Relevant bibliographies by topics / Myc Genes / Journal articles
To see the other types of publications on this topic, follow the link: Myc Genes.

Journal articles on the topic 'Myc Genes'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Myc Genes.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Grandori, C. "Myc target genes." Trends in Biochemical Sciences 22, no. 5 (May 1997): 177–81. http://dx.doi.org/10.1016/s0968-0004(97)01025-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Collum, R. G., D. F. Clayton, and F. W. Alt. "Structure and expression of canary myc family genes." Molecular and Cellular Biology 11, no. 3 (March 1991): 1770–76. http://dx.doi.org/10.1128/mcb.11.3.1770.

Full text
Abstract:
We found that the canary N-myc gene is highly related to mammalian N-myc genes in both the protein-coding region and the long 3' untranslated region. Examined coding regions of the canary c-myc gene were also highly related to their mammalian counterparts, but in contrast to N-myc, the canary and mammalian c-myc genes were quite divergent in their 3' untranslated regions. We readily detected N-myc and c-myc expression in the adult canary brain and found N-myc expression both at sites of proliferating neuronal precursors and in mature neurons.
APA, Harvard, Vancouver, ISO, and other styles
3

Collum, R. G., D. F. Clayton, and F. W. Alt. "Structure and expression of canary myc family genes." Molecular and Cellular Biology 11, no. 3 (March 1991): 1770–76. http://dx.doi.org/10.1128/mcb.11.3.1770-1776.1991.

Full text
Abstract:
We found that the canary N-myc gene is highly related to mammalian N-myc genes in both the protein-coding region and the long 3' untranslated region. Examined coding regions of the canary c-myc gene were also highly related to their mammalian counterparts, but in contrast to N-myc, the canary and mammalian c-myc genes were quite divergent in their 3' untranslated regions. We readily detected N-myc and c-myc expression in the adult canary brain and found N-myc expression both at sites of proliferating neuronal precursors and in mature neurons.
APA, Harvard, Vancouver, ISO, and other styles
4

Kinzler, K. W., B. A. Zehnbauer, G. M. Brodeur, R. C. Seeger, J. M. Trent, P. S. Meltzer, and B. Vogelstein. "Amplification units containing human N-myc and c-myc genes." Proceedings of the National Academy of Sciences 83, no. 4 (February 1, 1986): 1031–35. http://dx.doi.org/10.1073/pnas.83.4.1031.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Li, Feng, Yunyue Wang, Karen I. Zeller, James J. Potter, Diane R. Wonsey, Kathryn A. O'Donnell, Jung-whan Kim, Jason T. Yustein, Linda A. Lee, and Chi V. Dang. "Myc Stimulates Nuclearly Encoded Mitochondrial Genes and Mitochondrial Biogenesis." Molecular and Cellular Biology 25, no. 14 (July 2005): 6225–34. http://dx.doi.org/10.1128/mcb.25.14.6225-6234.2005.

Full text
Abstract:
ABSTRACT Although several genes involved in mitochondrial function are direct Myc targets, the role of Myc in mitochondrial biogenesis has not been directly established. We determined the effects of ectopic Myc expression or the loss of Myc on mitochondrial biogenesis. Induction of Myc in P493-6 cells resulted in increased oxygen consumption and mitochondrial mass and function. Conversely, compared to wild-type Myc fibroblasts, Myc null rat fibroblasts have diminished mitochondrial mass and decreased number of normal mitochondria. Reconstitution of Myc expression in Myc null fibroblasts partially restored mitochondrial mass and function and normal-appearing mitochondria. Concordantly, we also observed in primary hepatocytes that acute deletion of floxed murine Myc by Cre recombinase resulted in diminished mitochondrial mass in primary hepatocytes. Our microarray analysis of genes responsive to Myc in human P493-6 B lymphocytes supports a role for Myc in mitochondrial biogenesis, since genes involved in mitochondrial structure and function are overrepresented among the Myc-induced genes. In addition to the known direct binding of Myc to many genes involved in mitochondrial structure and function, we found that Myc binds the TFAM gene, which encodes a key transcriptional regulator and mitochondrial DNA replication factor, both in P493-6 lymphocytes with high ectopic MYC expression and in serum-stimulated primary human 2091 fibroblasts with induced endogenous MYC. These observations support a pivotal role for Myc in regulating mitochondrial biogenesis.
APA, Harvard, Vancouver, ISO, and other styles
6

Versteeg, R., C. van der Minne, A. Plomp, A. Sijts, A. van Leeuwen, and P. Schrier. "N-myc expression switched off and class I human leukocyte antigen expression switched on after somatic cell fusion of neuroblastoma cells." Molecular and Cellular Biology 10, no. 10 (October 1990): 5416–23. http://dx.doi.org/10.1128/mcb.10.10.5416.

