Relevant bibliographies by topics / C-Myc

Academic literature on the topic 'C-Myc'

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Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "C-Myc"

1

Ibrahim, Dina, Léa Prévaud, Nathalie Faumont, Danielle Troutaud, Jean Feuillard, Mona Diab-Assaf, and Ahmad Oulmouden. "Alternative c-MYC mRNA Transcripts as an Additional Tool for c-Myc2 and c-MycS Production in BL60 Tumors." Biomolecules 12, no. 6 (June 16, 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 with the production of c-Myc2 and c-MycS, and loss of c-Myc1. The contribution of these transcripts to the oncogenic activation of the t(8;22) c-MYC is discussed.
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Lechable, Marion, Xuechen Tang, Stefan Siebert, Angelika Feldbacher, Monica L. Fernández-Quintero, Kathrin Breuker, Celina E. Juliano, Klaus R. Liedl, Bert Hobmayer, and Markus Hartl. "High Intrinsic Oncogenic Potential in the Myc-Box-Deficient Hydra Myc3 Protein." Cells 12, no. 9 (April 26, 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 function in adult stem cell maintenance. In contrast, an additional Hydra Myc protein termed Myc3 is highly divergent, lacking the common N-terminal domain and all conserved Myc-boxes. Single cell transcriptome analysis revealed that the myc3 gene is expressed in a distinct population of interstitial precursor cells committed to nerve- and gland-cell differentiation, where the Myc3 protein may counteract the stemness actions of Myc1 and Myc2 and thereby allow the implementation of a differentiation program. In vitro DNA binding studies showed that Myc3 dimerizes with Hydra Max, and this dimer efficiently binds to DNA containing the canonical Myc consensus motif (E-box). In vivo cell transformation assays in avian fibroblast cultures further revealed an unexpected high potential for oncogenic transformation in the conserved Myc3 C-terminus, as compared to Hydra Myc2 or Myc1. Structure modeling of the Myc3 protein predicted conserved amino acid residues in its bHLH-LZ domain engaged in Myc3/Max dimerization. Mutating these amino acid residues in the human c-Myc (MYC) sequence resulted in a significant decrease in its cell transformation potential. We discuss our findings in the context of oncogenic transformation and cell differentiation, both relevant for human cancer, where Myc represents a major driver.
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Liu, Zhiliang, Tiantian Han, Rongrong Kong, Didi Guo, Mengjuan Wang, Yuwei Dong, Siqi Chen, et al. "Clinical characterization of MYC family proto-oncogene amplification in solid tumors from Chinese patients." Journal of Clinical Oncology 41, no. 16_suppl (June 1, 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 (NGS) in 23990 chinese solid tumors tissues to reveal the prevalence of MYC family proto-oncogene amplification(MYC AMP) and the association with Tumor mutational burden(TMB) and microsatellite instability(MSI). Results: The prevalence of MYC AMP (copy number, CN≥5) in the cohort was 2.1% (504/23,990), in which ovarian cancer (7.6%, 22/289) showed the highest prevalence, followed by breast cancer (6.1%, 26/429), esophagus cancer (5.9%, 17/287). Only one glioma patient(pt) carried co-amplification of MYCN and c-MYC. In 504 MYC AMP pts, c-MYC AMP accounted for 93.7%(472/504), MYCN and MYCL AMP accounted for 6.5%(33/504) in total. The CN was significantly higher in MYCN and MYCL AMP pts than c-MYC AMP pts (22.9 vs 7.6, p < 0.0001). MSI-H showed a lower detection rate in MYC AMP pts other than Non-MYC AMP pts (0% vs 1.2%, p < 0.05). The proportion of TMB-L in MYC AMP pts was similar to Non-MYC AMP pts (90.9% vs. 90.1%, p > 0.05). Conclusions: In totally, 2.1% of chinese solid tumor pts had MYC high level AMP, mainly c-MYC Amp. The CN was higer in MYCN/ MYCL AMP pts than c-MYC AMP pts. In addition, MYC AMP pts tended to have MSS and TMB-L, suggesting that MYC may be a novel target for tumor immunotherapy. MYC inhibitor combines with immunotherapy may be an important direction for the treatment of MYC AMP pts.
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Yuan, Ye, Mohammad Alzrigat, Aida Rodriguez-Garcia, Xueyao Wang, Tomas Sjöberg Bexelius, John Inge Johnsen, Marie Arsenian-Henriksson, Judit Liaño-Pons, and Oscar C. Bedoya-Reina. "Target Genes of c-MYC and MYCN with Prognostic Power in Neuroblastoma Exhibit Different Expressions during Sympathoadrenal Development." Cancers 15, no. 18 (September 16, 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 expression of MYCN and/or c-MYC targets could more accurately stratify NB patients in different risk groups rather than using the expression of either MYC gene alone. We employed an integrative approach using the transcriptome of 498 NB patients from the SEQC cohort and previously defined c-MYC and MYCN target genes to model a multigene transcriptional risk score. Our findings demonstrate that defined sets of c-MYC and MYCN targets with significant prognostic value, effectively stratify NB patients into different groups with varying overall survival probabilities. In particular, patients exhibiting a high-risk signature score present unfavorable clinical parameters, including increased clinical risk, higher INSS stage, MYCN amplification, and disease progression. Notably, target genes with prognostic value differ between c-MYC and MYCN, exhibiting distinct expression patterns in the developing sympathoadrenal system. Genes associated with poor outcomes are mainly found in sympathoblasts rather than in chromaffin cells during the sympathoadrenal development.
