3 results match your criteria: "USA Institute of Pathology[Affiliation]"
MYC regulates the antitumor immune response through CD47 and PD-L1.
Science
April 2016
Division of Oncology, Departments of Medicine and Pathology, Stanford University School of Medicine, Stanford, CA 94305, USA.
The MYC oncogene codes for a transcription factor that is overexpressed in many human cancers. Here we show that MYC regulates the expression of two immune checkpoint proteins on the tumor cell surface: the innate immune regulator CD47 (cluster of differentiation 47) and the adaptive immune checkpoint PD-L1 (programmed death-ligand 1). Suppression of MYC in mouse tumors and human tumor cells caused a reduction in the levels of CD47 and PD-L1 messenger RNA and protein.
View Article and Find Full Text PDFp27 variant and corticotropinoma susceptibility: a genetic and in vitro study.
Endocr Relat Cancer
June 2014
Endocrine Genetics Unit LIM-25 Neuroendocrinology Unit Adrenal Unit (LIM-42) Experimental Oncology Laboratory (LIM-24), School of Medicine, Hospital das Clinicas, University of Sao Paulo, Sao Paulo, Brazil Nursing School School of Public Health, University of Sao Paulo, Sao Paulo, Brazil Endocrinology Division, Santa Casa Hospital, Sao Paulo, Brazil Brigadeiro Hospital, Sao Paulo, Brazil Federal University of Sao Paulo, Sao Paulo, Brazil Human Genome Research Center Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, Sao Paulo, Brazil Instituto do Cérebro, Instituto Israelita de Ensino e Pesquisa Albert Einstein, Sao Paulo, Brazil National Institute of Aging, National Institutes of Health (NIH), Bethesda, Maryland, USA Institute of Pathology, Helmholtz Zentrum München, Neuherberg, Germany.
Germline mutations in p27(kip1) are associated with increased susceptibility to multiple endocrine neoplasias (MEN) both in rats and humans; however, the potential role of common polymorphisms of this gene in endocrine tumor susceptibility and tumorigenesis remains mostly unrecognized. To assess the risk associated with polymorphism rs2066827 (p27-V109G), we genotyped a large cohort of Brazilian patients with sporadic endocrine tumors (pituitary adenomas, n=252; pheochromocytomas, n=125; medullary thyroid carcinoma, n=51; and parathyroid adenomas, n=19) and 885 population-matched healthy controls and determined the odds ratios and 95% CIs. Significant associations were found for the group of patients with pituitary adenomas (P=0.
View Article and Find Full Text PDFMicroRNA profile of poorly differentiated thyroid carcinomas: new diagnostic and prognostic insights.
J Mol Endocrinol
April 2014
Department of Pathology and Laboratory Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania 15213, USA Institute of Pathology, University of Bern, Murtenstrasse 31, 3010 Bern, Switzerland Institute of Surgical Pathology, University Hospital Zurich, 8091 Zurich, Switzerland Institute of Surgical Pathology, Triemlispital Zurich, 8063 Zurich, Switzerland.
The diagnosis of conventional and oncocytic poorly differentiated (oPD) thyroid carcinomas is difficult. The aim of this study is to characterise their largely unknown miRNA expression profile and to compare it with well-differentiated thyroid tumours, as well as to identify miRNAs which could potentially serve as diagnostic and prognostic markers. A total of 14 poorly differentiated (PD), 13 oPD, 72 well-differentiated thyroid carcinomas and eight normal thyroid specimens were studied for the expression of 768 miRNAs using PCR-Microarrays.
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