Full text
Abstract:
Neuroblastomas often show amplification and high expression of the N-myc oncogene. N-myc expression could be explained as a consequence of gene amplification, but an alternative possibility is that expression primarily results from the inactivation or loss of some factor that normally represses the N-myc gene. To test this idea, we fused N-myc-overexpressing neuroblastoma cell lines with lines that do not express N-myc. In the resulting hybrids, N-myc expression turned out to be switched off, although amplified N-myc copies were still present. This suggests that N-myc overexpression in neuroblastomas results, at least in part, from the inactivation of a suppressor gene that is present in normal cells. In rat neuroblastomas, it has been found that N-myc can switch off class I major histocompatibility complex (MHC) expression. Therefore, we analyzed in our hybrid cells whether suppression of N-myc results in reexpression of human class I MHC genes. Because this was found to be the case, the picture emerges of a hierarchic pathway that connects a putative tumor-suppressor gene with the expression of N-myc and consequently of class I MHC, thus affecting the potential immunogenic properties of neuroblastomas.
APA, Harvard, Vancouver, ISO, and other styles
7

Versteeg, R., C. van der Minne, A. Plomp, A. Sijts, A. van Leeuwen, and P. Schrier. "N-myc expression switched off and class I human leukocyte antigen expression switched on after somatic cell fusion of neuroblastoma cells." Molecular and Cellular Biology 10, no. 10 (October 1990): 5416–23. http://dx.doi.org/10.1128/mcb.10.10.5416-5423.1990.

Full text
Abstract:
Neuroblastomas often show amplification and high expression of the N-myc oncogene. N-myc expression could be explained as a consequence of gene amplification, but an alternative possibility is that expression primarily results from the inactivation or loss of some factor that normally represses the N-myc gene. To test this idea, we fused N-myc-overexpressing neuroblastoma cell lines with lines that do not express N-myc. In the resulting hybrids, N-myc expression turned out to be switched off, although amplified N-myc copies were still present. This suggests that N-myc overexpression in neuroblastomas results, at least in part, from the inactivation of a suppressor gene that is present in normal cells. In rat neuroblastomas, it has been found that N-myc can switch off class I major histocompatibility complex (MHC) expression. Therefore, we analyzed in our hybrid cells whether suppression of N-myc results in reexpression of human class I MHC genes. Because this was found to be the case, the picture emerges of a hierarchic pathway that connects a putative tumor-suppressor gene with the expression of N-myc and consequently of class I MHC, thus affecting the potential immunogenic properties of neuroblastomas.
APA, Harvard, Vancouver, ISO, and other styles
8

Dunnick, Wesley, James Baumgartner, Lee Fradkin, Cynthia Schultz, and Paul Szurek. "Methylation of plasmacytoma c-myc genes." Gene 39, no. 2-3 (January 1985): 287–92. http://dx.doi.org/10.1016/0378-1119(85)90325-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Rimpi, S., and J. A. Nilsson. "Metabolic enzymes regulated by the Myc oncogene are possible targets for chemotherapy or chemoprevention." Biochemical Society Transactions 35, no. 2 (March 20, 2007): 305–10. http://dx.doi.org/10.1042/bst0350305.

Full text
Abstract:
The Myc oncogenes are dysregulated in 70% of human cancers. They encode transcription factors that bind to E-box sequences in DNA, driving the expression of a vast amount of target genes. The biological outcome is enhanced proliferation (which is counteracted by apoptosis), angiogenesis and cancer. Based on the biological effects of Myc overexpression it was originally assumed that the important Myc target genes are those encoding components of the cell cycle machinery. Recent work has challenged this notion and indicates that Myc target genes encoding metabolic enzymes deserve attention, as they may be critical arbiters of Myc in cancer. Thus targeting metabolic enzymes encoded by Myc-target genes may provide a new means to treat cancer that have arisen in response to deregulated Myc oncogenes.
APA, Harvard, Vancouver, ISO, and other styles
10

Leffak, M., and C. D. James. "Opposite replication polarity of the germ line c-myc gene in HeLa cells compared with that of two Burkitt lymphoma cell lines." Molecular and Cellular Biology 9, no. 2 (February 1989): 586–93. http://dx.doi.org/10.1128/mcb.9.2.586.

Full text
Abstract:
To study the cell type specificity of the direction of replication of the human c-myc genes and the relationship of replication polarity to transcriptional activity, we analyzed the directions of replication of the c-myc genes in two Burkitt lymphoma cell lines, CA46 and ST486, and in HeLa cells. On the basis of in vitro runoff replication of forks initiated in intact cells, we found that transcribed c-myc genes in the germ line configuration in HeLa cells were replicated in the direction of transcription from origins in the 5'-flanking DNA, while the repressed, unrearranged c-myc genes of CA46 and ST486 cells were replicated in the antitranscriptional direction. In contrast, the transcribed c-myc genes of CA46 cells were replicated in the transcriptional direction, while the translocated, amplified c-myc genes of ST486 cells showed no preferred polarity of replication. The data also provided evidence for the existence of an endogenous barrier to DNA polymerases in the flanking DNA immediately 5' to the HeLa c-myc genes.
APA, Harvard, Vancouver, ISO, and other styles
11

Leffak, M., and C. D. James. "Opposite replication polarity of the germ line c-myc gene in HeLa cells compared with that of two Burkitt lymphoma cell lines." Molecular and Cellular Biology 9, no. 2 (February 1989): 586–93. http://dx.doi.org/10.1128/mcb.9.2.586-593.1989.

