Relevant bibliographies by topics / MiR-17(similar to)92

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Academic literature on the topic 'MiR-17(similar to)92'

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Published: 4 June 2021
Last updated: 10 February 2022

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Journal articles on the topic "MiR-17(similar to)92"

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Khuu, Cuong, Tor Paaske Utheim, and Amer Sehic. "The Three Paralogous MicroRNA Clusters in Development and Disease, miR-17-92, miR-106a-363, and miR-106b-25." Scientifica 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/1379643.

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MicroRNAs (miRNAs) form a class of noncoding RNA genes whose products are small single-stranded RNAs that are involved in the regulation of translation and degradation of mRNAs. There is a fine balance between deregulation of normal developmental programs and tumor genesis. An increasing body of evidence suggests that altered expression of miRNAs is entailed in the pathogenesis of human cancers. Studies in mouse and human cells have identified the miR-17-92 cluster as a potential oncogene. The miR-17-92 cluster is often amplified or overexpressed in human cancers and has recently emerged as th
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Bi, Chengfeng, Chunsun Jiang, Xiaoxing Jiang, et al. "The Mir-17∼92 Cluster Activates mTORC1 Signaling in MCL by Targeting Multiple Regulators of the LKB1/AMPK/mTOR Pathway." Blood 120, no. 21 (2012): 5118. http://dx.doi.org/10.1182/blood.v120.21.5118.5118.

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Abstract Abstract 5118 Mantle cell lymphoma (MCL) is an aggressive hematological malignancy with a median survival ranging between 3 and 5 years. Novel therapeutic strategies are urgently needed to improve the outcome. Mammalian target of rapamycin (mTOR) pathway which plays a central role in controlling cell growth, proliferation and metabolism has been shown to be deregulated in MCL. mTOR inhibitors, such as rapamycin and its analogues, have been approved for treatment of relapsed/refractory MCL. However, the molecular mechanism of mTOR activation in MCL has yet to be defined. MiRNA (miR)-17
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Liao, Ya-Chun, Tzu-Heng Lin, Chih-Ying Chen, Shwu-Bin Lin, and Lo-Chun Au. "The Antileukemia Activity of Natural Product HQ17(3) Is Possibly Associated with Downregulation of miR-17-92 Cluster." BioMed Research International 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/306718.

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The compound 10′(Z),13′(E),15′(E)-heptadecatrienylhydroquinone [HQ17(3)] was purified from the sap of the lacquer treeRhus succedanea. HQ17(3) has cytotoxic effect on cancer cells and can inhibit topoisomerase (topo) IIαactivity. We treated various cancer cells with different doses of HQ17(3) and found that leukemia cells were most sensitive to HQ17(3). After analysis of microRNA (miRNA) profiling, we found that treatment with HQ17(3) caused downregulation of miR-17-92 cluster in some leukemia cells. These changes partially restored the normal levels from leukemia-specific miRNA expression sig
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Cao, H., W. Yu, X. Li, et al. "A new plasmid-based microRNA inhibitor system that inhibits microRNA families in transgenic mice and cells: a potential new therapeutic reagent." Gene Therapy 23, no. 6 (2016): 527–42. http://dx.doi.org/10.1038/gt.2016.22.

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Abstract Current tools for the inhibition of microRNA (miR) function are limited to modified antisense oligonucleotides, sponges and decoy RNA molecules and none have been used to understand miR function during development. CRISPR/Cas-mediated deletion of miR sequences within the genome requires multiple chromosomal deletions to remove all functional miR family members because of duplications. Here, we report a novel plasmid-based miR inhibitor system (PMIS) that expresses a new RNA molecule, which inhibits miR family members in cells and mice. The PMIS engineered RNA optimal secondary structu
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Robertus, Jan-Lukas, Miao Wang, Geert Harms, et al. "Differences in the C13orf25 miRNA Cluster in Non-Hodgkin Lymphoma and Normal B-Cell Subtypes." Blood 110, no. 11 (2007): 3586. http://dx.doi.org/10.1182/blood.v110.11.3586.3586.

