may play an autocrine/paracrine role in regulating
ACTH
release in
Cushing's disease
.
Our findings provide a plausible cellular basis for the exaggerated
ACTH
response to ghrelin in
Cushing's disease
and suggest novel research strategies to develop medical treatments for this
disease
.
[MeSH-major]
Adenoma
/ secretion. Adrenocorticotropic Hormone / secretion. Peptide Hormones / physiology.
Pituitary
Neoplasms / secretion
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.
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CALCIUM, ELEMENTAL
.
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Corticotropin
.
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(PMID = 16551736.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Ghrelin; 0 / Peptide Hormones; 0 / RNA, Messenger; 0 / Receptors, G-Protein-Coupled; 0 / Receptors, Ghrelin; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; SY7Q814VUP / Calcium
75.
Roelfsema F, Pereira AM, Keenan DM, Veldhuis JD, Romijn JA:
Thyrotropin secretion by thyrotropinomas is characterized by increased pulse frequency, delayed diurnal rhythm, enhanced basal secretion, spikiness, and disorderliness.
J Clin Endocrinol Metab
; 2008 Oct;93(10):4052-7
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CONTEXT: Hormone secretion by somatotropinomas,
corticotropinomas
, and prolactinomas exhibits increased pulsatility and basal secretion, accompanied by greater disorderliness.
CONCLUSION: TSH secretion by thyrotropinomas shares many characteristics with other
pituitary
hormone-
secreting
adenomas
.
[MeSH-major]
Adenoma
/ physiopathology.
Adenoma
/ secretion. Circadian Rhythm / physiology.
Pituitary
Neoplasms / physiopathology.
Pituitary
Neoplasms / secretion. Pulsatile Flow / physiology. Thyrotropin / secretion
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.
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(PMID = 18682501.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
9002-71-5 / Thyrotropin
76.
Tauchmanovà L, Pivonello R, De Martino MC, Rusciano A, De Leo M, Ruosi C, Mainolfi C, Lombardi G, Salvatore M, Colao A:
Effects of sex steroids on bone in women with subclinical or overt endogenous hypercortisolism.
Eur J Endocrinol
; 2007 Sep;157(3):359-66
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PATIENTS: Seventy-one consecutive women were enrolled: 36 with overt hypercortisolism (26 with
ACTH
-
secreting pituitary adenoma
and 10 with cortisol-
secreting
adrenal
tumor
) and 35 with subclinical hypercortisolism due to adrenal incidentalomas.
METHODS: At
diagnosis
, we measured serum cortisol, FSH, LH, estradiol, testosterone, androstenedione and DHEAS, and urinary cortisol excretion.
RESULTS: Between women with overt and subclinical hypercortisolism BMD values and prevalence of any vertebral (69 vs 57%, P = 0.56), clinical (28 vs 11.4%, P = 0.22), and multiple vertebral fractures (36 vs 31%, P = 0.92) did
not
differ.
The deleterious effects of hypercortisolism on the spine may be partly counterbalanced by DHEAS increase at any degree of cortisol excess, and by preserved menstrual cycles in women with subclinical but
not
in those with overt hypercortisolism.
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.
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.
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.
Hazardous Substances Data Bank.
HYDROCORTISONE
.
Hazardous Substances Data Bank.
ESTRADIOL
.
Hazardous Substances Data Bank.
TESTOSTERONE
.
Hazardous Substances Data Bank.
ANDROSTENEDIONE
.
Hazardous Substances Data Bank.
MENOTROPINS
.
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(PMID = 17766720.001).
[ISSN]
0804-4643
[Journal-full-title]
European journal of endocrinology
[ISO-abbreviation]
Eur. J. Endocrinol.
[Language]
ENG
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
England
[Chemical-registry-number]
0 / Gonadal Steroid Hormones; 3XMK78S47O / Testosterone; 409J2J96VR / Androstenedione; 4TI98Z838E / Estradiol; 57B09Q7FJR / Dehydroepiandrosterone Sulfate; 9002-68-0 / Follicle Stimulating Hormone; WI4X0X7BPJ / Hydrocortisone
77.
Jankowska A, Wasko R, Waligorska-Stachura J, Andrusiewicz M, Jaskula M, Liebert W, Sowinski J:
Survivin products in pituitary tumors.
Neuro Endocrinol Lett
; 2008 Dec;29(6):1033-7
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[Title]
Survivin products in
pituitary
tumors.
Still very little is known about survivin expression in
pituitary
tumors.
In spite of the fact that
pituitary
tumors in histological examination are usually benign, in the clinical process a certain number
of pituitary
adenomas
is capable of aggressive growth, recurrence and invasion of the surrounding structures.
The aim of the present study was to assess the presence of survivin transcripts and protein in different types
of pituitary
tumors and to evaluate survivin expression levels in invasive and non-invasive
pituitary
tumors.
DESIGN AND METHODS: The analyzed material consisted of
tumor
tissue samples obtained during standard neurosurgical removal of the
tumor
from 23 patients in whom acromegaly (n=14), non-functioning
pituitary
tumor
(n=6), prolactinoma (n=2) and
corticotropinoma
(n=1) were diagnosed.
As a control of the study normal
pituitary
tissue obtained at autopsy was used.
RESULTS: Our study demonstrated the presence of survivin mRNA in all 23 analyzed
pituitary
tumors.
Survivin expression was also observed in normal
pituitary
, but the level of its expression was 6-fold lower than in tumors tissue when studied by real time RT-PCR.
The difference between the levels of survivin expression in invasive and non-invasive tumors was
not
statistically significant.
Immunohistochemical analyses revealed the presence of the protein in both normal and
tumor
tissue
of pituitary
.
Immunostaining of
tumor
tissue was
not
uniform.
The presence of the protein in normal
pituitary
was restricted to small population of cells.
CONCLUSIONS: The present study showed that overexpression of survivin is characteristic for
pituitary
tumors.
Further analysis of this protein expression profile should demonstrate whether survivin might be use as a prognostic marker in
diagnosis
and therapy
of pituitary
adenomas
.
[MeSH-major]
Adenoma
/ metabolism. Apoptosis Regulatory Proteins / metabolism. Microtubule-Associated Proteins / metabolism.
Neoplasm
Proteins / metabolism.
Pituitary
Gland
/ metabolism.
Pituitary
Neoplasms / metabolism
[MeSH-minor]
ACTH
-
Secreting Pituitary Adenoma
/ metabolism. Adult. Female. Growth Hormone-
Secreting Pituitary Adenoma
/ metabolism. Humans. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Prolactinoma / metabolism. RNA, Messenger / analysis
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.
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(PMID = 19112393.001).
[ISSN]
0172-780X
[Journal-full-title]
Neuro endocrinology letters
[ISO-abbreviation]
Neuro Endocrinol. Lett.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
Sweden
[Chemical-registry-number]
0 / Apoptosis Regulatory Proteins; 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
78.
