Relevant bibliographies by topics / C-Myc

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'C-Myc'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 July 2025

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Journal articles on the topic "C-Myc"

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Ibrahim, Dina, Léa Prévaud, Nathalie Faumont, et al. "Alternative c-MYC mRNA Transcripts as an Additional Tool for c-Myc2 and c-MycS Production in BL60 Tumors." Biomolecules 12, no. 6 (2022): 836. http://dx.doi.org/10.3390/biom12060836.

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While studying c-Myc protein expression in several Burkitt lymphoma cell lines and in lymph nodes from a mouse model bearing a translocated c-MYC gene from the human BL line IARC-BL60, we surprisingly discovered a complex electrophoretic profile. Indeed, the BL60 cell line carrying the t(8;22) c-MYC translocation exhibits a simple pattern, with a single c-Myc2 isoform. Analysis of the c-MYC transcripts expressed by tumor lymph nodes in the mouse λc-MYC (Avy/a) showed for the first time five transcripts that are associated with t(8;22) c-MYC translocation. The five transcripts were correlated w
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Lechable, Marion, Xuechen Tang, Stefan Siebert, et al. "High Intrinsic Oncogenic Potential in the Myc-Box-Deficient Hydra Myc3 Protein." Cells 12, no. 9 (2023): 1265. http://dx.doi.org/10.3390/cells12091265.

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The proto-oncogene myc has been intensively studied primarily in vertebrate cell culture systems. Myc transcription factors control fundamental cellular processes such as cell proliferation, cell cycle control and stem cell maintenance. Myc interacts with the Max protein and Myc/Max heterodimers regulate thousands of target genes. The genome of the freshwater polyp Hydra encodes four myc genes (myc1-4). Previous structural and biochemical characterization showed that the Hydra Myc1 and Myc2 proteins share high similarities with vertebrate c-Myc, and their expression patterns suggested a functi
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Liu, Zhiliang, Tiantian Han, Rongrong Kong, et al. "Clinical characterization of MYC family proto-oncogene amplification in solid tumors from Chinese patients." Journal of Clinical Oncology 41, no. 16_suppl (2023): e15140-e15140. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.e15140.

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e15140 Background: The dysregulation of the MYC family oncogenes ( c-MYC, MYCN and MYCL) play critical roles in tumorigenesis, prognosis and immune escape. MYC inactivation can result in sustained tumour regression and many therapeutic agents that directly target MYC are under development. MYC signaling is associated with tumor cell PD-L1, overall immune cell infiltration. Herein, we explore MYC family proto-oncogene amplification profiles and clinical characterization in chinese solid tumors. Methods: This research comprehensively characterized gene mutations by next-generation sequencing (NG
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Yuan, Ye, Mohammad Alzrigat, Aida Rodriguez-Garcia, et al. "Target Genes of c-MYC and MYCN with Prognostic Power in Neuroblastoma Exhibit Different Expressions during Sympathoadrenal Development." Cancers 15, no. 18 (2023): 4599. http://dx.doi.org/10.3390/cancers15184599.

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Deregulation of the MYC family of transcription factors c-MYC (encoded by MYC), MYCN, and MYCL is prevalent in most human cancers, with an impact on tumor initiation and progression, as well as response to therapy. In neuroblastoma (NB), amplification of the MYCN oncogene and over-expression of MYC characterize approximately 40% and 10% of all high-risk NB cases, respectively. However, the mechanism and stage of neural crest development in which MYCN and c-MYC contribute to the onset and/or progression of NB are not yet fully understood. Here, we hypothesized that subtle differences in the exp
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Chen, Yihui, Ricardo A. León-Letelier, Ali Hussein Abdel Sater, et al. "c-MYC-Driven Polyamine Metabolism in Ovarian Cancer: From Pathogenesis to Early Detection and Therapy." Cancers 15, no. 3 (2023): 623. http://dx.doi.org/10.3390/cancers15030623.

