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Journal articles on the topic 'C-Myc'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

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.bloodjournal6951542.

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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

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12

Clurman, B. E., and W. S. Hayward. "Multiple proto-oncogene activations in avian leukosis virus-induced lymphomas: evidence for stage-specific events." Molecular and Cellular Biology 9, no. 6 (1989): 2657–64. http://dx.doi.org/10.1128/mcb.9.6.2657-2664.1989.

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We have examined avian leukosis virus-induced B-cell lymphomas for multiple, stage-specific oncogene activations. Three targets for viral integration were identified: c-myb, c-myc, and a newly identified locus termed c-bic. The c-myb and c-myc genes were associated with different lymphoma phenotypes. The c-bic locus was a target for integration in one class of lymphomas, usually in conjunction with c-myc activation. The data indicate that c-myc and c-bic may act synergistically during lymphomagenesis and that c-bic is involved in late stages of tumor progression.

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13

Clurman, B. E., and W. S. Hayward. "Multiple proto-oncogene activations in avian leukosis virus-induced lymphomas: evidence for stage-specific events." Molecular and Cellular Biology 9, no. 6 (1989): 2657–64. http://dx.doi.org/10.1128/mcb.9.6.2657.

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We have examined avian leukosis virus-induced B-cell lymphomas for multiple, stage-specific oncogene activations. Three targets for viral integration were identified: c-myb, c-myc, and a newly identified locus termed c-bic. The c-myb and c-myc genes were associated with different lymphoma phenotypes. The c-bic locus was a target for integration in one class of lymphomas, usually in conjunction with c-myc activation. The data indicate that c-myc and c-bic may act synergistically during lymphomagenesis and that c-bic is involved in late stages of tumor progression.

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14

Lüscher, B., and R. N. Eisenman. "c-myc and c-myb protein degradation: effect of metabolic inhibitors and heat shock." Molecular and Cellular Biology 8, no. 6 (1988): 2504–12. http://dx.doi.org/10.1128/mcb.8.6.2504-2512.1988.

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The proteins encoded by both viral and cellular forms of the c-myc oncogene have been previously demonstrated to have exceptionally short in vivo half-lives. In this paper we report a comparative study on the parameters affecting turnover of nuclear oncoproteins c-myc, c-myb, and the rapidly metabolized cytoplasmic enzyme ornithine decarboxylase. The degradation of all three proteins required metabolic energy, did not result in production of cleavage intermediates, and did not involve lysosomes or ubiquitin. A five- to eightfold increase in the half-life of c-myc proteins, and a twofold increa

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15

Lüscher, B., and R. N. Eisenman. "c-myc and c-myb protein degradation: effect of metabolic inhibitors and heat shock." Molecular and Cellular Biology 8, no. 6 (1988): 2504–12. http://dx.doi.org/10.1128/mcb.8.6.2504.

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The proteins encoded by both viral and cellular forms of the c-myc oncogene have been previously demonstrated to have exceptionally short in vivo half-lives. In this paper we report a comparative study on the parameters affecting turnover of nuclear oncoproteins c-myc, c-myb, and the rapidly metabolized cytoplasmic enzyme ornithine decarboxylase. The degradation of all three proteins required metabolic energy, did not result in production of cleavage intermediates, and did not involve lysosomes or ubiquitin. A five- to eightfold increase in the half-life of c-myc proteins, and a twofold increa

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16

Qiu, Bo, Bo Qiu, and Bo Qiu. "TMOD-27. IDENTIFYING ONCOGENIC C-MYC AND MYCN COMPLEXES IN HIGH-RISK PEDIATRIC CANCERS." Neuro-Oncology 23, Supplement_6 (2021): vi221. http://dx.doi.org/10.1093/neuonc/noab196.888.