Meinardi JR, Wolffenbuttel BH, Dullaart RP:
Cyclic Cushing's syndrome: a clinical challenge.
Eur J Endocrinol
; 2007 Sep;157(3):245-54
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[Title]
Cyclic
Cushing's
syndrome: a clinical challenge.
Cyclic
Cushing's
syndrome (CS) is a rare
disorder
, characterized by repeated episodes of cortisol excess interspersed by periods of normal cortisol secretion.
Our review of 65 reported cases demonstrates that cyclic CS originates in 54% of cases from a
pituitary
corticotroph
adenoma
, in 26% from an ectopic
ACTH
-
producing
tumour and in about 11% from an adrenal tumour, the remainder being unclassified.
When cyclic CS is biochemically confirmed, further imaging and laboratory studies are guided by the presence or absence of
ACTH
dependency.
In cases of suspected ectopic
ACTH
production, specific biochemical testing for carcinoids or neuroendocrine tumours is required, including measurements of serotonin in platelets and/or urine, chromogranin A and calcitonin.
Genetic Alliance.
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.
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.
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HYDROCORTISONE
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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(PMID = 17766705.001).
[ISSN]
0804-4643
[Journal-full-title]
European journal of endocrinology
[ISO-abbreviation]
Eur. J. Endocrinol.
[Language]
ENG
[Publication-type]
Journal Article; Review
[Publication-country]
England
[Chemical-registry-number]
WI4X0X7BPJ / Hydrocortisone
[Number-of-references]
108
79.
Mortini P, Losa M, Barzaghi R, Boari N, Giovanelli M:
Results of transsphenoidal surgery in a large series of patients with pituitary adenoma.
Neurosurgery
; 2005 Jun;56(6):1222-33; discussion 1233
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[Title]
Results of transsphenoidal surgery in a large series of patients with
pituitary adenoma
.
OBJECTIVE: To report the efficacy and safety of microsurgical transsphenoidal surgery in a series of previously untreated patients with
pituitary adenoma
.
METHODS: One thousand one hundred forty consecutive patients undergoing transsphenoidal resection of a
pituitary adenoma
at our department from January 1990 through December 2002 were included in our study.
Patients were considered in remission of
disease
when strict hormonal and radiological criteria of cure were met.
RESULTS: The most frequent
tumor
type was clinically nonfunctioning
adenoma
(NFPA) (33.2%), followed by growth hormone-
secreting adenoma
(28.1%),
adrenocorticotropin
-
secreting adenoma
(23.0%), prolactin-
secreting adenoma
(13.2%), and last, thyrotropin-
secreting adenoma
(2.5%).
There were 788 macroadenomas (69.1%), and in 233 patients (20.4%), the
tumor
invaded one or both cavernous sinuses.
The overall rate of early surgical success was achieved in 504 (66.1%) of the 762 patients with a hormone-active
adenoma
.
In patients with NFPA, no residual
adenoma
was present in 234 patients (64.8%).
CONCLUSION: Transsphenoidal surgery is an effective and safe treatment for most patients with
pituitary adenoma
and could be considered the first-choice therapy in all cases except for prolactinomas responsive to dopamine agonists.
Other treatment methods, such as radiotherapy, stereotactic radiosurgery, and medical therapy, play an important role in patients
not
cured by surgery.
[MeSH-major]
Adenoma
/ surgery. Hypophysectomy / methods.
Pituitary
Neoplasms / surgery. Sphenoid Sinus / surgery
[MeSH-minor]
Adult. Female. Humans. Male. Middle Aged.
Pituitary
Hormones / metabolism. Postoperative Complications. Retrospective Studies. Treatment Outcome. Vision Disorders / etiology
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.
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(PMID = 15918938.001).
[ISSN]
1524-4040
[Journal-full-title]
Neurosurgery
[ISO-abbreviation]
Neurosurgery
[Language]
eng
[Publication-type]
Clinical Trial; Comparative Study; Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Pituitary Hormones
80.
Pawlikowski M, Kunert-Radek J, Radek M:
"Silent"corticotropinoma.
Neuro Endocrinol Lett
; 2008 Jun;29(3):347-50
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[Title]
"Silent"
corticotropinoma
.
OBJECTIVES: The aim of the study was to evaluate the
ACTH
-immunopositive
pituitary
adenomas
, especially those without manifestation of
Cushing's disease
MATERIAL AND METHODS: 148
pituitary
adenomas
removed surgically in years 1994--2007 were studied.
The paraffin sections were immunostained with antibodies against
the pituitary
hormones.
In 79
adenomas
the immunostaining with anti-
ACTH
antibody was performed Additionally, 23 tumors were also immunostained with anti-Ki-67 (MIB-1) antibody.
RESULTS:
ACTH
immunopositivity was found in 34 cases (23%).
Fourteen
ACTH
-immunopositive tumors manifested themselves as
Cushing's disease
(including 1 case of Nelson's syndrome).
In the remaining 20 cases in spite of the positive immunostaining for
ACTH
of the
tumor
cells, no features of hypercortisolism were observed (in several cases even hypocortisolism was found).
Thus, those tumors represented so-called "silent"
corticotropinomas
.
Over one third (37%) of "clinically" nonfunctioning
pituitary
adenomas
, when immunostained with anti-
ACTH
antibody, showed
ACTH
immunopositivity.
Three
adenomas
in patients with
Cushing's disease
(21.4%) and 7 "silent"
corticotropinomas
(35%) were recurrent tumors.
In contrast, the recurrence rate in the group of
ACTH
-immunonegative clinically nonfunctioning
pituitary
adenomas
was 14.7%.
The "silent"
corticotropinomas
exhibited a tendency towards the higher expression of a proliferation marker, Ki-67 antigen as compared to the "active"
corticotropinomas
.
CONCLUSIONS: (i) "Silent"
corticotropinomas
are rather frequent. (ii) This
adenoma
type should be considered as aggressive. (iii) It is hypothetized that--like in Nelson's syndrome--the lack of hypercortisolism or even presence of hypocortisolism favorizes the exaggerated growth of tumoral corticotrophs.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ metabolism.
Adenoma
/ metabolism. Adrenocorticotropic Hormone / metabolism
[MeSH-minor]
Adult. Cushing Syndrome / blood. Cushing Syndrome / pathology. Female. Humans. Immunohistochemistry. Ki-67 Antigen / blood. Male. Nelson Syndrome / blood. Paraffin Embedding.
Pituitary
Hormones / metabolism
Hazardous Substances Data Bank.
Corticotropin
.
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(PMID = 18580839.001).
[ISSN]
0172-780X
[Journal-full-title]
Neuro endocrinology letters
[ISO-abbreviation]
Neuro Endocrinol. Lett.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
Sweden
[Chemical-registry-number]
0 / Ki-67 Antigen; 0 / Pituitary Hormones; 9002-60-2 / Adrenocorticotropic Hormone
81.