Full text
Abstract:
To study the cell type specificity of the direction of replication of the human c-myc genes and the relationship of replication polarity to transcriptional activity, we analyzed the directions of replication of the c-myc genes in two Burkitt lymphoma cell lines, CA46 and ST486, and in HeLa cells. On the basis of in vitro runoff replication of forks initiated in intact cells, we found that transcribed c-myc genes in the germ line configuration in HeLa cells were replicated in the direction of transcription from origins in the 5'-flanking DNA, while the repressed, unrearranged c-myc genes of CA46 and ST486 cells were replicated in the antitranscriptional direction. In contrast, the transcribed c-myc genes of CA46 cells were replicated in the transcriptional direction, while the translocated, amplified c-myc genes of ST486 cells showed no preferred polarity of replication. The data also provided evidence for the existence of an endogenous barrier to DNA polymerases in the flanking DNA immediately 5' to the HeLa c-myc genes.
APA, Harvard, Vancouver, ISO, and other styles
12

Hirvonen, H., V. Hukkanen, TT Salmi, TP Makela, TT Pelliniemi, S. Knuutila, and R. Alitalo. "Expression of L-myc and N-myc proto-oncogenes in human leukemias and leukemia cell lines." Blood 78, no. 11 (December 1, 1991): 3012–20. http://dx.doi.org/10.1182/blood.v78.11.3012.3012.

Full text
Abstract:
Abstract The myc proto-oncogenes encode nuclear phosphoproteins, which are believed to participate in the control of cell proliferation and differentiation. Deregulated expression of c-myc has been implicated in several human hematopoietic malignancies. We have studied the expression and mRNA processing of human L-myc, N-myc, and c-myc genes in a panel of human leukemias, leukemia cell lines, and normal hematopoietic cells. L-myc mRNA was expressed in three acute myeloid leukemias (AML) studied and in several myeloid leukemia cell lines. Only low expression levels were observed in adult bone marrow and in fetal spleen and thymus. The K562 and Dami leukemia cell lines showed a unique pattern of L-myc mRNA processing, with approximately 40% of L- myc mRNA lacking exon III and intron I. N-myc was expressed in five of six AML cases studied, in one of nine acute lymphocytic leukemia (ALL) cases, and in several leukemia cell lines, while c-myc mRNA was detected in all leukemias and leukemia cell lines studied. Coexpression of all three myc genes was observed in Dami and MOLT-4 cell lines and in two AMLs, and either L-myc or N-myc was coexpressed with c-myc in several other cases. These results show that in addition to c-myc, the L-myc and N-myc genes are expressed in some human leukemias and leukemia cell lines, and suggest a lack of mutually exclusive cross- regulation of the myc genes in human leukemia cells.
APA, Harvard, Vancouver, ISO, and other styles
13

Hirvonen, H., V. Hukkanen, TT Salmi, TP Makela, TT Pelliniemi, S. Knuutila, and R. Alitalo. "Expression of L-myc and N-myc proto-oncogenes in human leukemias and leukemia cell lines." Blood 78, no. 11 (December 1, 1991): 3012–20. http://dx.doi.org/10.1182/blood.v78.11.3012.bloodjournal78113012.

Full text
Abstract:
The myc proto-oncogenes encode nuclear phosphoproteins, which are believed to participate in the control of cell proliferation and differentiation. Deregulated expression of c-myc has been implicated in several human hematopoietic malignancies. We have studied the expression and mRNA processing of human L-myc, N-myc, and c-myc genes in a panel of human leukemias, leukemia cell lines, and normal hematopoietic cells. L-myc mRNA was expressed in three acute myeloid leukemias (AML) studied and in several myeloid leukemia cell lines. Only low expression levels were observed in adult bone marrow and in fetal spleen and thymus. The K562 and Dami leukemia cell lines showed a unique pattern of L-myc mRNA processing, with approximately 40% of L- myc mRNA lacking exon III and intron I. N-myc was expressed in five of six AML cases studied, in one of nine acute lymphocytic leukemia (ALL) cases, and in several leukemia cell lines, while c-myc mRNA was detected in all leukemias and leukemia cell lines studied. Coexpression of all three myc genes was observed in Dami and MOLT-4 cell lines and in two AMLs, and either L-myc or N-myc was coexpressed with c-myc in several other cases. These results show that in addition to c-myc, the L-myc and N-myc genes are expressed in some human leukemias and leukemia cell lines, and suggest a lack of mutually exclusive cross- regulation of the myc genes in human leukemia cells.
APA, Harvard, Vancouver, ISO, and other styles
14

Richman, A., and A. Hayday. "Serum-inducible expression of transfected human c-myc genes." Molecular and Cellular Biology 9, no. 11 (November 1989): 4962–69. http://dx.doi.org/10.1128/mcb.9.11.4962.

Full text
Abstract:
Activation of the c-myc proto-oncogene is implicated in the initiation or progression of many vertebrate cancers. In nontransformed cells, the expression of c-myc is induced by growth factors. Studies have indicated that such induction is effected by multiple mechanisms. To study regulation of c-myc expression, a transfection system has been developed in which introduced c-myc genes exhibit serum-responsive activity. The responsiveness assayed is not mediated by increased transcription initiation. Rather, it is effected at a point(s) between transcription and stabilization of the RNA.
APA, Harvard, Vancouver, ISO, and other styles
15

Richman, A., and A. Hayday. "Serum-inducible expression of transfected human c-myc genes." Molecular and Cellular Biology 9, no. 11 (November 1989): 4962–69. http://dx.doi.org/10.1128/mcb.9.11.4962-4969.1989.