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Chen, Yihui, Ricardo A. León-Letelier, Ali Hussein Abdel Sater, Jody Vykoukal, Jennifer B. Dennison, Samir Hanash, and Johannes F. Fahrmann. "c-MYC-Driven Polyamine Metabolism in Ovarian Cancer: From Pathogenesis to Early Detection and Therapy." Cancers 15, no. 3 (January 19, 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 cancer tumorigenesis. We highlight the potential of targeting c-MYC-driven polyamine metabolism for the treatment of ovarian cancers and the utility of polyamine signatures in biofluids for early detection applications.
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Cogswell, J. P., P. C. Cogswell, W. M. Kuehl, A. M. Cuddihy, T. M. Bender, U. Engelke, K. B. Marcu, and J. P. Ting. "Mechanism of c-myc regulation by c-Myb in different cell lineages." Molecular and Cellular Biology 13, no. 5 (May 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 responsiveness in two T-cell lines, a distal site upstream of P1 and a proximal site within the first noncoding exon. In contrast, only the proximal site was required for other cell lineages examined. Five separate Myb-binding sites were located in this proximal site and found to be important for c-Myb trans activation. DNA binding was necessary for c-myc activation, as shown by the loss of function associated with mutation of Myb's DNA-binding domain and by trans-dominant repressor activity of the DNA binding, trans-activation-defective mutant. The involvement of additional protein factors was addressed by inhibiting protein synthesis with cycloheximide in a conditional expression system in which the activity of presynthesized Myb was under the control of estrogen. These experiments indicate that de novo synthesis of additional proteins was not necessary for c-myc trans activation. Together these data reveal two cell lineage-dependent pathways by which c-Myb regulates c-myc; however, both pathways are mechanistically indistinguishable in that direct DNA binding by Myb is required for activating c-myc whereas neither de novo protein synthesis nor other labile proteins are necessary.
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Cogswell, J. P., P. C. Cogswell, W. M. Kuehl, A. M. Cuddihy, T. M. Bender, U. Engelke, K. B. Marcu, and J. P. Ting. "Mechanism of c-myc regulation by c-Myb in different cell lineages." Molecular and Cellular Biology 13, no. 5 (May 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 responsiveness in two T-cell lines, a distal site upstream of P1 and a proximal site within the first noncoding exon. In contrast, only the proximal site was required for other cell lineages examined. Five separate Myb-binding sites were located in this proximal site and found to be important for c-Myb trans activation. DNA binding was necessary for c-myc activation, as shown by the loss of function associated with mutation of Myb's DNA-binding domain and by trans-dominant repressor activity of the DNA binding, trans-activation-defective mutant. The involvement of additional protein factors was addressed by inhibiting protein synthesis with cycloheximide in a conditional expression system in which the activity of presynthesized Myb was under the control of estrogen. These experiments indicate that de novo synthesis of additional proteins was not necessary for c-myc trans activation. Together these data reveal two cell lineage-dependent pathways by which c-Myb regulates c-myc; however, both pathways are mechanistically indistinguishable in that direct DNA binding by Myb is required for activating c-myc whereas neither de novo protein synthesis nor other labile proteins are necessary.
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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 (March 1, 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 half-lives of greater than 75 minutes. c-fos RNA turnover was rapid in blasts from all eight patients, with half-lives of approximately 15 minutes. Stabilization of GM-CSF transcripts was not observed. In contrast, c-myb RNA half-lives were greater than 75 minutes in cells of the two patients with prolonged c-myc RNA turnover, as compared to 30 minutes in cells of the other six patients. Enhanced stability of both c-myc and c-myb RNA species suggests that a defect exists in a trans-acting factor that destabilizes both of these normally labile RNAs. Incomplete correlation between c-myc RNA levels and half-lives indicates regulation of c-myc expression at the level of transcription or nuclear transport in addition to posttranscriptional regulation.