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c-MYC and its paralogues MYCN and MYCL are among the most frequently amplified and/or overexpressed oncoproteins in ovarian cancer. c-MYC plays a key role in promoting ovarian cancer initiation and progression. The polyamine pathway is a bona fide target of c-MYC signaling, and polyamine metabolism is strongly intertwined with ovarian malignancy. Targeting of the polyamine pathway via small molecule inhibitors has garnered considerable attention as a therapeutic strategy for ovarian cancer. Herein, we discuss the involvement of c-MYC signaling and that of its paralogues in promoting ovarian ca
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Cogswell, J. P., P. C. Cogswell, W. M. Kuehl, et al. "Mechanism of c-myc regulation by c-Myb in different cell lineages." Molecular and Cellular Biology 13, no. 5 (1993): 2858–69. http://dx.doi.org/10.1128/mcb.13.5.2858-2869.1993.

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Activation of the murine c-myc promoter by murine c-Myb protein was examined in several cell lines by using a transient expression system in which Myb expression vectors activate the c-myc promoter linked to a chloramphenicol acetyltransferase reporter gene or a genomic beta-globin gene. S1 nuclease protection analyses confirmed that the induction of c-myc by c-Myb was transcriptional and affected both P1 and P2 start sites in a murine T-cell line, EL4, and a myelomonocytic line, WEHI-3. Mutational analyses of the c-myc promoter revealed that two distinct regions could confer Myb responsivenes
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Cogswell, J. P., P. C. Cogswell, W. M. Kuehl, et al. "Mechanism of c-myc regulation by c-Myb in different cell lineages." Molecular and Cellular Biology 13, no. 5 (1993): 2858–69. http://dx.doi.org/10.1128/mcb.13.5.2858.

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Activation of the murine c-myc promoter by murine c-Myb protein was examined in several cell lines by using a transient expression system in which Myb expression vectors activate the c-myc promoter linked to a chloramphenicol acetyltransferase reporter gene or a genomic beta-globin gene. S1 nuclease protection analyses confirmed that the induction of c-myc by c-Myb was transcriptional and affected both P1 and P2 start sites in a murine T-cell line, EL4, and a myelomonocytic line, WEHI-3. Mutational analyses of the c-myc promoter revealed that two distinct regions could confer Myb responsivenes
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Baer, MR, P. Augustinos, and AJ Kinniburgh. "Defective c-myc and c-myb RNA turnover in acute myeloid leukemia cells." Blood 79, no. 5 (1992): 1319–26. http://dx.doi.org/10.1182/blood.v79.5.1319.1319.

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Abstract Dysregulated expression of the c-myc and c-myb protooncogenes has been implicated in the pathogenesis of acute myeloid leukemia (AML). To elucidate mechanisms of c-myc dysregulation in AML cells, we studied c- myc RNA turnover in peripheral blood blasts from eight patients using actinomycin D transcription blockade. Rapid c-myc RNA turnover was seen in cells from six patients, with half-lives of approximately 30 minutes, similar to those reported in normal myeloid cells, in HL-60 cells, and in other cell lines. c-myc RNA turnover was prolonged in cells of the other two patients, with
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Baer, MR, P. Augustinos, and AJ Kinniburgh. "Defective c-myc and c-myb RNA turnover in acute myeloid leukemia cells." Blood 79, no. 5 (1992): 1319–26. http://dx.doi.org/10.1182/blood.v79.5.1319.bloodjournal7951319.

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Dysregulated expression of the c-myc and c-myb protooncogenes has been implicated in the pathogenesis of acute myeloid leukemia (AML). To elucidate mechanisms of c-myc dysregulation in AML cells, we studied c- myc RNA turnover in peripheral blood blasts from eight patients using actinomycin D transcription blockade. Rapid c-myc RNA turnover was seen in cells from six patients, with half-lives of approximately 30 minutes, similar to those reported in normal myeloid cells, in HL-60 cells, and in other cell lines. c-myc RNA turnover was prolonged in cells of the other two patients, with half-live
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Lee, J., K. Mehta, MB Blick, JU Gutterman, and G. Lopez-Berestein. "Expression of c-fos, c-myb, and c-myc in human monocytes: correlation with monocytic differentiation." Blood 69, no. 5 (1987): 1542–45. http://dx.doi.org/10.1182/blood.v69.5.1542.1542.