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Abstract Introduction Amplification of chromosome 13q31 is a frequent occurrence in lymphoma and solid tumors. The C13orf25 gene at 13q31.3 is the primary miRNA transcript for seven miRNAs. This specific cluster of miRNAs is sequentially related to the homologous miR-106a-92 cluster on chromosome X and the miR-106b-25 cluster on chromosome 7. The miR17-92 cluster has been shown to be over expressed in various non-Hodgkin Lymphoma (NHL). As a specific group of miRNAs which are derived from the same primary miRNA transcript, each miRNA in the cluster may be expected to show a similar expression
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He, Ming, Bo Zhang, Qianqian Yin, Meng Guo, Qian Zhao, and Guo-Qiang Chen. "MicroRNA Expression Contributes to Hypoxia-Inducible Factor-1a-Induced Differentiation of Myeloid Leukemic Cells." Blood 114, no. 22 (2009): 1007. http://dx.doi.org/10.1182/blood.v114.22.1007.1007.

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Abstract Abstract 1007 Poster Board I-29 In our previous study, we showed that the hypoxia or hypoxia-mimetic agents induces differentiation of myeloid leukemic cells. During this event, hypoxia-inducible factor-1a (HIF-1a) exerts a critical role in its transcriptional activity-independent manner. MicroRNAs (miRNAs) regulate the expression of 30% of the transcripts of human genome on a posttranscriptional level. Recent work on miRNA has shed light on the possible involvement of miRNA genes in biological processes such as cell proliferation, differentiation and hematopoiesis. To reveal the miRN
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Mosakhani, Neda, Mohamed El Missiry, Emmi Vakkila, Päivi Heikkilä, Sakari Knuutila, and Jukka Vakkila. "Low Epression of MiR-18a Distinguishes Pediatric and Adult Acute Lymphoblastic Leukemia from Each Other." Blood 126, no. 23 (2015): 4991. http://dx.doi.org/10.1182/blood.v126.23.4991.4991.

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Abstract In several adult solid cancers the presence or absence of an inflammatory microenvironment has turned out to be an important prognostic factor. Acute lymphoblastic leukemia (ALL) is seen in both adults and children but the response to chemotherapy and survival is significantly worse in adults than children. Therefore, we wanted to study whether the expression of immune system associated molecular markers would be different in adult and pediatric ALL patients at the time of diagnosis. IDO and FOXP3 were studied from paraffin embedded tissue samples by immunohistochemistry in 12 pediatr
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Wang, Yi, Yaohui Tian, Zonghao Li, Zhaoke Zheng, and Liangliang Zhu. "miR-92 regulates the proliferation, migration, invasion and apoptosis of glioma cells by targeting neogenin." Open Medicine 15, no. 1 (2020): 283–91. http://dx.doi.org/10.1515/med-2020-0040.

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AbstractThis study aimed to explore the pathological mechanism in regulating glioma progression. The expression of miR-92 and neogenin was evaluated by qRT-PCR and western blot. Cell viability and apoptosis were measured by MTT and flow cytometry assays, respectively. The migration and invasion abilities were examined by transwell assays. The interaction between miR-92 and neogenin was conducted by dual-luciferase reporter system. As a result, we found that the expression of miR-92 was up-regulated in glioma tissues and cell lines. Down-regulation of miR-92 inhibited glioma cell proliferation,
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Souza, Felipe C., Josiane L. Schiavinato, Antonio R. Lucena-Araujo, et al. "High Aurora Kinase and Low Dido Levels Characterizes a Sub-Group of Chronic Lymphocytic Leukemia with Chromosomal Gains and High White Blood Cell Counts: Potential Inter-Regulatory Role of E2F1 and Mir-17-92 Cluster." Blood 128, no. 22 (2016): 2029. http://dx.doi.org/10.1182/blood.v128.22.2029.2029.

