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Roger Gejman

Researcher at Pontifical Catholic University of Chile

Publications -  21
Citations -  1580

Roger Gejman is an academic researcher from Pontifical Catholic University of Chile. The author has contributed to research in topics: Adenoma & Pituitary adenoma. The author has an hindex of 10, co-authored 21 publications receiving 1449 citations. Previous affiliations of Roger Gejman include Harvard University & Centre national de la recherche scientifique.

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Activation of p53 by MEG3 non-coding RNA.

TL;DR: It is found that transfection of expression constructs for MEG3 and its isoforms results in a significant increase in p53 protein levels and dramatically stimulates p 53-dependent transcription from a p53-responsive promoter, supporting the concept that M EG3 functions as a non-coding RNA.
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Maternally Expressed Gene 3, an Imprinted Noncoding RNA Gene, Is Associated with Meningioma Pathogenesis and Progression

TL;DR: Data are consistent with the hypothesis that MEG3, which encodes a noncoding RNA, may be a tumor suppressor gene at chromosome 14q32 involved in meningioma progression via a novel mechanism.
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The effects of SOM230 on cell proliferation and adrenocorticotropin secretion in human corticotroph pituitary adenomas.

TL;DR: The hypothesis that somatostatin analog pasireotide (SOM230) may have a role in the medical therapy of corticotroph tumors is supported by in vitro results that significantly suppressed cell proliferation and ACTH secretion in primary cultures of human corticOTroph tumors.
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Role of Ki-67 proliferation index and p53 expression in predicting progression of pituitary adenomas☆

TL;DR: There was no significant difference between the 2 groups with regard to invasion, suprasellar extension, size, tumor type, postoperative radiotherapy, extent of resection, sex, and age.
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Lipophilic but not hydrophilic statins selectively induce cell death in gynaecological cancers expressing high levels of HMGCoA reductase

TL;DR: It is demonstrated that lipophilic but not hydrophilic statins induce cell death through activation of extrinsic and intrinsic apoptotic cascades in cancerous cells from the human female genital tract, which express high levels of HMG‐CoA reductase.