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Abstract Terminal differentiation of human monocytic leukemia cells (THP-1 cells) was associated with the induction of c-fos, the down regulation of c-myb, and no significant change in the level of c-myc expression. Gamma interferon, which resulted in a slight decrease in c-myb but no change in c-fos or c-myc expression, had a transient antiproliferative effect without a morphological or functional differentiation of THP-1 cells. Resting human peripheral blood monocytes have a high c-fos, a low c-myc, and no detectable c-myb expression. These findings suggest that a switch in c-fos/c-myb expre
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Dissertations / Theses on the topic "C-Myc"

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Evans, Joanne R. "The investigation of internal ribosome entry in the c-myc and c-myb genes." Thesis, University of Leicester, 2003. http://hdl.handle.net/2381/29681.

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The c-myc gene contains an internal ribosome entry site (IRES) within its 5' untranslated region. The IRES was shown to have different activities between cell lines suggesting a requirement for protein trans-acting factors that are present in these cell lines in varying amounts. In addition a number of proteins have been shown to interact with the IRES by north-western and UV cross-linking analysis. Investigation of the protein factors involved in c-myc IRES translation identified PCBP1 (Poly (rC) binding protein 1), PCBP2, HnRNPK (heterogeneous nuclear ribonucleoprotein K), UNR (upstream of N
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Beaudoin, Nicolas. "L’inhibition de c-MYC : l’approche MAX*." Mémoire, Université de Sherbrooke, 2015. http://hdl.handle.net/11143/6739.

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c-MYC est un facteur de transcription oncogénique dont l’expression est dérégulée dans 78% des gliomes. On observe d’ailleurs une corrélation positive entre sa surexpression et le grade des gliomes. De plus, cette surexpression serait essentielle à la survie des cellules souches tumorales, cellules qui seraient davantage résistantes à la chimiothérapie et à la radiothérapie en plus d’avoir un caractère plus invasif. Il a aussi été démontré que l’inhibition de c-MYC par ARN interférents peut sensibiliser les cellules cancéreuses à l’apoptose et réduire leur prolifération. S
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Hotti, Anneli. "Caspases in c-Myc-induced apoptosis." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/haart/vk/hotti/.

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Vervoorts, Jörg. "Molekulare Mechanismen der c-Myc-Transaktivierung Identifikation von hASH2, Nucleolin und CBP als neue c-Myc-Koaktivatoren /." [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=97123163X.

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Le, Quesne John P. C. "The c-myc IRES : structure and mechanism." Thesis, University of Leicester, 2000. http://hdl.handle.net/2381/29652.

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The proto-oncogene c-myc is central to the process whereby the cell commits itself to quiescence, differentiation, proliferation of apoptosis, and the expression of Myc protein is controlled at several levels, including translation. The 5' UTR of c-myc has been shown to contain an internal ribosome entry segment (IRES), allowing translation to proceed via an internally initiated mechanism. To determine the secondary structure of the IRES, structural data were obtained by chemical probing of 5' UTR RNA in vitro. These data were used as constraints upon the "mFold" RNA secondary structure predic
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Cannell, Ian G. "Regulation of c-Myc by miR-34c." Thesis, University of Nottingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.523121.

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Straaten, J. P. van. "Studies on the human c-myc gene product." Thesis, University of Cambridge, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.377708.

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Fleser, Angelica. "Resténose et expression des proto-oncogènes, c-myc, c-fos et c-jun." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ35590.pdf.

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GIOVANNINI, VALENTINA, and VALENTINA GIOVANNINI. "NUOVE STRATEGIE ANTITUMORALI: PEPTIDI RETROINVERSI CHE MIMANO DOMINI FUNZIONALI SPECIFICI DI REGIONI DI C-MYC, COME INIBITORI COMPETITIVI DELLA PROTEINA C-MYC NATIVA." Doctoral thesis, La Sapienza, 2005. http://hdl.handle.net/11573/916799.

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Marhin, Wilson. "Characterization of c-myc as a transcriptional repressor." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq41469.pdf.

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Books on the topic "C-Myc"

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Dang, Chi V., and Linda A. Lee. c-Myc Function in Neoplasia. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0.

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A, Lee Linda, ed. c-Myc function in neoplasia. R.G. Landes Co., 1995.

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Dang, Chi V. C-myc function in neoplasia. Springer, 1995.

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Potter, Michael, and Fritz Melchers, eds. C-Myc in B-Cell Neoplasia. Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60801-8.