Full text
Abstract:
Activation of the c-myc proto-oncogene is implicated in the initiation or progression of many vertebrate cancers. In nontransformed cells, the expression of c-myc is induced by growth factors. Studies have indicated that such induction is effected by multiple mechanisms. To study regulation of c-myc expression, a transfection system has been developed in which introduced c-myc genes exhibit serum-responsive activity. The responsiveness assayed is not mediated by increased transcription initiation. Rather, it is effected at a point(s) between transcription and stabilization of the RNA.
APA, Harvard, Vancouver, ISO, and other styles
16

Schweinfest, C. W., S. Fujiwara, L. F. Lau, and T. S. Papas. "c-myc can induce expression of G0/G1 transition genes." Molecular and Cellular Biology 8, no. 8 (August 1988): 3080–87. http://dx.doi.org/10.1128/mcb.8.8.3080.

Full text
Abstract:
The human c-myc oncogene was linked to the heat shock-inducible Drosophila hsp70 promoter and used to stably transfect mouse BALB/c 3T3 cells. Heat shock of the transfectants at 42 degrees C followed by recovery at 37 degrees C resulted in the appearance of the human c-myc protein which was appropriately localized to the nuclear fraction. Two-dimensional analysis of the proteins of density-arrested cells which had been heat shock treated revealed the induction of eight protein species and the repression of five protein species. All of the induced and repressed proteins were nonabundant. cDNA clones corresponding to genes induced during the G0/G1 transition were used as probes to assay for c-myc inducibility of these genes. Two anonymous sequences previously identified as serum inducible (3CH77 and 3CH92) were induced when c-myc was expressed. In response to serum stimulation, 3CH77 and 3CH92 were expressed before c-myc mRNA levels increased. However, in response to specific induction of c-myc by heat shock of serum arrested cells, 3CH77 and 3CH92 mRNA levels increased after the rise in c-myc mRNA. Therefore, we hypothesize that abnormal expression of c-myc can induce genes involved in the proliferative response.
APA, Harvard, Vancouver, ISO, and other styles
17

Schweinfest, C. W., S. Fujiwara, L. F. Lau, and T. S. Papas. "c-myc can induce expression of G0/G1 transition genes." Molecular and Cellular Biology 8, no. 8 (August 1988): 3080–87. http://dx.doi.org/10.1128/mcb.8.8.3080-3087.1988.

Full text
Abstract:
The human c-myc oncogene was linked to the heat shock-inducible Drosophila hsp70 promoter and used to stably transfect mouse BALB/c 3T3 cells. Heat shock of the transfectants at 42 degrees C followed by recovery at 37 degrees C resulted in the appearance of the human c-myc protein which was appropriately localized to the nuclear fraction. Two-dimensional analysis of the proteins of density-arrested cells which had been heat shock treated revealed the induction of eight protein species and the repression of five protein species. All of the induced and repressed proteins were nonabundant. cDNA clones corresponding to genes induced during the G0/G1 transition were used as probes to assay for c-myc inducibility of these genes. Two anonymous sequences previously identified as serum inducible (3CH77 and 3CH92) were induced when c-myc was expressed. In response to serum stimulation, 3CH77 and 3CH92 were expressed before c-myc mRNA levels increased. However, in response to specific induction of c-myc by heat shock of serum arrested cells, 3CH77 and 3CH92 mRNA levels increased after the rise in c-myc mRNA. Therefore, we hypothesize that abnormal expression of c-myc can induce genes involved in the proliferative response.
APA, Harvard, Vancouver, ISO, and other styles
18

Inglés, Marta, Cristina Mas-Bargues, Alejandro Berna-Erro, Ander Matheu, Paula Sanchís, Juan-Antonio Avellana, Consuelo Borrás, and José Viña. "Centenarians Overexpress Pluripotency-Related Genes." Journals of Gerontology: Series A 74, no. 9 (July 19, 2018): 1391–95. http://dx.doi.org/10.1093/gerona/gly168.

Full text
Abstract:
Abstract Human mesenchymal cells can become pluripotent by the addition of Yamanaka factors OCT3/4, SOX2, c-MYC, KLF4. We have recently reported that centenarians overexpress BCL-xL, which has been shown to improve pluripotency; thus, we aimed to determine the expression of pluripotency-related genes in centenarians. We recruited 22 young, 32 octogenarian, and 47 centenarian individuals and determined the mRNA expression of Yamanaka factors and other stemness-related cell surface marker genes (VIM, BMP4, NCAM, BMPR2) in peripheral blood mononuclear cells by reverse transcription polymerase chain reaction. We found that centenarians overexpress OCT3/4, SOX2, c-MYC, VIM, BMP4, NCAM, and BMPR2, when compared with octogenarians (p < .05). We further tested the functional role of BCL-xL in centenarians’ ability to express pluripotency-related genes: lymphocytes from octogenarians transduced with BCL-xL overexpressed SOX2, c-MYC, and KLF4. We conclude that centenarians overexpress Yamanaka Factors and other stemness-related cell surface marker genes, which may contribute to their successful aging.
APA, Harvard, Vancouver, ISO, and other styles
19

Doose, Gero, Andrea Haake, Stephan H. Bernhart, Cristina López, Sujitha Duggimpudi, Franziska Wojciech, Anke K. Bergmann, et al. "MINCR is a MYC-induced lncRNA able to modulate MYC’s transcriptional network in Burkitt lymphoma cells." Proceedings of the National Academy of Sciences 112, no. 38 (September 8, 2015): E5261—E5270. http://dx.doi.org/10.1073/pnas.1505753112.