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Abstract During cell cycle division Aurora kinases (AURKA and AURKB) participate in the formation and control of mitotic spindle fibers, while, protein isoforms (DIDO1, DIDO2 and DIDO3), derived by alternative splicing of the DIDO gene, assist at the junction of microtubules to kinetochores. Thus, both are relevant to cell cycle maintenance. Interestingly, overexpression (or gain of function) of AURKs or low expression (or loss of function of DIDO) are both associated with centrosomal amplification and chromosomal instability (CIN), leading to aneuploidy. Among hematological diseases with CIN
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Bouska, Alyssa, Chengfeng Bi, Waseem Lone, et al. "Comprehensive Genomic Analysis of Adult Burkitt Lymphoma Identifies the B-Cell Receptor Signaling Pathway As a Potential Therapeutic Target." Blood 128, no. 22 (2016): 4095. http://dx.doi.org/10.1182/blood.v128.22.4095.4095.

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Abstract Burkitt lymphoma (BL) is the most common non-Hodgkin lymphoma (NHL) in children. Although it accounts for only 1-5% of NHL in adults, approximately 60% of the BL cases diagnosed each year in western countries occur in patients >40 years of age. Although adult and pediatric BL cases are indistinguishable by molecular classification, pediatric patients have a significantly better outcome than adults. While translocation of MYC to the immunoglobulin heavy or light chain genes is characteristic of pediatric and adult BL, genetic differences may contribute to the superior clinical outco
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Dissertations / Theses on the topic "MiR-17(similar to)92"

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Chen, Tianji, Qiyuan Zhou, Haiyang Tang, et al. "miR‐17/20 Controls Prolyl Hydroxylase 2 (PHD2)/Hypoxia‐Inducible Factor 1 (HIF1) to Regulate Pulmonary Artery Smooth Muscle Cell Proliferation." WILEY-BLACKWELL, 2016. http://hdl.handle.net/10150/622697.

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Background-Previously we found that smooth muscle cell (SMC)-specific knockout of miR-17 similar to 92 attenuates hypoxia-induced pulmonary hypertension. However, the mechanism underlying miR-17 similar to 92-mediated pulmonary artery SMC (PASMC) proliferation remains unclear. We sought to investigate whether miR-17 similar to 92 regulates hypoxia-inducible factor (HIF) activity and PASMC proliferation via prolyl hydroxylases (PHDs). Methods and Results-We show that hypoxic sm-17 similar to 92(-/-) mice have decreased hematocrit, red blood cell counts, and hemoglobin contents. The sm-17 simila
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Fuziwara, Cesar Seigi. "Influência do MicroRNA let-7 e miR-17-92 como oncomiRs no câncer." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-27092010-152352/.

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No câncer, alterações em microRNAs (miRNAs), pequenos RNAs que regulam a tradução protéica, exerce efeito oncogênico (oncomiR). Os oncomiRs regulam genes chave para a proliferação celular e apoptose, sendo importantes para a biologia do câncer. O carcinoma papilífero de tiróide apresenta alterações genéticas alinhadas na via MAPK (RET>RAS>BRAF>ERK). Observamos que a indução do oncogene RET/PTC diminui a expressão de let-7 em células foliculares tiroidianas. Na linhagem TPC-1 (com RET/PTC-1), a introdução de let-7 diminui a proliferação celular e a fosforilaçãode ERK, indicando papel de gene su
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Prakash, Meeta B. "Deletion of Cardiac miR-17-92 Cluster Increases Ischemia/ Reperfusion Injury via PTEN Upregulation." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4956.

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The miR-17- 92 cluster is necessary for cell proliferation and development of the cardiovascular system. Deletion of this cluster leads to death in neonatal mice. The role of this cluster still needs to be defined following ischemia and reperfusion. Methods and Results: Adult male mice were injected with Tamoxifen- was to induce inducible cardiac-specific miR-17- 92-deficient (miR-17- 92-def: MCM:TG:miR-17- 92 flox/flox ) and wild type (WT: MCM:NTG:miR-17-92 flox/flox ) mice were subjected to 30 minutes of myocardial ischemia via left anterior descending coronary artery ligation followed by re
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Kayali, Samer. "Spi-1,Fli-1et miR-17-92 contribuent au même réseau oncogénique impliqué dans le contrôle de la prolifération dans l’érythroleucémie de Friend." Thesis, Lyon 1, 2012. http://www.theses.fr/2012LYO10100.