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Rottleb, Christoph. Modulation der c-myc-Expression durch exogene Stimuli. [s.n.], 1991.

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Collum, Robert Gerard. Studies on the structure and function of N-m y c. [Columbia University], 1992.

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Devine, Paula. Molecular analysis of C-MYC chromosome dosage in uveal melanoma. The Author], 1994.

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Schräder-Carlberg, Magdalena. Kartierung kleiner RNA Schleifen im Chromatin des c-myc Gens. Karoi-Verlag, 1992.

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Kappes-Roth, Thomas. Chemoenzymatische Synthese eines charakteristischen Glycophospho-Nonapeptids aus dem c-Myc Transkriptionsfaktor. [s.n.], 1998.

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Giessen, Justus Liebig-Universität, ed. Molekulargenetische Studien am porcinen c-myc-Locus zur Phylogenie und Assoziation mit konstitutionellen Merkmalen. Köhler, 1999.

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Book chapters on the topic "C-Myc"

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Schmierer, Bernhard. "c-Myc." In Encyclopedia of Systems Biology. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_771.

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van Roy, Frans, Volker Nimmrich, Anton Bespalov, et al. "c-MYC." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100292.

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Shrivastava, A., and K. Calame. "Association with C-Myc: An Alternated Mechanism for c-Myc Function." In Current Topics in Microbiology and Immunology. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_32.

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Dang, Chi V., and Linda A. Lee. "Max Association with Myc." In c-Myc Function in Neoplasia. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0_8.

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Dang, Chi V., and Linda A. Lee. "DNA Binding Properties of Myc." In c-Myc Function in Neoplasia. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0_9.

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Dang, Chi V., and Linda A. Lee. "Introduction." In c-Myc Function in Neoplasia. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0_1.

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Dang, Chi V., and Linda A. Lee. "Myc Target Genes in Cell Proliferation and Programmed Cell Death." In c-Myc Function in Neoplasia. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0_10.

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Dang, Chi V., and Linda A. Lee. "Retroviruses, Cancer Genes, and Tumor Suppressor Genes." In c-Myc Function in Neoplasia. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0_2.

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Dang, Chi V., and Linda A. Lee. "Historical Perspectives of myc Gene Studies." In c-Myc Function in Neoplasia. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0_3.

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Dang, Chi V., and Linda A. Lee. "Structure of the c-myc Gene and its Transcription." In c-Myc Function in Neoplasia. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22681-0_4.

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Conference papers on the topic "C-Myc"

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Neghabi, Mehrnoosh, Parisa Nategh, Busenur Ceyhan, et al. "Quantifying the Effects of Chemotherapy-Induced Toxicity and Knockout of the Transcription Factor c-Myc on Mice Kidney Metabolism Using Optical Imaging." In CLEO: Applications and Technology. Optica Publishing Group, 2024. http://dx.doi.org/10.1364/cleo_at.2024.jtu2a.72.

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The study explores knockout of c-Myc and doxorubicin toxicity influence on mouse kidney’s metabolism. Cryo-imaging unveils knockout is significantly more oxidized compared to control group while this was not observed between doxorubicin and saline group.
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Kumari, Alpana, Tetsushi Iwasaki, Walson P. Folk, et al. "Abstract PR09: c-MYC preserves genomic integrity during DNA replication: a paradigm shift of c-MYC." In Abstracts: AACR Precision Medicine Series: Cancer Cell Cycle - Tumor Progression and Therapeutic Response; February 28 - March 2, 2016; Orlando, FL. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1557-3125.cellcycle16-pr09.

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Riquelme, Erick M., Milind B. Suraokar, Maria I. Nunez, et al. "Abstract 4031: CNG c-myc in mesothelioma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4031.

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Fan-Minogue, Hua, Zhongwei Cao, Paulmurugan Ramasamy, et al. "Abstract 5223: Towards MYC targeted cancer therapy: Noninvasive molecular imaging of c-Myc signaling." 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.am10-5223.

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Rezzoug, Francine, Shelia D. Thomas, Eric C. Rouchka, and Donald M. Miller. "Abstract 3811: G-quadruplex-forming genomic sequences homologous to Pu27 interact with c-Myc promoter and regulate c-Myc transcription." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-3811.