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Abstract The MYC family of proto-oncogenes is activated in a variety of cancers, including multiple high-risk pediatric malignancies. c-MYC (MYC) is ubiquitously expressed in human tissues, while MYCN (MYCN) has tissue and developmentally restricted expression patterns. In both neuroblastoma and medulloblastoma, enhanced activity of either MYCN or c-MYC drives high-risk disease. As transcription factors, MYC proteins exert oncogenic functions through protein-protein interaction networks that alter gene expression, but also mediate a growing list of target-gene independent nuclear functions (tr

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17

Shipp, M. A., and E. L. Reinherz. "Differential expression of nuclear proto-oncogenes in T cells triggered with mitogenic and nonmitogenic T3 and T11 activation signals." Journal of Immunology 139, no. 7 (1987): 2143–48. http://dx.doi.org/10.4049/jimmunol.139.7.2143.

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Abstract The relationship between induction of nuclear proto-oncogenes and cellular proliferation is not fully understood. To better define this relationship, we have studied c-fos, c-myc, and c-myb mRNA induction in T lymphocytes where early and late activation events have been clearly delineated. In T cells, initial activation from G0 to G1 results from stimulation of either the antigen/major histocompatibility complex receptor (T3-Ti) or the T11 structure; further cycle progression and proliferation follow interaction of interleukin 2 (IL-2) with the IL-2 receptor. These events can be disse

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18

Evans, J. L., T. L. Moore, W. M. Kuehl, T. Bender, and J. P. Ting. "Functional analysis of c-Myb protein in T-lymphocytic cell lines shows that it trans-activates the c-myc promoter." Molecular and Cellular Biology 10, no. 11 (1990): 5747–52. http://dx.doi.org/10.1128/mcb.10.11.5747-5752.1990.

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The function of c-Myb protein was revealed by transfecting an expression vector containing the entire c-Myb protein-coding sequence into the murine CTLL-2 T-cell line. Expressions of high levels of c-Myb protein did not alter the expression of several T-cell markers, c-fos mRNA expression, responses to interleukin-2, and growth characteristics of these cells. Interestingly, expression of the c-myc gene was drastically increased in this clone. Further, the c-myb expression plasmid, but not a frameshift mutant of c-myb, enhanced the expression of a hybrid construct of c-myc promoter linked to a

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19

Evans, J. L., T. L. Moore, W. M. Kuehl, T. Bender, and J. P. Ting. "Functional analysis of c-Myb protein in T-lymphocytic cell lines shows that it trans-activates the c-myc promoter." Molecular and Cellular Biology 10, no. 11 (1990): 5747–52. http://dx.doi.org/10.1128/mcb.10.11.5747.

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The function of c-Myb protein was revealed by transfecting an expression vector containing the entire c-Myb protein-coding sequence into the murine CTLL-2 T-cell line. Expressions of high levels of c-Myb protein did not alter the expression of several T-cell markers, c-fos mRNA expression, responses to interleukin-2, and growth characteristics of these cells. Interestingly, expression of the c-myc gene was drastically increased in this clone. Further, the c-myb expression plasmid, but not a frameshift mutant of c-myb, enhanced the expression of a hybrid construct of c-myc promoter linked to a

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20

Miner, J. H., and B. J. Wold. "c-myc inhibition of MyoD and myogenin-initiated myogenic differentiation." Molecular and Cellular Biology 11, no. 5 (1991): 2842–51. http://dx.doi.org/10.1128/mcb.11.5.2842-2851.1991.

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In vertebrate development, a prominent feature of several cell lineages is the coupling of cell cycle regulation with terminal differentiation. We have investigated the basis of this relationship in the skeletal muscle lineage by studying the effects of the proliferation-associated regulator, c-myc, on the differentiation of MyoD-initiated myoblasts. Transient cotransfection assays in NIH 3T3 cells using MyoD and c-myc expression vectors demonstrated c-myc suppression of MyoD-initiated differentiation. A stable cell system was also developed in which MyoD expression was constitutive, while myc

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21

Miner, J. H., and B. J. Wold. "c-myc inhibition of MyoD and myogenin-initiated myogenic differentiation." Molecular and Cellular Biology 11, no. 5 (1991): 2842–51. http://dx.doi.org/10.1128/mcb.11.5.2842.

