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1 itary adenomas (NFPAs) are the most frequent pituitary tumors.
2 us sinus fistulae, parasellar syndromes, and pituitary tumors.
3 posed as novel oral medications for managing pituitary tumors.
4 rmone receptor PPAR-gamma in all of 39 human pituitary tumors.
5 role for selective antiestrogens in treating pituitary tumors.
6 -378 RB-producing ES cells failed to develop pituitary tumors.
7 tiation and increases the susceptibility for pituitary tumors.
8 of human anterior pituitary cells and human pituitary tumors.
9 al cell proliferation, and susceptibility to pituitary tumors.
10 ce and increased penetrance of hGHRH-induced pituitary tumors.
11 pressed in malignant human cell lines and in pituitary tumors.
12 e utility of this tracer in the detection of pituitary tumors.
13 the recently proposed genetic treatments for pituitary tumors.
14 ous role for these cells in the induction of pituitary tumors.
15 fects in the Rb gene are not common in human pituitary tumors.
16 44) rat induces growth of large, hemorrhagic pituitary tumors.
17 product occurs at a high frequency in human pituitary tumors.
18 tiple parathyroid, pancreatic, duodenal, and pituitary tumors.
19 CTH) and adrenal steroid secretion caused by pituitary tumors.
20 potential to improve care for patients with pituitary tumors.
21 adenomas compared with that in nonsecreting pituitary tumors.
22 Gli function may contribute to these common pituitary tumors.
23 anding mechanisms underlying uniquely benign pituitary tumors.
24 was significantly reduced due to aggressive pituitary tumors.
25 expressed in a specific cell-type manner in pituitary tumors.
26 statin ligand design to treat ACTH-secreting pituitary tumors.
27 gnostic and potential therapeutic targets in pituitary tumors.
28 sible therapeutic target in the treatment of pituitary tumors.
29 Gal-3 in the development and progression of pituitary tumors.
32 ter, white matter, gliomas, meningiomas, and pituitary tumors, allowing their ready discrimination by
33 l pituitaries; however, in a small number of pituitary tumors analysed, 11 beta-HSD2 was readily demo
34 dentified a miRNA signature for GH-producing pituitary tumors and found that miR-26b and miR-128 regu
35 of mRNA for 11 beta-HSD1 and 2 in 105 human pituitary tumors and have performed enzyme expression an
36 types of normal anterior pituitary cells and pituitary tumors and in other neuroendocrine cells and t
39 chanism of silencing of the p27 gene in some pituitary tumors and possibly in other types of neoplasm
41 review current research in the treatment of pituitary tumors and summarize emerging medical, surgica
42 ads to an overall increase in animal growth, pituitary tumors, and hyperplasia of hematopoietic organ
44 total number of reproductive system tumors, pituitary tumors, and metastases was increased in the of
45 ent therapy can generate menin expression in pituitary tumors, and significantly reduce tumor cell pr
47 drenocorticotrophic hormone (ACTH)-secreting pituitary tumors are associated with high morbidity due
48 dels of these neoplasms simply do not exist: pituitary tumors are common in rodents, but their histol
55 hown to significantly reduce the severity of pituitary tumors arising in Rb1(+/-) animals by enhancin
56 o investigate the expression of p16 in human pituitary tumors as an indirect mechanism of Rb inactiva
60 beta-catenin in Sox2(+) cells gives rise to pituitary tumors, but, unexpectedly, the tumor mass is n
62 cate that the suppression of pars intermedia pituitary tumors by p27(Kip1) is cell-autonomous and doe
63 stioned the mechanism of Gal-3 expression in pituitary tumors, by using methylation-specific PCR and
65 identified that miR-26b and miR-128 affected pituitary tumor cell behavior through regulation of thei
66 genesis we treated primary rat pituitary and pituitary tumor cell cultures with recombinant FGF-4 and
72 hibits the growth and DNA synthesis of mouse pituitary tumor cells and human choriocarcinoma cells.