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Kawauchi, Daisuke, Giles Robinson, Tamar Uziel, et al. "Abstract 3444: Enforced expression of MycN and C-Myc induces different medulloblastoma subtypes." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3444.

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Liu, Wenting, Guanhui Wu, Clement Lin, et al. "Abstract 4853: BMVC specifically binds the major G-quadruplex structure formed in the c-MYC promoter to lower c-MYC levels." 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.am2016-4853.

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Holien, Toril, Thea K. Våtsveen, Hanne Hella, Anders Waage, and Anders Sundan. "Abstract 3130: Dependency on c-MYC in multiple myeloma." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3130.

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Ma, Liandong, Youzhi Tong, Qianxiang Zhou, et al. "Abstract 1265: Discovery of GT19077, a c-Myc/Max protein-protein Interaction (PPI) small molecule inhibitor, and GT19506 a c-Myc PROTAC molecule, for targeting c-Myc-driven blood cancers and small cell lung cancers." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1265.

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Hu, Angela, Huabo Wang, Kelsey Pendleton, and Edward V. Prochownik. "Abstract 4760: Inhibition of c-myc by the triterpenoid celastrol." In 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.am2012-4760.

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Reports on the topic "C-Myc"

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ธัญญะกิจไพศาล, พสุธา, та Bidwell, Joseph P. การศึกษาคุณสมบัติของสารซิมวาสเตติน ต่อการกระตุ้นการเพิ่มจำนวนเซลล์ และระดับอาร์เอ็นเอนำรหัสของ c-fos และ c-myc ในเซลล์สร้างกระดูก : รายงานวิจัยฉบับสมบูรณ์. จุฬาลงกรณ์มหาวิทยาลัย, 2003. https://doi.org/10.58837/chula.res.2003.9.

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งานวิจัยนี้มีวัตถุประสงค์เพื่อศึกษาผลของสารซิมวาสเตตินต่อการเพิ่มจำนวนเซลล์และระดับอาร์เอ็นนำรหัสของจีน c-fos และ c-myc ของเซลล์สร้างกระดูกที่แยกจากกระโหลกศีรษะของหนูแรกเกิดและเซลล์สร้างกระดูกที่แยกจากไขกระดูกของหนู โดยเซลล์จะถูกทดสอบด้วยสารซิมวาสเตตินในระดับความเข้มข้นที่กำหนดเป็นเวลา 24 ชั่วโมง จากนั้นเซลล์จะถูกวิเคราะห์ด้วยสารเอ็มทีที, [[superscript 3]H] thymidine incorporation assay และ Northern blot ตามลำดับ ผลการทดลองพบสารซิมวาสเตตินที่ระดับความเข้มข้น 2 ไมโครโมลาร์มีความเป็นพิษต่อเซลล์สร้างกระดูกที่แยกจากกระโหลกศีรษะและไขกระดูกของหนูอย่างมีนัยสำคัญทางสถิติเมื่อเปรียบเทียบกับกลุ่มควบคุม
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Prochownik, Edward. Evaluation of Molecular Inhibitors of the c-Myc Oncoprotein. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada502505.

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Blakely, Collin M. Interactions Between C-Myc and Development in Mammary Carcinogenesis. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada426178.

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Prochownik, Edward V. Evaluation of Molecular Inhibitors of the c-Myc Oncoprotein. Defense Technical Information Center, 2005. http://dx.doi.org/10.21236/ada434552.

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Prochownik, Edward. Evaluation of Molecular Inhibitors of the c-Myc Oncoprotein. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada475675.

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Jamerson, Matthew. Cooperation of Bcl-XL and c-Myc in Mammary Tumorigenesis. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada396438.

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Jamerson, Matthew H. Cooperation of Bc1-XL and c-Myc in Mammary Tumorigenesis. Defense Technical Information Center, 1998. http://dx.doi.org/10.21236/ada363615.

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Coticchia, Christine M., and Robert B. Dickson. Fas/FasL System in c-Myc Expressing Mammary Carcinoma Cells. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada411302.

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Coticchia, Christine M., and Robert B. Dickson. Fas/FasL System in c-Myc Expressing Mammary Carcinoma Cells. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada422986.

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Jamerson, Matthew H. Cooperation of Bcl-xL and c-Myc in Mammary Tumorigenesis. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada391341.

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