|
Metabolic Bone Disorder
|
0.300 |
Biomarker
|
group |
CTD_human |
Skeletal Mineralization Deficits and Impaired Biogenesis and Function of Chondrocyte-Derived Matrix Vesicles in Phospho1(-/-) and Phospho1/Pi t1 Double-Knockout Mice.
|
26773408 |
2016 |
|
Osteopenia
|
0.300 |
Biomarker
|
disease |
CTD_human |
Skeletal Mineralization Deficits and Impaired Biogenesis and Function of Chondrocyte-Derived Matrix Vesicles in Phospho1(-/-) and Phospho1/Pi t1 Double-Knockout Mice.
|
26773408 |
2016 |
|
Liver Cirrhosis, Experimental
|
0.300 |
Biomarker
|
disease |
CTD_human |
Systems level analysis and identification of pathways and networks associated with liver fibrosis.
|
25380136 |
2014 |
|
Aortic valve calcification
|
0.300 |
Biomarker
|
disease |
CTD_human |
High expression of the Pi-transporter SLC20A1/Pit1 in calcific aortic valve disease promotes mineralization through regulation of Akt-1.
|
23308213 |
2013 |
|
Endometriosis
|
0.300 |
Biomarker
|
disease |
CTD_human |
Unique transcriptome, pathways, and networks in the human endometrial fibroblast response to progesterone in endometriosis.
|
20864642 |
2011 |
|
Endometrioma
|
0.300 |
Biomarker
|
disease |
CTD_human |
Unique transcriptome, pathways, and networks in the human endometrial fibroblast response to progesterone in endometriosis.
|
20864642 |
2011 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This disorder is associated with a thymoma or neoplasm that ectopically expresses PIT-1 protein.
|
31513261 |
2020 |
|
Adenoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We discussed the 2 published cases and describe another case of poorly-differentiated plurihormonal PIT-1 positive adenoma with moderate SSTR2 expression and intense STTR5 expression succeffuly treated with PAS-LAR 40mg/month.
|
31167164 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Through the release of CXCL12, Pit-1 in tumor cells was found to mediate the recruitment and polarization of macrophages into tumor-associated macrophages (TAMs).
|
31292963 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Following surgery, pathology revealed a collision tumor; the dominant lesion was positive for GH, βTSH, βFSH, and αSU and expressed both Pit-1 and SF-1.The smaller lesion was a corticotroph tumor.
|
30610567 |
2019 |
|
Adenoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
SSTR2A expression was higher compared to gonadotroph and nonfunctioning pituitary adenomas (<i>p</i> = 0.0217 and 0.0126, respectively) while PIT-1-positive adenomas showed even higher SSTR2A expression (<i>p</i> < 0.0001).
|
30627156 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Diagnosis is invariably made post-operatively of a tumor immunopositive for GH (and Pit-1 in selected cases) but without clinical acromegaly.
|
29305680 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Knock-down of CXCR4 reduces tumor growth and spread of Pit-1 overexpressing cells in a zebrafish xenograft model.
|
29321662 |
2018 |
|
Panhypopituitarism
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We also found combinations of de novo (SLC20A1/SLC15A4) and transmitted variants (GLI2/LHX3) in the same individuals, leading to the full-blown CPHD phenotype.
|
29261175 |
2018 |
|
Adenoma
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data suggests that Pit-1 can be utilized as a second tier immunostain in cases of clinically non-functioning adenomas that are immunonegative for ACTH, prolactin, growth hormone, TSH, and SF-1 in order to further segregate rare cases of Pit-1-positive adenomas from null cell adenomas.
|
28994039 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Additionally, Pit-1 expression was reduced in the ACTH-positive cells from tumor tissue primary culture.
|
28865461 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Increased expression of Pit-1 was detected in the tumor tissues compared with the normal tissues (1.086 vs. 0.541) and the abnormal expression was associated with tumor size, clinical stage, tumor grade, and lymph node metastasis (P<0.05).
|
27798557 |
2016 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Administration of 1α, 25-dihydroxy-3-epi-vitamin D3 (3-Epi, an endogenous low calcemic vitamin D metabolite) reduced Pit-1 expression, and synergized with cisplatin, thus, decreasing cell proliferation and apoptosis in vitro, and reducing tumor growth in vivo.
|
25992773 |
2015 |
|
Panhypopituitarism
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
To test the role of wtPIT-1 (PITWT) or PIT-1 (R271W) (PIT271) in somatolactotroph cells, we established, using inducible lentiviral vectors, sublines of GH4C1 somatotroph cells that allow the blockade of the expression of endogenous PIT-1 and/or the expression of PITWT or PIT271, a dominant negative mutant of PIT-1 responsible for Combined Pituitary Hormone Deficiency in patients.
|
25822178 |
2015 |
|
Panhypopituitarism
|
0.100 |
Biomarker
|
disease |
BEFREE |
Anti-PIT-1 (pituitary-specific transcription factor 1) antibody syndrome is a novel clinical entity that presents an acquired combined pituitary hormone deficiency characterized by a specific defect in growth hormone, prolactin, and thyroid-stimulating hormone.
|
25962206 |
2015 |
|
Adenoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Interestingly, these adenomas showed very high expression levels of PIT1, a transcriptional factor that regulates the gene expression of Gh, Prl, Ghrhr and Pit1 itself, playing a key role in pituitary gland development and physiology.
|
22199144 |
2012 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The Pit-1/Pou1f1 transcription factor regulates and correlates with prolactin expression in human breast cell lines and tumors.
|
19808898 |
2010 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In patients with invasive ductal carcinoma of the breast and node-positive tumor, high expression of Pit-1 was significantly correlated with Snai1 positivity.
|
21060149 |
2010 |
|
Adenoma
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The functional differentiation of pituitary cells and adenomas follows the combination of transcription factors and co-factors in three cell lineages [growth hormone-prolactin-thyroid-stimulating hormone lineage, adrenocorticotrophic hormone (ACTH)/pro-opiomelanocortin (POMC) lineage, and follicular stimulating hormone (FSH)/luteinizing hormone (LH) lineage], which include Pit-1, GATA-2, SF-1, NeuroD1/beta2, Tpit, ERalpha, and others.
|
18228160 |
2008 |
|
Panhypopituitarism
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The genetic form of CPHD may originate from mutations in pituitary transcription factor (PTF) genes and the pituitary image in these cases may give a clue of what PTF is most probably mutated: defects in LHX4 are usually associated with ectopic posterior pituitary (EPP); defects in LHX3, PIT1, and PROP1, with normally placed posterior pituitary (NPPP); HESX1 mutations are associated with both.
|
18157385 |
2007 |