Stilling G, Sun Z, Zhang S, Jin L, Righi A, Kovācs G, Korbonits M, Scheithauer BW, Kovacs K, Lloyd RV:
MicroRNA expression in ACTH-producing pituitary tumors: up-regulation of microRNA-122 and -493 in pituitary carcinomas.
Endocrine
; 2010 Aug;38(1):67-75
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[Title]
MicroRNA expression in
ACTH
-
producing
pituitary
tumors: up-regulation of microRNA-122 and -493 in
pituitary
carcinomas.
MicroRNAs (miRNAs) are involved in
cell
proliferation, differentiation, and apoptosis, and can function as
tumor
suppressor genes or oncogenes.
The expression of miRNAs in
pituitary
carcinomas has
not
been previously examined.
We used miRNA profiling with 1,145 probes to study miRNA expression in normal anterior
pituitary
(6 cases),
adrenocorticotropin
(
ACTH
)-
producing adenomas
(8 cases), and
ACTH
-
producing
pituitary
carcinomas (two cases).
Real-time RT-PCR and in situ hybridization were used to confirm and independently validate miRNAs that were significantly up-regulated or down-regulated between
the pituitary
tissues.
There were more miRNAs up- (188) or down-regulated (160) between
adenomas
and normal pituitaries compared to carcinomas and normal pituitaries (92 up- and 91 down-regulated) or between carcinomas and
adenomas
(46 up- and 52 down-regulated).
Both real-time RT-PCR and in situ hybridization showed significant up-regulation of miRNA-122 between
pituitary
carcinomas and
adenomas
.
MiRNA-493 was also up-regulated in carcinomas compared to
ACTH adenomas
.
Analysis of genes that miRNA-493 interacts with included LGALS3 and RUNX2 ( http://microrna.sanger.ac.uk ) both of which have been shown to have roles in
pituitary
tumor cell
growth.
These results provide information about marker miRNAs that may lead to further insights into the regulation
of pituitary
tumor
growth and development.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ genetics.
Adenoma
/ genetics. Gene Expression Profiling. Gene Expression Regulation, Neoplastic. MicroRNAs / genetics
[MeSH-minor]
Adult. Aged. Female. Humans. In Situ Hybridization. Oligonucleotide Array Sequence Analysis.
Pituitary
Gland
, Anterior / pathology.
Pituitary
Gland
, Anterior / physiology. Reverse Transcriptase Polymerase Chain Reaction. Up-Regulation / genetics
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[ISSN]
1559-0100
[Journal-full-title]
Endocrine
[ISO-abbreviation]
Endocrine
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / MIRN122 microRNA, human; 0 / MIRN493 microRNA, human; 0 / MicroRNAs
82.
Dehdashti AR, Gentili F:
Current state of the art in the diagnosis and surgical treatment of Cushing disease: early experience with a purely endoscopic endonasal technique.
Neurosurg Focus
; 2007;23(3):E9
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[Title]
Current state of the art in the
diagnosis
and surgical treatment of Cushing
disease
: early experience with a purely endoscopic endonasal technique.
OBJECT: Transsphenoidal
pituitary
surgery is the primary therapy for Cushing
disease
because of its potential to produce lasting remission without the need for long-term drug or hormone replacement therapy.
The authors evaluated the current role of pure endoscopic endonasal
pituitary
surgery in the treatment of Cushing
disease
.
METHODS: Twenty-five patients underwent pure endoscopic surgery for confirmed Cushing
disease
.
Final histological results were consistent with
adrenocorticotropin
hormone (
ACTH
)-
secreting adenoma
in 20 patients.
Three patients presented with new anterior
pituitary
deficiency, but no one had permanent diabetes insipidus.
Treatment failure was attributable to involvement of the cavernous sinus in two patients, incomplete
tumor
removal in one, negative exploration in one, and nodular
corticotroph
hyperplasia of the
pituitary
gland
in one.
CONCLUSIONS: Early results indicated that endoscopic endonasal surgery is a safe and effective treatment for
ACTH
-
producing adenomas
.
Further studies with a larger number of patients and longer follow-ups are required to determine whether this more minimally invasive pure endoscopic approach should become the standard of care for the surgical treatment of Cushing
disease
.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ surgery.
Adenoma
/ surgery. Endoscopy. Paranasal Sinuses / surgery.
Pituitary
ACTH
Hypersecretion /
diagnosis
.
Pituitary
ACTH
Hypersecretion / surgery
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.
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(PMID = 17961027.001).
[ISSN]
1092-0684
[Journal-full-title]
Neurosurgical focus
[ISO-abbreviation]
Neurosurg Focus
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
83.
Giorgi RR, Correa-Giannella ML, Casarini AP, Machado MC, Bronstein MD, Cescato VA, Giannella-Neto D:
Metallothionein isoform 3 gene is differentially expressed in corticotropin-producing pituitary adenomas.
Neuroendocrinology
; 2005;82(3-4):208-14
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[Title]
Metallothionein isoform 3 gene is differentially expressed in
corticotropin
-
producing
pituitary
adenomas
.
In order to search for candidate genes related to
pituitary adenoma
aggressiveness, the present investigation was intended to compare the mRNA expression profile from a pool of four nonfunctional
pituitary
adenomas
(NFPA) with a spinal cord metastasis of a nonfunctional
pituitary
carcinoma (MNFPC).
The metallothionein isoform 3 (MT3) gene was differentially expressed in nonfunctional
adenomas
in comparison to the metastasis of nonfunctional carcinoma.
A microarray dataset comprising 19,881 probes was employed for comparing expression profiles of a spinal cord metastasis of a nonfunctional
pituitary
carcinoma with a pool of four nonfunctional
pituitary
adenomas
.
RT-qPCR confirmed the microarray findings and was used to investigate MT3 mRNA gene expression in
tumor
samples of a series of 52 different
pituitary adenoma
subtypes comprising 10
corticotropin
(
ACTH
)-
producing
, 18 growth hormone (GH)-
producing
, 8 prolactin (PRL)-
producing
, and 16 nonfunctional
adenomas
.
MT3 mRNA expression was statistically significantly higher in
ACTH
-
producing
pituitary
adenomas
and in nonfunctional
pituitary
adenomas
in comparison to the other
pituitary adenoma
subtypes.
The more abundant expression of this gene in
ACTH
-
producing
pituitary
adenomas
suggests that MT3 could be related to distinct
pituitary
cell
lineage regulating the activity of some transcription factor of importance in hormone production and/or secretion.
[MeSH-major]
Adenoma
/ metabolism. Adrenocorticotropic Hormone / metabolism. Nerve Tissue Proteins / biosynthesis.
Pituitary
Neoplasms / metabolism
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.
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Corticotropin
.
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(PMID = 16601360.001).