Full text
Abstract:
Despite the established role of the transcription factor MYC in cancer, little is known about the impact of a new class of transcriptional regulators, the long noncoding RNAs (lncRNAs), on MYC ability to influence the cellular transcriptome. Here, we have intersected RNA-sequencing data from two MYC-inducible cell lines and a cohort of 91 B-cell lymphomas with or without genetic variants resulting in MYC overexpression. We identified 13 lncRNAs differentially expressed in IG-MYC-positive Burkitt lymphoma and regulated in the same direction by MYC in the model cell lines. Among them, we focused on a lncRNA that we named MYC-induced long noncoding RNA (MINCR), showing a strong correlation with MYC expression in MYC-positive lymphomas. To understand its cellular role, we performed RNAi and found that MINCR knockdown is associated with an impairment in cell cycle progression. Differential gene expression analysis after RNAi showed a significant enrichment of cell cycle genes among the genes down-regulated after MINCR knockdown. Interestingly, these genes are enriched in MYC binding sites in their promoters, suggesting that MINCR acts as a modulator of the MYC transcriptional program. Accordingly, MINCR knockdown was associated with a reduction in MYC binding to the promoters of selected cell cycle genes. Finally, we show that down-regulation of Aurora kinases A and B and chromatin licensing and DNA replication factor 1 may explain the reduction in cellular proliferation observed on MINCR knockdown. We, therefore, suggest that MINCR is a newly identified player in the MYC transcriptional network able to control the expression of cell cycle genes.
APA, Harvard, Vancouver, ISO, and other styles
20

Chong, Lauren C., Susana Ben-Neriah, Graham W. Slack, Ciara Freeman, Daisuke Ennishi, Anja Mottok, Brett Collinge, et al. "High-resolution architecture and partner genes of MYC rearrangements in lymphoma with DLBCL morphology." Blood Advances 2, no. 20 (October 22, 2018): 2755–65. http://dx.doi.org/10.1182/bloodadvances.2018023572.

Full text
Abstract:
Abstract Genomic rearrangements in the MYC locus occur in ∼12% of lymphomas with diffuse large B-cell lymphoma (DLBCL) morphology and are associated with inferior outcome. Previous studies exploring MYC rearrangements have primarily used fluorescence in situ hybridization (FISH) assays to characterize break-apart status but have rarely examined breakpoint location, and in some cases have not examined partner identity. We performed targeted sequencing of MYC, BCL2, BCL6, and the immunoglobulin (IG) loci in 112 tumors with DLBCL morphology harboring MYC rearrangement. We characterized the location of the MYC rearrangement at base pair resolution and identified the partner in 88 cases. We observed a cluster of breakpoints upstream of the MYC coding region and in intron 1 (the “genic cluster”). Genic cluster rearrangements were enriched for translocations involving IGH (80%), whereas nongenic rearrangements occurred mostly downstream of the MYC gene with a variety of partners, including IGL and IGK. Other recurrent partners included BCL6, ZCCHC7, and RFTN1, which has not previously been described as a MYC partner. We compared 2 commercially available FISH break-apart assays for the MYC locus and observed discordant results in 32% of cases examined, including some with MYC-IGL and MYC-IGK rearrangements. In cases of high-grade B-cell lymphoma with MYC and BCL2 and/or BCL6 rearrangement (HGBL-DH), so-called “double-hit” lymphomas, the majority of MYC rearrangements had non-IG partners (65%), with breakpoints outside the genic cluster (72%). In patients with de novo HGBL-DH of DLBCL morphology, MYC-IG rearrangements showed a trend toward inferior time to progression and overall survival compared with MYC–non-IG rearrangements. Our data reveal clinically relevant architecture of MYC rearrangements in lymphomas with DLBCL morphology.
APA, Harvard, Vancouver, ISO, and other styles
21

Greenberg, R., R. Hawley, and K. B. Marcu. "Acquisition of an intracisternal A-particle element by a translocated c-myc gene in a murine plasma cell tumor." Molecular and Cellular Biology 5, no. 12 (December 1985): 3625–28. http://dx.doi.org/10.1128/mcb.5.12.3625.