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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 (March 1, 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-lives of greater than 75 minutes. c-fos RNA turnover was rapid in blasts from all eight patients, with half-lives of approximately 15 minutes. Stabilization of GM-CSF transcripts was not observed. In contrast, c-myb RNA half-lives were greater than 75 minutes in cells of the two patients with prolonged c-myc RNA turnover, as compared to 30 minutes in cells of the other six patients. Enhanced stability of both c-myc and c-myb RNA species suggests that a defect exists in a trans-acting factor that destabilizes both of these normally labile RNAs. Incomplete correlation between c-myc RNA levels and half-lives indicates regulation of c-myc expression at the level of transcription or nuclear transport in addition to posttranscriptional regulation.
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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 (May 1, 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 expression is associated with the terminal differentiation of cells of the monocytic lineage.
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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-ras) and UNRIP (unr interacting protein) as having a role in c-myc IRES translation, PCBP1, PCBP2, HnRNPK and UNR were found to directly interact with the IRES RNA by UV cross-linking and electrophoretic mobility shift assays (EMSAs). Investigation of the proteins effect on c-myc IRES activity showed stimulation of IRES activity in HeLa cells by PCBP1 and PCBP2. The factor HnRNPK was found to have a slight stimulatory effect in vivo. In addition PCBP1 and PCBP2 were found to stimulate IRES activity in vitro in combination with UNR and UNRIP. Using the yeast three-hybrid system a number of additional proteins were found to interact with the c-myc IRES RNA. A novel Fibrillarin-like protein was identified and shown to strongly interact with the IRES by EMSA. Studies to determine a direct role of this factor in c-myc IRES translation were inconclusive. The study of translation of the c-myc gene identified an IRES within its 5'UTR. Investigation of the role of trans-acting factors in its translation showed a possible role of the factors PCBP2, HnRNPk and ITAF45 (IRES trans-acting factor 45).
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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. Sa surexpression relative dans les glioblastomes (GBM) est signe de la malignité et l’espérance de vie des patients atteints par ces tumeurs est réduite chez les patients plus âgés. c-MYC doit s’hétérodimériser avec MAX, son partenaire obligatoire afin de se lier aux promoteurs de ses gènes cibles contenant des EBox (CANNTG) et ainsi activer leur transcription. Cependant, il a été proposé que MAX pourrait homodimériser et agir comme antagoniste en compétitionnant pour les mêmes sites de reconnaissance que l’hétérodimère c-MYC/MAX sur l’ADN. Notre étude vise donc à évaluer l’effet dose-dépendant d’un traitement exogène de MAX*WT, correspondant à une version tronquée du facteur de transcription MAX, sur différentes lignées cellulaires de GBM. Nous avons d’abord étudié les capacités de la protéine à transloquer dans les cellules par microscopie. Ceci a permis de déterminer que le peptide s’internalise rapidement (15 minutes) pour ensuite s’accumuler au niveau nucléaire (24 h, 48 h). Par la suite, des analyses de FACScan ont démonté qu’un traitement de 72 heures provoque une inhibition de la prolifération cellulaire. À l’aide de chambres de Boyden et d’essais de croissance en sphéroïdes dans une matrice de Matrigel(indice supérieur TM]), nous avons observé une diminution importante du caractère invasif des lignées de gliomes malins suite au traitement avec MAX*WT. Ces résultats démontrent que la protéine MAX*WT semble avoir un effet antinéoplasique sur plusieurs lignées de gliomes malins et que la voie de signalisation de c-MYC pourrait constituer une cible thérapeutique intéressante.
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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 prediction algorithm, and the model was refined by phylogenetic analysis. The resulting model contains a number of interesting features. There is no detectable structural homology with viral IRESs. Mutations were introduced to determine the importance of various IRES moieties. Surprisingly, the IRES seemed resistant to relatively gross structural changes, and a number of mutations were seen to significantly activate IRES function, suggesting that the IRES is in a state of constitutive repression. The point at which the ribosome enters and begins scanning was investigated, revealing that entry occurs in an unstructured region of the IRES, upstream of an inhibitory pseudoknot element that must be disrupted before ribosome entry can occur. It has previously been noted that the c-myc IRES fails to function in RRL in vitro translation assays. In order to obtain an in vitro assay to aid isolation of specific trans-acting factors, several cellular extracts were tested for their ability to stimulate IRES activity in vitro. Nevertheless, the IRES was not activated in vitro. From these data, a picture of the c-myc IRES that is distinctly different from the viral paradigms has emerged, and a model of the IRES mechanism is presented and discussed.
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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. C-myc function in neoplasia. New York: Springer, 1995.