[ISSN]
0028-3835
[Journal-full-title]
Neuroendocrinology
[ISO-abbreviation]
Neuroendocrinology
[Language]
eng
[Publication-type]
Comparative Study; Journal Article
[Publication-country]
Switzerland
[Chemical-registry-number]
0 / Nerve Tissue Proteins; 0 / Protein Isoforms; 0 / RNA, Messenger; 0 / growth inhibitory factor; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin
84.
Daems T, Verhelst J, Michotte A, Abrams P, De Ridder D, Abs R:
Modification of hormonal secretion in clinically silent pituitary adenomas.
Pituitary
; 2009;12(1):80-6
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[Title]
Modification of hormonal secretion in clinically silent
pituitary
adenomas
.
BACKGROUND: Silent
pituitary
adenomas
are a subtype of
adenomas
characterized by positive immunoreactivity for one or more hormones classically secreted by normal
pituitary
cells but without clinical expression, although in some occasions enhanced or changed secretory activity can develop over time.
Silent
corticotroph adenomas
are the classical example of this phenomenon.
PATIENTS AND METHODS: A series of about 500
pituitary
adenomas
seen over a period of 20 years were screened for modification in hormonal secretion.
RESULTS: Two cases were retrieved, one silent somatotroph
adenoma
and one thyrotroph
adenoma
, both without specific clinical features or biochemical abnormalities, which presented 20 years after initial surgery with evidence of acromegaly and hyperthyroidism, respectively.
While the acromegaly was controlled by a combination of somatostatin analogs and growth hormone (GH) receptor antagonist therapy, neurosurgery was necessary to manage the thyrotroph
adenoma
.
Apparently, the mechanisms responsible for the secretory modifications are different, being a change in secretory capacity in the silent somatotroph
adenoma
and a quantitative change in the silent thyrotroph
adenoma
.
CONCLUSIONS: These two cases, one somatotroph and one thyrotroph
adenoma
, are an illustration that clinically silent
pituitary
adenomas
may in rare circumstances evolve over time and become active, as previously demonstrated in silent
corticotroph adenomas
.
[MeSH-major]
Pituitary
Neoplasms / metabolism
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.
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[Cites]
Neurosurgery. 2000 Sep;47(3):723-9; discussion 729-30
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(PMID = 18350381.001).
[ISSN]
1573-7403
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Publication-type]
Case Reports; Journal Article; Review
[Publication-country]
United States
[Chemical-registry-number]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I; 9002-71-5 / Thyrotropin
[Number-of-references]
30
85.
Hofland LJ, van der Hoek J, Feelders R, van Aken MO, van Koetsveld PM, Waaijers M, Sprij-Mooij D, Bruns C, Weckbecker G, de Herder WW, Beckers A, Lamberts SW:
The multi-ligand somatostatin analogue SOM230 inhibits ACTH secretion by cultured human corticotroph adenomas via somatostatin receptor type 5.
Eur J Endocrinol
; 2005 Apr;152(4):645-54
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[Title]
The multi-ligand somatostatin analogue SOM230 inhibits
ACTH
secretion by cultured human
corticotroph adenomas
via somatostatin receptor type 5.
OBJECTIVE: Currently, there is no effective medical treatment for patients with
pituitary
-dependent
Cushing's disease
.
We compared the in vitro effects of the sst(2)-preferring SS analogue octreotide (OCT) and the multi-ligand SOM230 on
ACTH
release by human and mouse
corticotroph
tumour cells.
METHODS: By quantitative RT-PCR the sst subtype expression level was determined in human
corticotroph adenomas
.
In vitro, the inhibitory effect of OCT and SOM230 on
ACTH
release by dispersed human
corticotroph
adenoma
cells and mouse AtT20
corticotroph
adenoma
cells was determined.
RESULTS:
Corticotroph adenomas
expressed predominantly sst(5) mRNA (six out of six
adenomas
), whereas sst(2) mRNA expression was detected at significantly lower levels.
In a 72 h incubation with 10 nmol/l SOM230,
ACTH
release was inhibited in three out of five cultures (range -30 to -40%).
Ten nmol/l OCT slightly inhibited
ACTH
release in only one of five cultures (- 28%).
In AtT20 cells, expressing sst(2), sst(3) and sst(5), SOM230 inhibited
ACTH
secretion with high potency (IC(50) 0.2 nmol/l).
Dexamethasone (10 nmol/l) pre-treatment did
not
influence the sensitivity of the cells to the inhibitory effect of SOM230, suggesting that sst(5) is relatively resistant to negative control by glucocorticoids.
CONCLUSIONS: The selective expression of sst(5) receptors in
corticotroph adenomas
and the preferential inhibition of
ACTH
release by human
corticotroph
adenoma
cells by SOM230 in vitro, suggest that SOM230 may have potential in the treatment of patients with
pituitary
-dependent
Cushing's disease
.
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consumer health - Pituitary Tumors
.
Faculty of 1000.
commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine.
(subscription/membership/fee required).
Hazardous Substances Data Bank.
Corticotropin
.
ORBi (University of Liege).
Free full Text at ORBi
.
The Lens.
Cited by Patents in
.
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(PMID = 15817922.001).
[ISSN]
0804-4643
[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 / Glucocorticoids; 0 / RNA, Messenger; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide; RWM8CCW8GP / Octreotide
86.
Jiang ZQ, Gui SB, Zhang YZ:
Differential gene expression by fiber-optic beadarray and pathway in adrenocorticotrophin-secreting pituitary adenomas.
Chin Med J (Engl)
; 2010 Dec;123(23):3455-61
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[Title]
Differential gene expression by fiber-optic beadarray and pathway in adrenocorticotrophin-
secreting pituitary
adenomas
.
BACKGROUND: Adrenocorticotrophin (
ACTH
)-
secreting pituitary
adenomas
account for approximately 7% - 14% of all
pituitary
adenomas
, but its pathogenesis is still enigmatic.
This study aimed to explore mechanisms underlying the pathogenesis of
ACTH
-
secreting pituitary
adenomas
.
METHODS: We used fiber-optic beadarray to examine gene expression in three
ACTH
-
secreting
adenomas
compared with three normal pituitaries.
Four differentially expressed genes from the three
ACTH
-
secreting
adenomas
and three normal pituitaries were chosen randomly for validation by reverse transcriptase-real time quantitative polymerase chain reaction (RT-qPCR).
Bioinformatic and pathway analysis showed that the genes HIGD1B, EPS8, HPGD, DAPK2, and IGFBP3 and the transforming growth factor (TGF)-β signaling pathway and extracellular matrix (ECM)-receptor interaction pathway may play important roles in tumorigenesis and progression of
ACTH
-
secreting pituitary
adenomas
.
CONCLUSIONS: Our data suggest that numerous aberrantly expressed genes and several pathways are involved in the pathogenesis of
ACTH
-
secreting pituitary
adenomas
.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ etiology.
Adenoma
/ etiology. Gene Expression Profiling. Oligonucleotide Array Sequence Analysis / methods. Signal Transduction / physiology
[MeSH-minor]
Adult.