Full text
Abstract:
The J558 plasma cell tumor contains two forms of a translocated c-myc gene which are distinguished by virtue of their 3' flanking sequences. The J558 alpha 4 and alpha 25 myc genes are broken by a 12;15 translocation which links c-myc exon 1 to C alpha switch sequences. Comparative restriction mapping and DNA sequence analyses demonstrated that an intracisternal A-particle (IAP) element inserted approximately 2 kilobases 3' of an alpha 4-type myc gene to generate the alpha 25 gene copy. The steady-state level of truncated myc RNAs in J558 was comparable to that in another plasma cell tumor line (MPC-11) which harbors a translocated c-myc locus without an IAP element. The significance of these observations for the putative role of IAP elements in the genesis or progression or both of plasma cell tumors is discussed.
APA, Harvard, Vancouver, ISO, and other styles
22

Greenberg, R., R. Hawley, and K. B. Marcu. "Acquisition of an intracisternal A-particle element by a translocated c-myc gene in a murine plasma cell tumor." Molecular and Cellular Biology 5, no. 12 (December 1985): 3625–28. http://dx.doi.org/10.1128/mcb.5.12.3625-3628.1985.

Full text
Abstract:
The J558 plasma cell tumor contains two forms of a translocated c-myc gene which are distinguished by virtue of their 3' flanking sequences. The J558 alpha 4 and alpha 25 myc genes are broken by a 12;15 translocation which links c-myc exon 1 to C alpha switch sequences. Comparative restriction mapping and DNA sequence analyses demonstrated that an intracisternal A-particle (IAP) element inserted approximately 2 kilobases 3' of an alpha 4-type myc gene to generate the alpha 25 gene copy. The steady-state level of truncated myc RNAs in J558 was comparable to that in another plasma cell tumor line (MPC-11) which harbors a translocated c-myc locus without an IAP element. The significance of these observations for the putative role of IAP elements in the genesis or progression or both of plasma cell tumors is discussed.
APA, Harvard, Vancouver, ISO, and other styles
23

Porro, Antonio, Simona Soverini, Daniel Diolaiti, Tiziana Grafone, Emanuela Ottaviani, Nunzio Iraci, Carolina Terragna, et al. "Direct and Coordinate Regulation of Multidrug Resistance Genes by the c-Myc Oncoprotein." Blood 108, no. 11 (November 16, 2006): 2594. http://dx.doi.org/10.1182/blood.v108.11.2594.2594.

Full text
Abstract:
Abstract The deregulation of ATP-binding cassette (ABC) transporters responsible for the efflux of anticancer agents may be achieved either by mutations or single nucleotide polymorphisms (SNPs) affecting the biophysical and biochemical properties of the transporters or by an increase in their expression level. Consequently, chemoresistance will develop. In this study we have investigated regulatory mechanisms involved in the activation of ABC transporters. We have first examined how ABC genes are regulated at the transcriptional level and which transcription factors concur to such a control. The expression level of all 48 human ABC drug transporters was determined as a function of c-Myc expression in a p493 lymphoblastoid cell line harboring c-Myc driven by a tetracycline-responsive promoter. Our results demonstrated that c-Myc affected the transcription of several ABC genes, such as ABCA2, ABCB1, ABCB9, ABCC1, ABCC4, ABCE1, ABCF1, ABCF2, ABCF3, a majority of which, has been found implicated in chemoresistance. To evaluate whether c-Myc affects the transcription of those ABC genes directly, chromatin immunoprecipitation (ChIP) was performed in p493 cells. The results have shown a direct binding of c-Myc to the promoters of the ABC genes tested, with the only exception of ABCB1. To further confirm a direct role of c-Myc on ABC gene transcription, ABC gene promoters were cloned into a luciferase reporter assay and their activity was tested in various lymphoblastoid cell line variants, expressing different levels of c-Myc. Results proved a dose-dependent transcription activation of ABC reporters induced by c-Myc, which suggested that the c-Myc oncoprotein could regulate the level of expression of a large number of ABC genes in lymphocytes. Furthermore, we have investigated the expression of c-Myc and ABC genes in chronic myeloid leukemia (CML) in order to verify whether high expression levels of c-Myc may affect transcription of ABC drug transporters also in CML cells. In fact, recent studies reported that Bcr-Abl may positively regulate c-Myc expression. Our results showed that c-Myc is highly expressed in CD34+ cells from newly diagnosed chronic phase (CP)-CML patients, and that it can significantly upregulate the expression of several ABC genes, particularly that of the ABCC1 and ABCC4. We have demonstrated that c-Myc was physically associated with the promoter of tested ABC genes and their direct regulator as assessed by ChIP in the Kasumi-4 cell line, which has been derived from a Ph+ CML patient and expresses the CD34 antigen. Taken together, our findings support the model of a direct and coordinate regulation of a large set of ABC genes by the c-Myc transcription factor. Our study suggests that c-myc deregulation of ABC genes could be an important molecular mechanism altering imatinib transport. Thus, we concluded that c-Myc could be involved in the development of chemoresistance in CML, as well as resistance to targeted drugs, such as imatinib. Currently, we are further assessing transcriptional deregulation of specific ABC genes, and SNPs affecting the functional properties of ABC transporters, by comparing CP-CML patients responsive to imatinib, which have been shown to represent over 90% of treated individuals, and patients who developed resistance.
APA, Harvard, Vancouver, ISO, and other styles
24

Stewart, Monica A., Douglas Forrest, Robert McFarlane, David Onions, Neil Wilkie, and James C. Neil. "Conservation of the c-myc coding sequence in transduced feline v-myc genes." Virology 154, no. 1 (October 1986): 121–34. http://dx.doi.org/10.1016/0042-6822(86)90435-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
25

Chen, Shoukun, Hongyan Zhao, Tengli Luo, Yue Liu, Xiaojun Nie, and Haifeng Li. "Characteristics and Expression Pattern of MYC Genes in Triticum aestivum, Oryza sativa, and Brachypodium distachyon." Plants 8, no. 8 (August 8, 2019): 274. http://dx.doi.org/10.3390/plants8080274.