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In vertebrate development, a prominent feature of several cell lineages is the coupling of cell cycle regulation with terminal differentiation. We have investigated the basis of this relationship in the skeletal muscle lineage by studying the effects of the proliferation-associated regulator, c-myc, on the differentiation of MyoD-initiated myoblasts. Transient cotransfection assays in NIH 3T3 cells using MyoD and c-myc expression vectors demonstrated c-myc suppression of MyoD-initiated differentiation. A stable cell system was also developed in which MyoD expression was constitutive, while myc

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22

Chana, J., R. Grover, G. D. Wilson, and R. Sanders. "c-myc." Melanoma Research 7, Supplement 1 (1997): S137. http://dx.doi.org/10.1097/00008390-199706001-00477.

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23

Boxer, Linda M., and Chi V. Dang. "Translocations involving c-myc and c-myc function." Oncogene 20, no. 40 (2001): 5595–610. http://dx.doi.org/10.1038/sj.onc.1204595.

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24

Hoffman-Liebermann, B., and D. A. Liebermann. "Interleukin-6- and leukemia inhibitory factor-induced terminal differentiation of myeloid leukemia cells is blocked at an intermediate stage by constitutive c-myc." Molecular and Cellular Biology 11, no. 5 (1991): 2375–81. http://dx.doi.org/10.1128/mcb.11.5.2375-2381.1991.

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Interleukin-6 (IL-6) and leukemia inhibitory factor (LIF), two multifunctional cytokines, recently have been identified as physiological inducers of hematopoietic cell differentiation which also induce terminal differentiation and growth arrest of the myeloblastic leukemic M1 cell line. In this work, it is shown that c-myc exhibited a unique pattern of expression upon induction of M1 terminal differentiation by LIF or IL-6, with an early transient increase followed by a decrease to control levels by 12 h and no detectable c-myc mRNA by 1 day; in contrast, c-myb expression was rapidly suppresse

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25

Hoffman-Liebermann, B., and D. A. Liebermann. "Interleukin-6- and leukemia inhibitory factor-induced terminal differentiation of myeloid leukemia cells is blocked at an intermediate stage by constitutive c-myc." Molecular and Cellular Biology 11, no. 5 (1991): 2375–81. http://dx.doi.org/10.1128/mcb.11.5.2375.

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Interleukin-6 (IL-6) and leukemia inhibitory factor (LIF), two multifunctional cytokines, recently have been identified as physiological inducers of hematopoietic cell differentiation which also induce terminal differentiation and growth arrest of the myeloblastic leukemic M1 cell line. In this work, it is shown that c-myc exhibited a unique pattern of expression upon induction of M1 terminal differentiation by LIF or IL-6, with an early transient increase followed by a decrease to control levels by 12 h and no detectable c-myc mRNA by 1 day; in contrast, c-myb expression was rapidly suppresse

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26

Ma, Liandong, Yuzhi Tong, Zhaohui Yang, et al. "Abstract A03: Discovery and evaluation of GT19630, a c-Myc/n-Myc degrader, for targeting c-Myc-driven B-cell malignancies, acute myeloid leukemia (AML) and n-Myc driven cancers." Blood Cancer Discovery 3, no. 5_Supplement (2022): A03. http://dx.doi.org/10.1158/2643-3249.lymphoma22-a03.

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Abstract Myc family members (MYC, MYCN and MYCL) are oncogenic transcriptional factors, which form dimers with Max to activate transcription activities to drive tumor initiation and progression. c-Myc deregulation has been identified in 80% of all tumor types, including B-cell malignancies, AML and a variety of solid tumors. N-Myc genetic alterations have been identified in small cell lung cancer, neuroblastoma, neuroendocrine prostate cancers and sarcoma. Myc-deregulation has been directly linked to the poor clinical outcome in these cancers, which makes Myc a therapeutic target for pharmacol

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27

Arsura, Marcello, Claudia S. Hofmann, Josee Golay, Martino Introna, and Gail E. Sonenshein. "A-myb rescues murine B-cell lymphomas from IgM-receptor–mediated apoptosis through c-myctranscriptional regulation." Blood 96, no. 3 (2000): 1013–20. http://dx.doi.org/10.1182/blood.v96.3.1013.