Disease
Progression. Expressed Sequence Tags. Extracellular Matrix Proteins / physiology. Female. Fiber Optic Technology. Humans. Male. Middle Aged. Real-Time Polymerase Chain Reaction. Reverse Transcriptase Polymerase Chain Reaction. Transforming Growth Factor alpha / physiology
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(PMID = 22166531.001).
[ISSN]
0366-6999
[Journal-full-title]
Chinese medical journal
[ISO-abbreviation]
Chin. Med. J.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
China
[Chemical-registry-number]
0 / Extracellular Matrix Proteins; 0 / Transforming Growth Factor alpha
87.
Bezerra MG, Latronico AC, Fragoso MC:
[Endocrine tumors associated to protein Gsalpha/Gi2alpha mutations].
Arq Bras Endocrinol Metabol
; 2005 Oct;49(5):784-90
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Many oncogenic mutations promote
tumor
growth by inducing autonomous activity of proteins that normally transmit proliferative signal initiated by extracellular factors.
The G proteins couple an array of seven transmembrane receptors at the
cell
surface with a variety of intracellular effectors, which produce second messenger molecules.
A subset of endocrine tumors, such as GH- or
ACTH
-
secreting pituitary
adenomas
, functioning thyroid
adenomas
, adrenocortical and gonadal tumors were associated with somatic activating mutations in the highly conserved codons of the Gs (Arg201 and Gln227) and Gi (Arg179 and Gln205) proteins.
[MeSH-major]
Endocrine
Gland
Neoplasms / genetics. GTP-Binding Protein alpha Subunits, Gi-Go / genetics. GTP-Binding Protein alpha Subunits, Gs / genetics. Mutation / genetics. Oncogenes / genetics
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(PMID = 16444361.001).
[ISSN]
0004-2730
[Journal-full-title]
Arquivos brasileiros de endocrinologia e metabologia
[ISO-abbreviation]
Arq Bras Endocrinol Metabol
[Language]
por
[Publication-type]
English Abstract; Journal Article; Review
[Publication-country]
Brazil
[Chemical-registry-number]
EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gi-Go; EC 3.6.5.1 / GTP-Binding Protein alpha Subunits, Gs
[Number-of-references]
64
88.
Durán-Prado M, Gahete MD, Martínez-Fuentes AJ, Luque RM, Quintero A, Webb SM, Benito-López P, Leal A, Schulz S, Gracia-Navarro F, Malagón MM, Castaño JP:
Identification and characterization of two novel truncated but functional isoforms of the somatostatin receptor subtype 5 differentially present in pituitary tumors.
J Clin Endocrinol Metab
; 2009 Jul;94(7):2634-43
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[Title]
Identification and characterization of two novel truncated but functional isoforms of the somatostatin receptor subtype 5 differentially present in
pituitary
tumors.
DESIGN AND RESULTS: A rapid amplification of cDNA ends PCR approach on samples from a human
pituitary
tumor
and a
cell
line enabled identification of two novel alternatively spliced sst5 receptor variants.
Both novel receptors show a differential expression pattern in normal tissues and are also present in
pituitary
tumors of diverse etiology including nonfunctioning
adenomas
,
corticotropinomas
, somatotropinomas, and a prolactinoma.
Specifically, whereas sst5TMD5 is selectivity activated by somatostatin compared with cortistatin, cells transfected with sst5TMD4 almost exclusively respond to cortistatin and
not
to somatostatin.
CONCLUSIONS: Our results demonstrate the existence of two previously unidentified sst5 spliced variants with distinct distribution in normal tissues and
pituitary
tumors, unique ligand-selective signaling properties, and subcellular distribution, which could contribute to somatostatin and cortistatin signaling in normal and tumoral cells.
[MeSH-major]
Adenoma
/ genetics.
Pituitary
Neoplasms / genetics. Receptors, Somatostatin / genetics
MedlinePlus Health Information.
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.
Guide to Pharmacology.
gene/protein/disease-specific - SST5 receptor - data and references
.
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.
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(PMID = 19401364.001).
[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; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / Protein Isoforms; 0 / Receptors, Somatostatin; 0 / somatostatin receptor 5
89.
Baldeweg SE, Pollock JR, Powell M, Ahlquist J:
A spectrum of behaviour in silent corticotroph pituitary adenomas.
Br J Neurosurg
; 2005 Feb;19(1):38-42
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[Title]
A spectrum of behaviour in silent
corticotroph
pituitary
adenomas
.
Silent
corticotroph adenomas
(SCA) are
pituitary
tumours positive on immunohistochemical staining for
ACTH
but without clinical evidence of
Cushing's disease
in the patient.
Previous reports suggest that these tumours may behave in a more aggressive way then other
pituitary
adenomas
.
We identified 22 patients in whom trans-sphenoidal surgery was performed for a non-functioning
adenoma
(NFA) with positive immunostaining for
ACTH
between 1990 and 2000 and examined the history of their
disease
.
In four cases hypercortisolaemia was observed later in the course of the
disease
.
Pathological indices (increased mitotic range and Ki-67) did
not
predict recurrence or malignant transformation.
We suggest that certain 'silent'
corticotroph
tumours may have the potential for
ACTH
secretion leading to hypercortisolaemia at a later stage in the
disease
.
[MeSH-major]
Adenoma
/ physiopathology.
Pituitary
Neoplasms / physiopathology
[MeSH-minor]
Adrenocorticotropic Hormone / analysis. Adult. Aged. Anti-Inflammatory Agents / analysis. Female. Humans. Hydrocortisone / analysis. Immunohistochemistry / methods. Magnetic Resonance Imaging / methods. Male. Middle Aged.
Neoplasm
Recurrence, Local / surgery. Reoperation. Treatment Outcome. Vision Disorders / etiology
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.
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(PMID = 16147581.001).
[ISSN]
0268-8697
[Journal-full-title]
British journal of neurosurgery
[ISO-abbreviation]
Br J Neurosurg
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Anti-Inflammatory Agents; 9002-60-2 / Adrenocorticotropic Hormone; WI4X0X7BPJ / Hydrocortisone
90.
Minniti G, Osti M, Jaffrain-Rea ML, Esposito V, Cantore G, Maurizi Enrici R:
Long-term follow-up results of postoperative radiation therapy for Cushing's disease.
J Neurooncol
; 2007 Aug;84(1):79-84
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[Title]
Long-term follow-up results of postoperative radiation therapy for
Cushing's disease
.
OBJECTIVES: Radiotherapy is currently used in patients with residual or recurrent
pituitary
adenomas
after surgery.
However, there is little information of long-term outcome of patients with
Cushing's disease
following radiotherapy.
We assessed the long-term efficacy and toxicity of conventional radiotherapy in the control of
Cushing's disease
after unsuccessful transsphenoidal surgery.
PATIENTS AND METHODS: Forty patients with
Cushing's disease
were treated with conventional external beam radiotherapy at our Institution between 1988 and 2002.