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Plus de 90% des érythroleucémies induites par le virus de Friend sont associées à l'activation récurrente de l’un ou l’autre des facteurs de transcription ETS Spi-1 ou Fli-1, ou du cluster miR-17-92. La contribution de ces trois oncogènes à la prolifération des clones érythroleucémiques correspondant a déjà été indépendamment démontrée. De plus, il a été montré dans l’équipe que Spi-1 active de façon directe l’expression de Fli-1 et que les deux facteurs activent des gènes cibles communs. Dans cette thèse, j’ai montré que Spi-1 et Fli-1 activent l’expression du cluster miR-17-92 en se liant su
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Stunden, Hilary James [Verfasser]. "The role of the miR-17-92 cluster in macrophage driven innate immunity / Hilary James Stunden." Bonn : Universitäts- und Landesbibliothek Bonn, 2018. http://d-nb.info/1173789715/34.

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Stunden, H. James [Verfasser]. "The role of the miR-17-92 cluster in macrophage driven innate immunity / Hilary James Stunden." Bonn : Universitäts- und Landesbibliothek Bonn, 2018. http://d-nb.info/1173789715/34.

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Dakhlallah, Duaa. "Cross-Talk Between Epigenetic Regulation And Mir-17~92 Cluster Expression In Idiopathic Pulmonary Fibrosis (IPF)." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1297960869.

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Fuziwara, Cesar Seigi. "O cluster de microRNAs miR-17-92 e seus alvos na oncogênese tiroidiana: influência de BRAFT1799A e de iodo." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-19112014-162309/.

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O excesso de iodo inibe a proliferação celular e secreção hormonal, enquanto retarda os efeitos oncogênicos da ativação de RET/PTC3 na célula folicular tiroidiana. A mutação BRAF (T1799A) é a mais prevalente no câncer de tiroide, e modelo transgênico desenvolve câncer que progride para histotipo agressivo. Altos níveis de microRNAs (miRNAs) do cluster miR-17-92 estão associados a histotipos agressivos de câncer de tiroide e modulam a tradução de mRNAs alvo componentes de vias de sinalização oncogênicas. Neste estudo, avaliamos a influência da alta dose de iodo sobre miRNAs frente ativação do o
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Paiva, Marcelo Machado. "Identificação de proteínas reguladoras do splicing associadas à microRNAs." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-10112016-101050/.

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Splicing é o processo de remoção de introns e ligação de exons em eucariotos. É realizado pelo spliceossomo, um complexo macromolecular composto por RNAs e mais de cem proteínas. Alguns introns possuem microRNAs, os quais devem ser processados para gerar moléculas maduras. O cluster intrônico miR-17-92 é composto por sete miRNAs que têm sido associados ao desenvolvimento de diferentes tumores em vários tecidos. Neste trabalho o splicing de dois miRNAs deste cluster foi analisado em células HeLa, BCPAP e TPC-I. Os resultados mostraram que introns com miR19a tem o splicing mais eficiente do que
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Meyer, Annekarin [Verfasser], and Jörn [Akademischer Betreuer] Lausen. "TAL1 und miR-17-92 bilden eine regulatorische Schleife in der Hämatopoese / Annekarin Meyer ; Betreuer: Jörn Lausen." Stuttgart : Universitätsbibliothek der Universität Stuttgart, 2020. http://d-nb.info/1218078847/34.

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Book chapters on the topic "MiR-17(similar to)92"

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Chaulk, Steven G., and Richard P. Fahlman. "Tertiary Structure Mapping of the Pri-miRNA miR-17~92." In RNA Mapping. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1062-5_5.