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Abstract A-myb is a member of the myb family of transcription factors, which regulates proliferation, differentiation, and apoptosis of hematopoietic cells. A-Myb expression is normally restricted to the proliferating B-cell centroblasts and transgenic mice overexpressing A-myb displayed enhanced hyperplasia of the lymph nodes. Because A-Myb is highly expressed in several subtypes of human B-cell neoplasias, we sought to determine whether the A-myb gene promoted proliferation and survival of B lymphocytes, using the WEHI 231 and CH33 murine B-cell lymphomas as models. Here, we show that ectopi

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28

Arsura, Marcello, Claudia S. Hofmann, Josee Golay, Martino Introna, and Gail E. Sonenshein. "A-myb rescues murine B-cell lymphomas from IgM-receptor–mediated apoptosis through c-myctranscriptional regulation." Blood 96, no. 3 (2000): 1013–20. http://dx.doi.org/10.1182/blood.v96.3.1013.015k06_1013_1020.

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A-myb is a member of the myb family of transcription factors, which regulates proliferation, differentiation, and apoptosis of hematopoietic cells. A-Myb expression is normally restricted to the proliferating B-cell centroblasts and transgenic mice overexpressing A-myb displayed enhanced hyperplasia of the lymph nodes. Because A-Myb is highly expressed in several subtypes of human B-cell neoplasias, we sought to determine whether the A-myb gene promoted proliferation and survival of B lymphocytes, using the WEHI 231 and CH33 murine B-cell lymphomas as models. Here, we show that ectopic express

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Spotts, G. D., and S. R. Hann. "Enhanced translation and increased turnover of c-myc proteins occur during differentiation of murine erythroleukemia cells." Molecular and Cellular Biology 10, no. 8 (1990): 3952–64. http://dx.doi.org/10.1128/mcb.10.8.3952-3964.1990.

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To determine whether regulation of c-myc proteins occurs during the differentiation of murine erythroleukemia cells, we examined c-myc protein synthesis and accumulation throughout dimethyl sulfoxide (DMSO)- or hypoxanthine-induced differentiation. c-myc protein expression exhibited an overall biphasic reduction, with an initial concomitant decrease in c-myc RNA, protein synthesis, and protein accumulation early during the commitment phase. However, as the mRNA and protein levels recovered, c-myc protein synthesis levels dissociated from the levels of c-myc mRNA and protein accumulation. This

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Spotts, G. D., and S. R. Hann. "Enhanced translation and increased turnover of c-myc proteins occur during differentiation of murine erythroleukemia cells." Molecular and Cellular Biology 10, no. 8 (1990): 3952–64. http://dx.doi.org/10.1128/mcb.10.8.3952.

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To determine whether regulation of c-myc proteins occurs during the differentiation of murine erythroleukemia cells, we examined c-myc protein synthesis and accumulation throughout dimethyl sulfoxide (DMSO)- or hypoxanthine-induced differentiation. c-myc protein expression exhibited an overall biphasic reduction, with an initial concomitant decrease in c-myc RNA, protein synthesis, and protein accumulation early during the commitment phase. However, as the mRNA and protein levels recovered, c-myc protein synthesis levels dissociated from the levels of c-myc mRNA and protein accumulation. This

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31

Schmidt, M., V. Nazarov, L. Stevens, R. Watson, and L. Wolff. "Regulation of the Resident Chromosomal Copy of c-myc by c-Myb Is Involved in Myeloid Leukemogenesis." Molecular and Cellular Biology 20, no. 6 (2000): 1970–81. http://dx.doi.org/10.1128/mcb.20.6.1970-1981.2000.