The persistence of active
disease
after surgery was diagnosed by the increased high plasma cortisol levels, high 24 h urinary cortisol levels and absence of cortisol suppression after administration of dexamethasone.
CONCLUSION: Radiotherapy is effective in the long-term tumour- and hormone hypersecretion control of
ACTH
-
secreting pituitary
adenomas
, however with a high prevalence of hypopituitarism.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ radiotherapy.
Adenoma
/ radiotherapy.
Neoplasm
Recurrence, Local / radiotherapy.
Neoplasm
, Residual / radiotherapy.
Pituitary
ACTH
Hypersecretion / radiotherapy
[MeSH-minor]
Adult.
Disease
-Free Survival. Female. Follow-Up Studies. Humans. Hydrocortisone / blood. Male. Middle Aged
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Clin Endocrinol (Oxf). 1989 Sep;31(3):309-23
[
2559823.001
]
(PMID = 17356896.001).
[ISSN]
0167-594X
[Journal-full-title]
Journal of neuro-oncology
[ISO-abbreviation]
J. Neurooncol.
[Language]
eng
[Publication-type]
Journal Article; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
WI4X0X7BPJ / Hydrocortisone
91.
Brito J, Sáez L, Lemp M, Liberman C, Michelsen H, Araya AV:
[Immunohistochemistry for pituitary hormones and Ki-67 in growth hormone producing pituitary adenomas].
Rev Med Chil
; 2008 Jul;136(7):831-6
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[Title]
[Immunohistochemistry for
pituitary
hormones and Ki-67 in growth hormone
producing
pituitary
adenomas
].
[Transliterated title]
Evaluación por inmunohistoquímica
de
la expresión
de
hormonas hipofisiarias y del marcador
de
proliferación celular Ki-67 en tejido
de adenomas
causantes
de
acromegalia.
BACKGROUND: Growth hormone (GH)
producing adenomas
, frequently express several hormones.
AIM: To measure the immunohistochemical hormone expression in
pituitary
adenomas
, excised from patients with acromegaly.
To determine if the plurihormonal condition of these
adenomas
is associated with a higher proliferative capacity, assessed through the expression of Ki-67.
MATERIAL AND METHODS: Forty one paraffin embedded surgical samples
of pituitary
adenomas
from patients with acromegalia were studied.
Immunohistochemistry for GH, prolactin (PRL), follicle stimulating hormone (FSH), luteinizing hormone (LH), thyroid stimulating hormone (TSH),
adrenocorticotropin
(
ACTH
) and for the expression of Ki-67 was carried out.
CONCLUSIONS: Half of GH
producing
pituitary
adenomas
are plurihormonal.
There are no differences in the expression of Ki-67 between mono and plurihormonal
adenomas
.
[MeSH-major]
Adenoma
/ metabolism. Growth Hormone-
Secreting Pituitary Adenoma
/ metabolism. Human Growth Hormone / metabolism. Ki-67 Antigen / metabolism.
Neoplasm
Proteins / metabolism.
Pituitary
Neoplasms / metabolism
[MeSH-minor]
Acromegaly / physiopathology. Acromegaly / surgery. Adrenocorticotropic Hormone / analysis. Adult. Aged. Female. Follicle Stimulating Hormone / analysis. Humans. Immunohistochemistry. Male. Middle Aged. Prolactin / analysis. Proliferating
Cell
Nuclear Antigen / analysis. Statistics, Nonparametric. Thyrotropin / analysis
MedlinePlus Health Information.
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.
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Corticotropin
.
Hazardous Substances Data Bank.
MENOTROPINS
.
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(PMID = 18949157.001).
[ISSN]
0034-9887
[Journal-full-title]
Revista médica de Chile
[ISO-abbreviation]
Rev Med Chil
[Language]
spa
[Publication-type]
English Abstract; Journal Article
[Publication-country]
Chile
[Chemical-registry-number]
0 / Ki-67 Antigen; 0 / Neoplasm Proteins; 0 / Proliferating Cell Nuclear Antigen; 12629-01-5 / Human Growth Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-62-4 / Prolactin; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin
92.
Teshima T, Hara Y, Shigihara K, Takekoshi S, Nezu Y, Harada Y, Yogo T, Teramoto A, Osamura RY, Tagawa M:
Coexistence of corticotroph adenoma and thyrotroph hyperplasia in a dog.
J Vet Med Sci
; 2009 Jan;71(1):93-8
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[Title]
Coexistence of
corticotroph
adenoma
and thyrotroph hyperplasia in a dog.
Pituitary
thyrotroph hyperplasia results from prolonged primary hypothyroidism in humans, mice and rats.
In dogs with
Cushing's disease
, many cases have low serum thyroid hormones concentrations due to euthyroid sick syndrome.
A 6-year-old castrated male Beagle diagnosed with
Cushing's disease
had a high serum thyroid stimulating hormone (TSH) concentration that was treated by hypophysectomy.
On histological examination, the resected
pituitary
gland
contained both a
corticotroph
adenoma
and thyrotroph hyperplasia.
The TSH-positive
cell
ratio in this case was greater than that of healthy Beagles.
In the present case,
the pituitary
thyrotroph hyperplasia was probably caused by primary hypothyroidism.
In conclusion, this Beagle is the first histological confirmation of the coexistence of a
corticotroph
adenoma
and thyrotroph hyperplasia.
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(PMID = 19194082.001).
[ISSN]
0916-7250
[Journal-full-title]
The Journal of veterinary medical science
[ISO-abbreviation]
J. Vet. Med. Sci.
[Language]
ENG
[Publication-type]
Case Reports; Journal Article
[Publication-country]
Japan
93.
Batista DL, Zhang X, Gejman R, Ansell PJ, Zhou Y, Johnson SA, Swearingen B, Hedley-Whyte ET, Stratakis CA, Klibanski A:
The effects of SOM230 on cell proliferation and adrenocorticotropin secretion in human corticotroph pituitary adenomas.
J Clin Endocrinol Metab
; 2006 Nov;91(11):4482-8
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[Title]
The effects of SOM230 on
cell
proliferation and
adrenocorticotropin
secretion in human
corticotroph
pituitary
adenomas
.
CONTEXT: There is no
tumor
-directed medical therapy available for
Cushing's disease
.
OBJECTIVE: The objective was to determine the in vitro effect of the somatostatin analog pasireotide (SOM230) on
cell
proliferation in human
corticotroph
tumors.
DESIGN/METHODS: Expression of somatostatin receptors (SSTR 1-5) was determined by quantitative RT-PCR in 13 human
corticotroph
tumors and by immunohistochemistry (IHC) in 12 of the 13 tumors.
SOM230 effects on
cell
proliferation and
ACTH
release were evaluated in vitro using primary cultures of six of the 13 human
corticotroph adenomas
.
RESULTS: In our series, we found expression of SSTR subtypes 1, 2, 4, and 5 in human
corticotroph
tumors by quantitative RT-PCR.