Full text
Abstract:
Myelocytomatosis oncogenes (MYC) transcription factors (TFs) belong to basic helix-loop-helix (bHLH) TF family and have a special bHLH_MYC_N domain in the N-terminal region. Presently, there is no detailed and systematic analysis of MYC TFs in wheat, rice, and Brachypodium distachyon. In this study, 26 TaMYC, 7 OsMYC, and 7 BdMYC TFs were identified and their features were characterized. Firstly, they contain a JAZ interaction domain (JID) and a putative transcriptional activation domain (TAD) in the bHLH_MYC_N region and a BhlH region in the C-terminal region. In some cases, the bHLH region is followed by a leucine zipper region; secondly, they display tissue-specific expression patterns: wheat MYC genes are mainly expressed in leaves, rice MYC genes are highly expressed in stems, and B. distachyon MYC genes are mainly expressed in inflorescences. In addition, three types of cis-elements, including plant development/growth-related, hormone-related, and abiotic stresses-related were identified in different MYC gene promoters. In combination with the previous studies, these results indicate that MYC TFs mainly function in growth and development, as well as in response to stresses. This study laid a foundation for the further functional elucidation of MYC genes.
APA, Harvard, Vancouver, ISO, and other styles
26

Kakkis, E., J. Prehn, and K. Calame. "An active chromatin structure acquired by translocated c-myc genes." Molecular and Cellular Biology 6, no. 4 (April 1986): 1357–61. http://dx.doi.org/10.1128/mcb.6.4.1357.

Full text
Abstract:
We used general sensitivity to DNase I digestion to analyze the chromatin structure of c-myc genes in seven murine plasmacytomas. In every case, the 3' portion of c-myc juxtaposed with C alpha displayed a much more DNase I-sensitive chromatin structure than untranslocated c-myc or, in one case analyzed, the reciprocally translocated 5' portion. Our data suggest the presence of regulatory sequences near the C alpha gene segment.
APA, Harvard, Vancouver, ISO, and other styles
27

Kakkis, E., J. Prehn, and K. Calame. "An active chromatin structure acquired by translocated c-myc genes." Molecular and Cellular Biology 6, no. 4 (April 1986): 1357–61. http://dx.doi.org/10.1128/mcb.6.4.1357-1361.1986.

Full text
Abstract:
We used general sensitivity to DNase I digestion to analyze the chromatin structure of c-myc genes in seven murine plasmacytomas. In every case, the 3' portion of c-myc juxtaposed with C alpha displayed a much more DNase I-sensitive chromatin structure than untranslocated c-myc or, in one case analyzed, the reciprocally translocated 5' portion. Our data suggest the presence of regulatory sequences near the C alpha gene segment.
APA, Harvard, Vancouver, ISO, and other styles
28

Satoh, Kiyotoshi, Shinichi Yachida, Masahiro Sugimoto, Minoru Oshima, Toshitaka Nakagawa, Shintaro Akamoto, Sho Tabata, et al. "Global metabolic reprogramming of colorectal cancer occurs at adenoma stage and is induced by MYC." Proceedings of the National Academy of Sciences 114, no. 37 (August 28, 2017): E7697—E7706. http://dx.doi.org/10.1073/pnas.1710366114.

Full text
Abstract:
Cancer cells alter their metabolism for the production of precursors of macromolecules. However, the control mechanisms underlying this reprogramming are poorly understood. Here we show that metabolic reprogramming of colorectal cancer is caused chiefly by aberrant MYC expression. Multiomics-based analyses of paired normal and tumor tissues from 275 patients with colorectal cancer revealed that metabolic alterations occur at the adenoma stage of carcinogenesis, in a manner not associated with specific gene mutations involved in colorectal carcinogenesis. MYC expression induced at least 215 metabolic reactions by changing the expression levels of 121 metabolic genes and 39 transporter genes. Further, MYC negatively regulated the expression of genes involved in mitochondrial biogenesis and maintenance but positively regulated genes involved in DNA and histone methylation. Knockdown of MYC in colorectal cancer cells reset the altered metabolism and suppressed cell growth. Moreover, inhibition of MYC target pyrimidine synthesis genes such as CAD, UMPS, and CTPS blocked cell growth, and thus are potential targets for colorectal cancer therapy.
APA, Harvard, Vancouver, ISO, and other styles
29

Kim, H. K., I. J. Choi, C. G. Kim, A. Oshima, and J. E. Green. "Gene expression signatures to predict the response of gastric cancer to cisplatin and fluorouracil." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 4628. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.4628.