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ABSTRACT c-myb is a frequent target of retroviral insertional mutagenesis in murine leukemia virus-induced myeloid leukemia. Induction of the leukemogenic phenotype is generally associated with inappropriate expression of this transcriptional regulator. Despite intensive investigations, the target genes of c-myb that are specifically involved in development of these myeloid lineage neoplasms are still unknown. In vitro assays have indicated that c-myc may be a target gene of c-Myb; however, regulation of the resident chromosomal gene has not yet been demonstrated. To address this question furt

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32

Gadde, Satyanarayana, Sin Wi Ng, Natalie Chung, et al. "Abstract 6863: Development of MYCN/MYC inhibitors." Cancer Research 85, no. 8_Supplement_1 (2025): 6863. https://doi.org/10.1158/1538-7445.am2025-6863.

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Abstract Background: Deregulated expression of MYC family transcription factors is present in more than 70% of human cancers. MYC is an intrinsically disordered protein without known drug binding pockets and is essential for adult cell replication, making clinical development of MYC inhibitors challenging. MYCN amplification and overexpression generate driver signals in the childhood cancers, neuroblastoma (NB), medulloblastoma (MB) and diffuse intrinsic pontine glioma (DIPG). Methods and Results: We previously reported a small molecule compound, SE486-11, which reduced MYCN protein levels in

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33

Golay, J., G. Cusmano, and M. Introna. "Independent regulation of c-myc, B-myb, and c-myb gene expression by inducers and inhibitors of proliferation in human B lymphocytes." Journal of Immunology 149, no. 1 (1992): 300–308. http://dx.doi.org/10.4049/jimmunol.149.1.300.

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Abstract Although a detailed picture is emerging about the nature of the second messengers involved in B cell activation and proliferation, little is yet known about the intracellular events taking place further downstream. The c-myb proto-oncogene, the structurally related B-myb gene, and c-myc probably code for transcription factors, have been demonstrated to be necessary for the proliferation of hemopoietic cells, and their expression is indeed induced after mitogenic stimulation of T and B lymphocytes. They are therefore likely to be key elements in the regulation of gene expression during

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Lüscher, B., and R. N. Eisenman. "Mitosis-specific phosphorylation of the nuclear oncoproteins Myc and Myb." Journal of Cell Biology 118, no. 4 (1992): 775–84. http://dx.doi.org/10.1083/jcb.118.4.775.

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The c-myc and c-myb proto-oncogenes encode phosphorylated nuclear DNA binding proteins that are likely to be involved in transcriptional regulation. Here we demonstrate that both Myc and Myb proteins are hyperphosphorylated during mitosis. In the case of Myb, hyperphosphorylation is accompanied by the appearance of three M phase-specific tryptic phosphopeptides. At least one of these phosphopeptides corresponds to a phosphopeptide generated after phosphorylation of Myb in vitro by p34cdc2 kinase. By contrast, the mitotic hyperphosphorylation of Myc does not correlate with the appearance of uni

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35

Dang, C. V., H. van Dam, M. Buckmire, and W. M. Lee. "DNA-binding domain of human c-Myc produced in Escherichia coli." Molecular and Cellular Biology 9, no. 6 (1989): 2477–86. http://dx.doi.org/10.1128/mcb.9.6.2477-2486.1989.

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We have identified the domain of the human c-myc protein (c-Myc) produced in Escherichia coli that is responsible for the ability of the protein to bind sequence-nonspecific DNA. Using analysis of binding of DNA by proteins transferred to nitrocellulose, DNA-cellulose chromatography, and a nitrocellulose filter binding assay, we examined the binding properties of c-Myc peptides generated by cyanogen bromide cleavage, of mutant c-Myc, and of proteins that fuse portions of c-Myc to staphylococcal protein A. The results of these analyses indicated that c-Myc amino acids 265 to 318 were responsibl

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36

Dang, C. V., H. van Dam, M. Buckmire, and W. M. Lee. "DNA-binding domain of human c-Myc produced in Escherichia coli." Molecular and Cellular Biology 9, no. 6 (1989): 2477–86. http://dx.doi.org/10.1128/mcb.9.6.2477.