Significant suppression of
cell
proliferation was observed in all tumors cultured (percent suppression range: 10-70%; P = 0.045-0.001).
SOM230 inhibited
ACTH
secretion in five of the six tumors cultured (percent suppression range: 23-56%; P = 0.042-0.001).
CONCLUSION:
Corticotroph
tumors express multiple SSTR subtypes.
SOM230 significantly suppressed
cell
proliferation and
ACTH
secretion in primary cultures of human
corticotroph
tumors.
These in vitro results support the hypothesis that SOM230 may have a role in the medical therapy of
corticotroph
tumors.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ drug therapy.
Adenoma
/ drug therapy. Adrenocorticotropic Hormone / secretion.
Cell
Proliferation / drug effects. Somatostatin / analogs & derivatives
[MeSH-minor]
Adolescent. Adult. Child. Female. Humans. Immunohistochemistry. In Vitro Techniques. Male. Middle Aged.
Pituitary
ACTH
Hypersecretion / drug therapy. RNA, Messenger / metabolism. Receptors, Somatostatin / metabolism.
Tumor
Cells, Cultured
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Corticotropin
.
The Lens.
Cited by Patents in
.
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(PMID = 16940446.001).
[ISSN]
0021-972X
[Journal-full-title]
The Journal of clinical endocrinology and metabolism
[ISO-abbreviation]
J. Clin. Endocrinol. Metab.
[Language]
eng
[Grant]
United States / Intramural NIH HHS / /
[Publication-type]
Evaluation Studies; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
[Publication-country]
United States
[Chemical-registry-number]
0 / RNA, Messenger; 0 / Receptors, Somatostatin; 51110-01-1 / Somatostatin; 9002-60-2 / Adrenocorticotropic Hormone; 98H1T17066 / pasireotide
94.
Vila G, Papazoglou M, Stalla J, Theodoropoulou M, Stalla GK, Holsboer F, Paez-Pereda M:
Sonic hedgehog regulates CRH signal transduction in the adult pituitary.
FASEB J
; 2005 Feb;19(2):281-3
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[Title]
Sonic hedgehog regulates CRH signal transduction in the adult
pituitary
.
It is known to be involved in
pituitary
development, but its role in the adult
pituitary
has
not
been investigated.
Here, we show Shh and Gli1 immunoreactivity in adult human
corticotroph
cells.
Administration of Shh (5 microg/ml) alone and in combination with corticotrophin-releasing hormone (CRH; 100 nM) in dispersed rat anterior
pituitary
and AtT-20 mouse
corticotrophinoma
cells increased corticotrophin (
ACTH
) secretion and pro-opiomelanocortin (POMC) promoter activity.
Shh and CRH
act
additively in increasing CRH receptor 1 (CRH-R1).
Taken together, our results demonstrate a new role for Shh and Gli1 in
corticotroph
function and provide a new link between Shh and CRH signaling pathways.
[MeSH-major]
Corticotropin
-Releasing Hormone / physiology.
Pituitary
Gland
/ chemistry.
Pituitary
Gland
/ metabolism. Signal Transduction / physiology. Trans-Activators / physiology
[MeSH-minor]
Adrenocorticotropic Hormone / secretion. Adult. Animals.
Cell
Line,
Tumor
. Cells, Cultured. Hedgehog Proteins. Humans. Kruppel-Like Transcription Factors. Male. Mice. Pro-Opiomelanocortin / genetics. Rats. Rats, Sprague-Dawley. Transcription Factors / antagonists & inhibitors. Transcription Factors / metabolism. Transcription, Genetic / physiology
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.
The Lens.
Cited by Patents in
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(PMID = 15572433.001).
[ISSN]
1530-6860
[Journal-full-title]
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
[ISO-abbreviation]
FASEB J.
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / GLI1 protein, human; 0 / Gli protein, mouse; 0 / Gli protein, rat; 0 / Hedgehog Proteins; 0 / Kruppel-Like Transcription Factors; 0 / SHH protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 66796-54-1 / Pro-Opiomelanocortin; 9002-60-2 / Adrenocorticotropic Hormone; 9015-71-8 / Corticotropin-Releasing Hormone
95.
Kovacs K, Horvath E, Coire C, Cusimano M, Smyth H, Scheithauer BW, Lloyd RV:
Pituitary corticotroph hyperplasia preceding adenoma in a patient with Nelson's syndrome.
Clin Neuropathol
; 2006 Mar-Apr;25(2):74-80
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[Title]
Pituitary
corticotroph
hyperplasia preceding
adenoma
in a patient with Nelson's syndrome.
We report the case of a 42-year-old woman with
Cushing's disease
and Nelson's syndrome.
A detailed morphologic study demonstrated nodular hyperplasia of
corticotroph
cells but no
adenoma
.
Following a long-lasting remission (14 years),
Cushing's disease
recurred.
After an unsuccessful second transsphenoidal surgery,
Cushing's disease
persisted and both adrenals were removed (at the age of 34).
The pituitary
tumor
proved to be a
corticotroph
adenoma
; it was removed by the transsphenoidal approach (at the age of 42).
Although in most patients
Cushing's disease
is due to an
ACTH
-
secreting pituitary
corticotroph
adenoma
which precedes the manifestation of Nelson's syndrome, our case indicates
not
only that
corticotroph
hyperplasia may cause
Cushing's disease
but that it may exist before the development of Nelson's syndrome after the removal of both adrenals.
Our study supports the view that protracted stimulation of corticotrophs resulting from the elimination of the negative inhibitory feedback effect by corticosteroids plays a role in
adenoma
initiation.
[MeSH-major]
ACTH
-
Secreting Pituitary Adenoma
/ etiology.
Adenoma
/ etiology. Hyperplasia / complications. Nelson Syndrome / etiology.
Pituitary
ACTH
Hypersecretion / complications
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(PMID = 16550740.001).
[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
96.
Erickson D, Scheithauer B, Atkinson J, Horvath E, Kovacs K, Lloyd RV, Young WF Jr:
Silent subtype 3 pituitary adenoma: a clinicopathologic analysis of the Mayo Clinic experience.
Clin Endocrinol (Oxf)
; 2009 Jul;71(1):92-9
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[Title]
Silent subtype 3
pituitary adenoma
: a clinicopathologic analysis of the Mayo Clinic experience.
BACKGROUND: Macroadenomas represent 50%
of pituitary
tumours and are often (30%) nonfunctioning.
Their immunophenotype suggests differentiation toward a specific
pituitary
cell
line.
A substantial proportion of tumours with particularly aggressive behaviour are so called 'silent subtype 3
adenoma
'.
Its
diagnosis
requires ultrastructural confirmation.
Although once included among silent
corticotroph adenomas
, this aggressive, morphologically distinctive tumour is now recognized as a major form of plurihormonal
adenoma
and, in fact, some patients might present with clinical hormonal excess.