73 ETS-2 repressor factor (ERF) is expressed in pituitary tumor cells and that overexpression of recombi
74 (p27) protein in rat GH3 and mouse GHRH-CL1 pituitary tumor cells compared with normal pituitary (NP
75 aneuploid GH-secreting cells, and GH(3) rat pituitary tumor cells overexpressing PTTG also exhibited
78 enesis and/or proliferation, and 3) cultured pituitary tumor cells respond to TGF-beta1 and PKC inhib
79 ctin promoter to dopamine was examined using pituitary tumor cells stably expressing dopamine D2 rece
80 e cell cycle and apoptotic response of these pituitary tumor cells to the dopamine analog bromocripti
81 ta-HCH occurs in estrogen-responsive GH3 rat pituitary tumor cells transfected with a luciferase repo
82 nsforming gene (PTTG1) was isolated from rat pituitary tumor cells, and subsequently identified as a
83 rat somatolactotroph, and murine gonadotroph pituitary tumor cells, and suppressed in vitro hormone s
93 nally discovered in a subpopulation of human pituitary tumors characterized by their invasive phenoty
96 fe-threatening disorder attributed to excess pituitary tumor-derived adrenocorticotrophic hormone (AC
97 e PAs and in the (nonfunctioning) HP75 human pituitary tumor-derived cell line treated with phorbol-1
103 oci reside on chromosome 6 [Estrogen-induced pituitary tumor (Ept)1], chromosome 3 (Ept2 and Ept6), c
104 cognized that most clinically nonfunctioning pituitary tumors express gonadotropin hormones or their
106 near-real-time detection and delineation of pituitary tumors for intraoperative surgical decision-ma
107 ulating the PTEN-AKT pathway in GH-producing pituitary tumor formation in the context of hyperplasia
108 We have identified a 17-miRNA signature of pituitary tumors formed in the background of hyperplasia
111 he role of p185(her2/neu)/ErbB3 signaling in pituitary tumor function, we examined these receptors in
113 on therapy and stereotactic radiosurgery for pituitary tumors gains more widespread use, long-term da
115 K+ (I(K)) and Ca++ currents in rat anterior pituitary tumor (GH3) cells were analyzed by using a who
116 and circulating sex steroid hormones promote pituitary tumor growth and expansion into large invasive
118 Aneuploid pituitary cell p21 may constrain pituitary tumor growth, thus accounting for the very low
121 land and induce development of PRL-producing pituitary tumors in certain inbred rat strains but not o
123 orm aggressive growth-hormone (GH)-producing pituitary tumors in the background of hyperplasia caused
124 i-estrogens reduced PTTG expression in human pituitary tumors in vitro and suppressed experimental tu
125 pression of sigma-1 receptors in spontaneous pituitary tumors is detected as an increase in uptake an
126 MP-dependent protein kinase pathway in human pituitary tumors; it also reviews briefly other pathways
127 cretion and ablation or stabilization of the pituitary tumor mass lead to improved comorbidities and
128 ty of therapeutic radiation in patients with pituitary tumor, medulloblastoma, and arteriovenous malf
129 e drugs are introduced for the management of pituitary tumors, more patients with hormone-secreting a
132 eclinical evaluation of MEN1 gene therapy in pituitary tumors of Men1(+/-) mice, using a recombinant
133 These symptoms were not associated with pituitary tumors or multiple endocrine neoplasia but wer
136 racrine growth factor-mediated mechanism for pituitary tumor pathogenesis and potentially other estro
137 pituitary carcinomas that may contribute to pituitary tumor pathogenesis and/or proliferation, and 3
140 undetectable levels of p16 mRNA in 13 of 14 pituitary tumors relative to 5 normal pituitary specimen
148 E2F3 loss suppresses the development of the pituitary tumors that normally account for the death of
149 rbB receptor family members are expressed in pituitary tumors, the effects of EGF signaling on pituit
154 ly, we cloned and sequenced cDNA of a potent pituitary tumor transforming gene (PTTG) from human test
161 transgenic zebrafish with overexpression of pituitary tumor transforming gene (PTTG/securin) targete
167 n was also independently identified as PTTG (pituitary tumor transforming gene), a gene overexpressed
177 identical to the product of the gene called pituitary tumor-transforming gene (PTTG), which is overe
178 revealed that known tumor promoters such as pituitary tumor-transforming gene were activated and tum
179 It is also known as the product of the human pituitary tumor-transforming gene, pttg, a proto-oncogen
180 y proliferation to study the pathogenesis of pituitary tumors, we crossed the glycoprotein hormone al
182 H4C1 cells, a clonal line derived from a rat pituitary tumor, were stably transfected with the gene e
183 16 gene product was undetectable in 25 human pituitary tumors, whereas high levels of p16 could be de
185 ice heterozygous for the Rb mutation develop pituitary tumors, with about 20% arising from the AL.
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