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Abstract:

We have identified the domain of the human c-myc protein (c-Myc) produced in Escherichia coli that is responsible for the ability of the protein to bind sequence-nonspecific DNA. Using analysis of binding of DNA by proteins transferred to nitrocellulose, DNA-cellulose chromatography, and a nitrocellulose filter binding assay, we examined the binding properties of c-Myc peptides generated by cyanogen bromide cleavage, of mutant c-Myc, and of proteins that fuse portions of c-Myc to staphylococcal protein A. The results of these analyses indicated that c-Myc amino acids 265 to 318 were responsibl

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Tang, Yuting, Xiaomei Yan, Rui Huang, et al. "Essential Role of c-MYC for Natural Killer Cell Development, Proliferation and Anti-Tumor Activity." Blood 130, Suppl_1 (2017): 786. http://dx.doi.org/10.1182/blood.v130.suppl_1.786.786.

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Abstract Natural killer (NK) cells are the major component of innate immunity with both cytotoxicity and cytokine producing effector functions. NK cells also regulate the interplay between innate immunity and adaptive immunity by secreting certain cytokines. Extrinsic regulators of NK cell development and function, including diverse ligands of NK cell receptors and cytokines from the microenvironment, have been extensively studied. However, intrinsic regulators for NK cell biology are still less understood. In our previous study on aggressive NK cell leukemia (ANKL), genomics and transcriptomi

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38

Prochownik, EV. "c-myb but not c-myc suppresses the hemin-induced nonterminal expression of hemoglobin by murine erythroleukemia cells." Blood 73, no. 3 (1989): 782–86. http://dx.doi.org/10.1182/blood.v73.3.782.782.

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Abstract Clonal lines of Friend murine erythroleukemia (F-MEL) cells have been generated following transfection with c-myc or c-myb expression plasmids. These clones produce high levels of abnormally regulated proto-oncogene transcripts and fail to terminally differentiate in the presence of dimethyl sulfoxide. To determine the relative levels at which the two proto-oncogenes might exert their inhibitory effects, we asked whether these clones could express differentiated functions in the absence of terminal differentiation. It was found that exposure of c-myc-transfected cells to hemin allows

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39

Prochownik, EV. "c-myb but not c-myc suppresses the hemin-induced nonterminal expression of hemoglobin by murine erythroleukemia cells." Blood 73, no. 3 (1989): 782–86. http://dx.doi.org/10.1182/blood.v73.3.782.bloodjournal733782.

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Clonal lines of Friend murine erythroleukemia (F-MEL) cells have been generated following transfection with c-myc or c-myb expression plasmids. These clones produce high levels of abnormally regulated proto-oncogene transcripts and fail to terminally differentiate in the presence of dimethyl sulfoxide. To determine the relative levels at which the two proto-oncogenes might exert their inhibitory effects, we asked whether these clones could express differentiated functions in the absence of terminal differentiation. It was found that exposure of c-myc-transfected cells to hemin allows for the i

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40

Sheen, Joon-Ho, and Robert B. Dickson. "Overexpression of c-Myc Alters G1/S Arrest following Ionizing Radiation." Molecular and Cellular Biology 22, no. 6 (2002): 1819–33. http://dx.doi.org/10.1128/mcb.22.6.1819-1833.2002.

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ABSTRACT Study of the mechanism(s) of genomic instability induced by the c-myc proto-oncogene has the potential to shed new light on its well-known oncogenic activity. However, an underlying mechanism(s) for this phenotype is largely unknown. In the present study, we investigated the effects of c-Myc overexpression on the DNA damage-induced G1/S checkpoint, in order to obtain mechanistic insights into how deregulated c-Myc destabilizes the cellular genome. The DNA damage-induced checkpoints are among the primary safeguard mechanisms for genomic stability, and alterations of cell cycle checkpoi

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Batsché, Eric, and Chantal Crémisi. "Opposite transcriptional activity between the wild type c-myc gene coding for c-Myc1 and c-Myc2 proteins and c-Myc1 and c-Myc2 separately." Oncogene 18, no. 41 (1999): 5662–71. http://dx.doi.org/10.1038/sj.onc.1202927.