The cytogenesis and pathobiology of silent subtype 3
adenomas
is unsettled.
DESIGN: This retrospective, single institution study found 27 confirmed examples of silent subtype 3
adenoma
, a frequency of 0.9% of
adenomas
.
RESULTS: The study group was comprised of 16 men (59%) and 11 women (41%); two patients (7%) had definitive
diagnosis
of multiple endocrine neoplasia type 1 (MEN1).
Most tumours were plurihormonal, featuring immunoreactivity for PRL (17), GH (15), TSH (16) or
ACTH
(3); only one lesion was immunonegative.
CONCLUSION: Silent subtype 3
adenoma
, a plurihormonal tumour, is rare and aggressive in nature.
This
adenoma
must be considered in the differential of often clinically nonfunctioning but plurihormonal
adenomas
featuring variable cytologic atypia.
Electron microscopy is required for confirmation of the
diagnosis
.
The cytogenesis of silent subtype 3
adenoma
remains unsettled.
[MeSH-major]
Pituitary
Neoplasms / pathology
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(PMID = 19170710.001).
[ISSN]
1365-2265
[Journal-full-title]
Clinical endocrinology
[ISO-abbreviation]
Clin. Endocrinol. (Oxf)
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
England
[Chemical-registry-number]
0 / Hormones
97.
Iino K, Oki Y, Matsushita F, Yamashita M, Hayashi C, Miura K, Nishizawa S, Nakamura H:
Immunohistochemical properties of silent corticotroph adenoma and Cushing's disease.
Pituitary
; 2007;10(1):35-45
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[Title]
Immunohistochemical properties of silent
corticotroph
adenoma
and
Cushing's disease
.
Proopiomelanocortin processing in
corticotroph
cells is known to be operated by prohormone convertase (PC) 1/3 which is activating several pro-proteins and prohormones by intracellular limited proteolysis processing.
In this study, we hypothesized that PC1/3 expression differs between
Cushing's disease
(CD) and silent
corticotroph
adenoma
(SCA), and investigated whether PC1/3 expression is involved in
the adrenocorticotropin
(
ACTH
) silence of SCA.
We performed immunohistochemical analysis
of pituitary adenoma
specimens for six adenohypophysial hormones, PC1/3 and chromogranin A (CgA).
Subjects for this study consisted of 12 anterior
pituitary
adenomas
of CD (1 male, 11 female; 14-70 years old) and 31 non-functioning
adenomas
(23 male, 8 female; 32-71 years old).
ACTH
immunoreactivity was observed in all of CD and three of 31 non-functioning
adenomas
.
Cushing's adenomas
and SCAs were all positive for PC1/3.
PC1/3-positive cells did
not
always colocalize with
ACTH
but some of them colocalized with CgA in SCAs.
Even if PC1/3 is
not
present in
corticotroph
cells, PC1/3 immunoreactivity in SCA may originate from CgA-positive cells.
We conclude that immunohistochemistry for PC1/3 is
not
helpful for differential
diagnosis
between CD and SCA in clinical practice, though the regulation of PC1/3 expression is likely to be an important etiological factor in
ACTH
silence of SCA.
The diversity of immunohistochemical properties of SCA leads us to speculate that it is
not
a single entity and may be a general diagnostic term for
adenomas
of varying etiology.
[MeSH-major]
Adenoma
/ metabolism.
Pituitary
ACTH
Hypersecretion / metabolism.
Pituitary
Neoplasms / metabolism
[MeSH-minor]
Adolescent. Adrenocorticotropic Hormone / metabolism. Adult. Aged. Chromogranin A / blood.
Corticotropin
-Releasing Hormone. Female. Follicle Stimulating Hormone / metabolism. Gonadotropin-Releasing Hormone. Growth Hormone-Releasing Hormone. Human Growth Hormone / metabolism. Humans. Immunohistochemistry. Male. Middle Aged. Proprotein Convertases / blood. Thyrotropin
MedlinePlus Health Information.
consumer health - Pituitary Tumors
.
Hazardous Substances Data Bank.
Corticotropin
.
Hazardous Substances Data Bank.
MENOTROPINS
.
NCI CPTC Antibody Characterization Program.
NCI CPTC Antibody Characterization Program
.
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[ISSN]
1386-341X
[Journal-full-title]
Pituitary
[ISO-abbreviation]
Pituitary
[Language]
eng
[Publication-type]
Journal Article
[Publication-country]
United States
[Chemical-registry-number]
0 / Chromogranin A; 12629-01-5 / Human Growth Hormone; 33515-09-2 / Gonadotropin-Releasing Hormone; 9002-60-2 / Adrenocorticotropic Hormone; 9002-68-0 / Follicle Stimulating Hormone; 9002-71-5 / Thyrotropin; 9015-71-8 / Corticotropin-Releasing Hormone; 9034-39-3 / Growth Hormone-Releasing Hormone; EC 3.4.21.- / Proprotein Convertases
98.
Swords FM, Monson JP, Besser GM, Chew SL, Drake WM, Grossman AB, Plowman PN:
Gamma knife radiosurgery: a safe and effective salvage treatment for pituitary tumours not controlled despite conventional radiotherapy.
Eur J Endocrinol
; 2009 Dec;161(6):819-28
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[Title]
Gamma knife radiosurgery: a safe and effective salvage treatment for
pituitary
tumours
not
controlled despite conventional radiotherapy.
OBJECTIVE: We report the use of 'gamma knife' (GK) radiosurgery in 25 patients with
pituitary
adenomas not
cured despite conventional therapy, including external beam radiotherapy.
PATIENTS AND METHODS: All patients had previously received conventional radiotherapy for a mean of 11.8 years prior to receiving GK; 23 out of 25 had also undergone
pituitary
surgery on at least one occasion.
Seventeen had hyperfunctioning
adenomas
that still required medical therapy without an adequate biochemical control--ten somatotroph
adenomas
, six
corticotroph adenomas
and one prolactinoma, while eight patients had non-functioning
pituitary
adenomas
(NFPAs).
A total of 75% NFPAs showed
disease
stabilisation or shrinkage post GK.
The results in
corticotroph adenomas
were variable.
Prior to GK, 72% of the patients were panhypopituitary, and 42% of the remainder have developed new anterior
pituitary
hormone deficiencies to date.
CONCLUSIONS: These data indicate that GK is a safe and effective adjunctive treatment for patients with NFPAs and acromegaly
not
satisfactorily controlled with surgery and radiotherapy.
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(PMID = 19773368.001).
[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]
12629-01-5 / Human Growth Hormone; 67763-96-6 / Insulin-Like Growth Factor I
99.
Moyes VJ, Alusi G, Sabin HI, Evanson J, Berney DM, Kovacs K, Monson JP, Plowman PN, Drake WM:
Treatment of Nelson's syndrome with temozolomide.
Eur J Endocrinol
; 2009 Jan;160(1):115-9
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