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Kumar, Premlata, and Carole R. Mendelson. "Functional Role of the MicroRNA (miR)-17-92 Cluster during Human Trophoblast Differentiation." In BASIC/TRANSLATIONAL - Female Reproductive Physiology: Uterus, Placenta & Pregnancy, Including Endometriosis. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part3.p25.p3-156.

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Liao, Ya-Chun, Tzu-Heng Lin, Chih-Ying Chen, Shwu-Bin Lin, and Lo-Chun Au. "The Antileukemia Activity of Natural Product HQ17(3) Is Possibly Associated with Downregulation of miR-17-92 Cluster." In Prime Archives in Biomedical Sciences. Vide Leaf, Hyderabad, 2020. http://dx.doi.org/10.37247/pabs.1.2020.15.

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Conference papers on the topic "MiR-17(similar to)92"

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Robbins, M. E., K. A. Smith, E. M. Mendralla, J. M. Taylor, and G. S. Budinger. "miR-17∼92 Cluster Haploinsufficiency Decreases Pulmonary and Cardiovascular Function Similar to the Phenotype Present in Murine Bronchopulmonary Dysplasia Models." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4447.

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Li, Yulin, Peter S. Choi, Stephanie C. Casey, David L. Dill, and Dean W. Felsher. "Abstract PR13: miR-17-92 mediates MYC oncogene addiction." In Abstracts: AACR Special Conference on Myc: From Biology to Therapy; January 7-10, 2015; La Jolla, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1557-3125.myc15-pr13.

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Dichtelmuller, H., and W. Stephan. "IN VIVO AND IN VITRO NEUTRALIZATION OF BACTERIAL TOXINES BY IGM ENRICHED AND CONVENTIONAL I. V. IMMUNOGLOBULINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644255.

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Severe septic phenomena are caused bybacterial toxins. We therefore investigated the neutralization of toxins derived from Staphylococcus aureus and Pseudcmonas aeruginosa by different i.v. irtmunoglobulin preparations using hemolysis inhibition tests and mouse protection tests. The efficacy of conventional i.v. immunoglobulin containing preparations were compared with an IgM enriched i.v. immunoglobulin (Pentaglobin).For hemolysis inhibition tests sterile filtered supernatant of Staphylococcusaureus was prepared and given to human erythrocytes. When IgM enriched immunoglobulin was added, toxi
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Sandhu, Sukhinder K., Reid Neinast, Veronica Balatti та ін. "Abstract 2947: B-cell lymphoma in eα-miR-17∼92 transgenic mice". У Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2947.

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Kohanbash, Gary, Kotaro Sasaki, Aki Hoji, Mitsugu Fujita, and Hideho Okada. "Abstract 4786: MiR-17-92 expression in differentiated T cells - Implications for cancer immunotherapy." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-4786.

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Kemp, Sanne R. Martens-de, Malgorzata A. Komor, Rosa Hegi, et al. "Abstract 4638: Colorectal adenoma-to-carcinoma progression: The role of miR-17-92 cluster." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4638.

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Kemp, Sanne R. Martens-de, Malgorzata A. Komor, Rosa Hegi, et al. "Abstract 4638: Colorectal adenoma-to-carcinoma progression: The role of miR-17-92 cluster." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4638.

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Varshney, Jyotika, Nicholas J. Slipek, John Osborne, et al. "Abstract 1097: The miR-17-92 microRNA cluster plays a crucial role in osteosarcoma progression." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1097.

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Dakhlallah, Duaa, Melissa Piper, and Clay B. Marsh. "DNA Methylation-Mediated Silencing Of The MiR-17~92 Cluster In Idiopathic Pulmonary Fibrosis (IPF)." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3915.

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He, Shun, Shangbin Yang, Guohua Deng, et al. "Abstract 2943: Aurora kinase A induces miR-17-92 cluster through regulation of E2F1 transcription factor." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-2943.

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