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Sheppard, Terry L. "Sidelining c-Myc." Nature Chemical Biology 7, no. 11 (2011): 756. http://dx.doi.org/10.1038/nchembio.701.

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Ross, D. A., R. Grover, R. Sanders, and G. Wilson. "C-MYC oncoprotein." Melanoma Research 7, Supplement 1 (1997): S78. http://dx.doi.org/10.1097/00008390-199706001-00274.

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Mao, Beibei, Guowei Zhao, Xiang Lv, et al. "Sirt1 deacetylates c-Myc and promotes c-Myc/Max association." International Journal of Biochemistry & Cell Biology 43, no. 11 (2011): 1573–81. http://dx.doi.org/10.1016/j.biocel.2011.07.006.

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Mestdagh, P., E. Fredlund, F. Pattyn, et al. "MYCN/c-MYC-induced microRNAs repress coding gene networks associated with poor outcome in MYCN/c-MYC-activated tumors." Oncogene 29, no. 9 (2009): 1394–404. http://dx.doi.org/10.1038/onc.2009.429.

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Coppola, J. A., J. M. Parker, G. D. Schuler, and M. D. Cole. "Continued withdrawal from the cell cycle and regulation of cellular genes in mouse erythroleukemia cells blocked in differentiation by the c-myc oncogene." Molecular and Cellular Biology 9, no. 4 (1989): 1714–20. http://dx.doi.org/10.1128/mcb.9.4.1714-1720.1989.

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Constitutive expression of the c-myc oncogene blocks dimethyl sulfoxide (DMSO)-induced differentiation of mouse erythroleukemia (MEL) cells. During the first 12 h of treatment with DMSO, MEL cells undergo a temporary decrease in the level of c-myc mRNA, followed by a temporary withdrawal from the cell cycle. We found the same shutoff of DNA synthesis during the first 12 to 30 h after DMSO induction in normal MEL cells (which differentiate) and in c-myc-transfected MEL cells (which do not differentiate). We also examined whether deregulated c-myc expression grossly interfered with the regulatio

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47

Coppola, J. A., J. M. Parker, G. D. Schuler, and M. D. Cole. "Continued withdrawal from the cell cycle and regulation of cellular genes in mouse erythroleukemia cells blocked in differentiation by the c-myc oncogene." Molecular and Cellular Biology 9, no. 4 (1989): 1714–20. http://dx.doi.org/10.1128/mcb.9.4.1714.

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Abstract:

Constitutive expression of the c-myc oncogene blocks dimethyl sulfoxide (DMSO)-induced differentiation of mouse erythroleukemia (MEL) cells. During the first 12 h of treatment with DMSO, MEL cells undergo a temporary decrease in the level of c-myc mRNA, followed by a temporary withdrawal from the cell cycle. We found the same shutoff of DNA synthesis during the first 12 to 30 h after DMSO induction in normal MEL cells (which differentiate) and in c-myc-transfected MEL cells (which do not differentiate). We also examined whether deregulated c-myc expression grossly interfered with the regulatio

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48

Mousavi, K., and V. Sartorelli. "Myc-Nick: The Force Behind c-Myc." Science Signaling 3, no. 152 (2010): pe49. http://dx.doi.org/10.1126/scisignal.3152pe49.

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Gopal, Venu, Ben Hulette, Ya Oin Li, et al. "c-myc and c-myb expression in acute myelogenous leukemia." Leukemia Research 16, no. 10 (1992): 1003–11. http://dx.doi.org/10.1016/0145-2126(92)90080-q.

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Zobel, Andrea, Frank Kalkbrenner, Gerd Vorbrueggen, and Karin Moelling. "Transactivation of the human c-myc gene by c-Myb." Biochemical and Biophysical Research Communications 186, no. 2 (1992): 715–22. http://dx.doi.org/10.1016/0006-291x(92)90805-u.

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