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

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

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

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

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

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

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Coulis, Christopher M. Inhibition of c-MYC expression through disruption of an RNA·protein interaction using antisense oligonucleotides. Ottawa: National Library of Canada, 1999.

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Ifandi, Vasiliki. Influence of over-expression of c-Myc and bcl-2 on proliferation, apoptosis and survival of cho-K1 cells. Birmingham: University of Birmingham, 2002.

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Wood, Alan Christopher. The role of the C-MYC oncogene during drug-induced apoptosis of the acute lymphoblastic leukaemia cell line CCRF C7A. Manchester: University of Manchester, 1994.

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Book chapters on the topic "C-Myc"

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Schmierer, Bernhard. "c-Myc." In Encyclopedia of Systems Biology, 434. New York, NY: 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, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis, et al. "c-MYC." In Encyclopedia of Signaling Molecules, 448. New York, NY: 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, 273–82. Berlin, Heidelberg: 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, 151–63. Berlin, Heidelberg: 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, 165–70. Berlin, Heidelberg: 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, 1–36. Berlin, Heidelberg: 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, 171–92. Berlin, Heidelberg: 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, 37–64. Berlin, Heidelberg: 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, 65–71. Berlin, Heidelberg: 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, 73–84. Berlin, Heidelberg: 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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Kumari, Alpana, Tetsushi Iwasaki, Walson P. Folk, Amy L. Abdulovic-Cui, Slovénie Pyndiah, George C. Prendergast, John M. Sedivy, and Daitoku Sakamuro. "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, Adi F. Gazdar, Laurent A. Byers, John V. Heymach, Reza J. Mehran, Anne Tsao, and Ignacio I. Wistuba. "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, Chan Carmel, Tarik Massound, Felsher Dean, and Sanjiv Gambhir. "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, Jerold Rehg, Frederique Zindy, Chunxu Qu, Amar Gajjar, Richard J. Gilbertson, and Martine F. Roussel. "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, Buket Onel, Ding Chen, Ta-Chau Chang, and Danzhou Yang. "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, Zhaohui Yang, Honghau Yan, Ye Chen, Ruo Xu, 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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Kim, Tae-Aug, Jin-Muk Kang, John Niderhuber, and Seong-Jin Kim. "Abstract LB-304: Smad7-Skp2 complex orchestrates c-Myc stability." 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-lb-304.

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Reports on the topic "C-Myc"

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Prochownik, Edward. Evaluation of Molecular Inhibitors of the c-Myc Oncoprotein. Fort Belvoir, VA: Defense Technical Information Center, February 2008. http://dx.doi.org/10.21236/ada502505.

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

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

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

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Jamerson, Matthew. Cooperation of Bcl-XL and c-Myc in Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, August 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. Fort Belvoir, VA: Defense Technical Information Center, August 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. Fort Belvoir, VA: Defense Technical Information Center, June 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. Fort Belvoir, VA: Defense Technical Information Center, June 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. Fort Belvoir, VA: Defense Technical Information Center, August 1999. http://dx.doi.org/10.21236/ada391341.

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Sheen, Joon-Ho. A Gene Amplification Phenotype in c-Myc-Induced Mammary Tumors Cells. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396567.

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