The role of microRNA genes in papillary thyroid carcinoma.
By Huiling He, K. Jażdżewski, Wei Li, S. Liyanarachchi, R. Nagy, Stefano Volinia, George A. Calin, Chang-Gong Liu, K. Franssila, S. Suster and 3 more. Proceedings of the National Academy of Sciences of the United States of America, 2005
1,259 citations recorded by the source corpus.
Subfields: Cancer Research, Endocrinology, Diabetes and Metabolism, Mechanical Engineering
View Paper: https://www.semanticscholar.org/paper/001c41c640543a02eb1cf2aa978093d80f719620
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In Cancer Research
- Carlo Maria Croce
- George A. Calin
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In Endocrinology, Diabetes and Metabolism
Citations in the corpus
- Common SNP in pre-miR-146a decreases mature miR expression and predisposes to papillary thyroid carcinoma (2008, methodology): “We and others have described several microRNAs showing transcriptional up-regulation in PTC tumors, the most striking being a 19-fold increase in the quantity of miR-146 (17, 18).”
- MiRNA-Directed Regulation of VEGF and Other Angiogenic Factors under Hypoxia (2006, neutral): “html) [25,26].”
- miR-221 overexpression contributes to liver tumorigenesis (2009, background): “The cyclin-dependent kinase inhibitor p27 (Kip1-CDKN1B) and the tyrosine-kinase receptor c-kit have been identified as targets of miR-221 and miR-222 (9, 10).”
- OncomiRs: the discovery and progress of microRNAs in cancers (2007, background): “Sequence changes in genes targeted by these miRNAs could contribute to the regulation of Kit involved in PTC pathogenesis [27].”
- MicroRNA expression profiling in human ovarian cancer: miR-214 induces cell survival and cisplatin resistance by targeting PTEN. (2008, background): “Subsequently, miRNA deregulation was detected in other human malignancies, including breast carcinoma (4, 5), primary glioblastoma (6, 7), lung cancer (8), papillary thyroid carcinoma (9), colon carcinoma (10), and pancreatic tumors (11, 12).”
- A small piece in the cancer puzzle: microRNAs as tumor suppressors and oncogenes (2006, methodology): “Direct evidence demonstrating in vivo oncogenic activity of the mir-17 cluster was provided by the Hannon, Hammond and Lowe laboratories (He et al., 2005b).”
- microRNAs as oncogenes and tumor suppressors. (2007, background): “Compared with normal tissues, the expression of mir- 17–92 is significantly increased in several cancer types, including lung cancer and lymphomas, especially in their most aggressive forms, such as small-cell lung cancer and human B-cell lymphomas (Hayashita et al., 2005; He et al., 2005b).”
- Reprogramming of miRNA networks in cancer and leukemia. (2010, neutral): “GSE8126 and GSE7055 (Ambs et al. 2008), GSE17155 (Fassan et al. 2009), GSE3467 (He et al. 2005), GSE7828 (Schetter et al. 2008), GSE6857 (Budhu et al. 2008), GSE16654 (Chin et al. 2009), and GSE14936 (Seike et al. 2009), and at ArrayExpress (www.ebi.ac.uk/microarray-as/ae) under accession nos.”
- MicroRNA-cancer connection: the beginning of a new tale. (2006, background): “Thyroid cancers in which the up-regulation of miR-221, miR-222 , and miR-146 was the strongest showed dramatic loss of KIT oncogene and, in half of the cases, the downregulation was associated with germ-line single-nucleotide polymorphisms in the two recognition sites in KIT for these three miRNAs (”
- MicroRNAs: key players in the immune system, differentiation, tumorigenesis and cell death (2008, background): “In contrast to miR-15/miR-16, whose expression is often reduced in cancers, the miR-17-92 cluster is overexpressed in many cancers including B-cell lymphoma (Ota et al., 2004; Hayashita et al., 2005; He et al., 2005b).”
- MiR-221 controls CDKN1C/p57 and CDKN1B/p27 expression in human hepatocellular carcinoma (2008, background): “, 2007), papillary tumors of the thyroid (He et al., 2005) and pancreatic cancer (Lee et al.”
- Molecular genetics and diagnosis of thyroid cancer (2011, background): “Many miRNAs have been found to be deregulated in thyroid cancer”
- MicroRNA signatures in human cancers (2006, background): “Furthermore, the role of polymorphisms in the complementary sites of target mRNAs in cancer patient”