Full text
Abstract:
4628 Background: A prospective high-throughput gene expression study was conducted to identify transcriptional profiles predictive of a clinical response to cisplatin and fluorouracil (CF) combination chemotherapy and to identify dysregulated genes associated with acquired resistance to CF. Methods: Endoscopic biopsy samples were collected from CF-treated metastatic gastric cancer (MGC) patients (pts) prior to CF (n = 123) and following the development of resistance (n = 22) at the National Cancer Center of Korea from 2001 to 2006, and analyzed using CGH and expression microarrays. We developed 2 survival risk predictors. The first predictor was constructed using genes in DNA amplicons and identified in the expression signature that correlates with survival (intrinsic resistance signature). The second predictor was based on the acquired resistance signature, which was identified by comparing matched expression array data from initially responsive patients prior to treatment with profiles obtained at progressive disease. Results: Array CGH revealed the gene amplification of MYC, EGFR, and FGFR2 whose Affymetrix U133A signals significantly correlated with a poor prognosis (P values, 0.0154, 0.0096, and 0.0057) of training set pts (n = 96). Three-gene-predicted high-risk group of the validation cohort (n = 10) demonstrated a shorter median survival than low-risk (n = 17) group (7.4 vs 16.8 months; p = 0.047). The 3-gene signature, as a continuous variable, was the independent predictor for overall survival (OS) and time to progression (TTP) (adjusted P, 0.021, and 0.012). Importantly, the acquired resistance signature strongly overlapped the intrinsic resistance signature (LS P<10-5), and was highly enriched for MYC target genes (LS p = 2x10-5). A predictor based on MYC target genes within the acquired resistance signature was the independent predictor for OS and TTP of 101 separate pts (adjusted p, 0.015, and 0.011). Conclusions: Combined overexpression of MYC, EGFR, and FGFR2 predicts a poor response of MGC pts to CF. There is significant overlap between intrinsic and acquired resistance signatures of MGC, where the MYC gene network plays a central role. This is the first demonstration that the acquired resistance signature predicts the initial response to chemotherapy. No significant financial relationships to disclose.
APA, Harvard, Vancouver, ISO, and other styles
30

Kim, Jung-whan, Karen I. Zeller, Yunyue Wang, Anil G. Jegga, Bruce J. Aronow, Kathryn A. O'Donnell, and Chi V. Dang. "Evaluation of Myc E-Box Phylogenetic Footprints in Glycolytic Genes by Chromatin Immunoprecipitation Assays." Molecular and Cellular Biology 24, no. 13 (July 1, 2004): 5923–36. http://dx.doi.org/10.1128/mcb.24.13.5923-5936.2004.

Full text
Abstract:
ABSTRACT Prediction of gene regulatory sequences using phylogenetic footprinting has advanced considerably but lacks experimental validation. Here, we report whether transcription factor binding sites predicted by dot plotting or web-based Trafac analysis could be validated by chromatin immunoprecipitation assays. MYC overexpression enhances glycolysis without hypoxia and hence may contribute to altered tumor metabolism. Because the full spectrum of glycolytic genes directly regulated by Myc is not known, we chose Myc as a model transcription factor to determine whether it binds target glycolytic genes that have conserved canonical Myc binding sites or E boxes (5′-CACGTG-3′). Conserved canonical E boxes in ENO1, HK2, and LDHA occur in 31- to 111-bp islands with high interspecies sequence identity (>65%). Trafac analysis revealed another region in ENO1 that corresponds to a murine region with a noncanonical E box. Myc bound all these conserved regions well in the human P493-6 B lymphocytes. We also determined whether Myc could bind nonconserved canonical E boxes found in the remaining human glycolytic genes. Myc bound PFKM, but it did not significantly bind GPI, PGK1, and PKM2. Binding to BPGM, PGAM2, and PKLR was not detected. Both GAPD and TPI1 do not have conserved E boxes but are induced and bound by Myc through regions with noncanonical E boxes. Our results indicate that Myc binds well to conserved canonical E boxes, but not nonconserved E boxes. However, the binding of Myc to unpredicted genomic regions with noncanonical E boxes reveals a limitation of phylogenetic footprinting. In aggregate, these observations indicate that Myc is an important regulator of glycolytic genes, suggesting that MYC plays a key role in a switch to glycolytic metabolism during cell proliferation or tumorigenesis.
APA, Harvard, Vancouver, ISO, and other styles
31

Robaina, Mazzoccoli, and Esteves Klumb. "Germinal Centre B Cell Functions and Lymphomagenesis: Circuits Involving MYC and MicroRNAs." Cells 8, no. 11 (October 31, 2019): 1365. http://dx.doi.org/10.3390/cells8111365.

Full text
Abstract:
Background: The transcription factor MYC regulates several biological cellular processes, and its target gene network comprises approximately 15% of all human genes, including microRNAs (miRNAs), that also contribute to MYC regulatory activity. Although miRNAs are emerging as key regulators of immune functions, the specific roles of miRNAs in the regulation/dysregulation of germinal centre B-cells and B-cell lymphomas are still being uncovered. The regulatory network that integrates MYC, target genes and miRNAs is a field of intense study, highlighting potential pathways to be explored in the context of future clinical approaches. Methods: The scientific literature that is indexed in PUBMED was consulted for publications involving MYC and miRNAs with validated bioinformatics analyses or experimental protocols. Additionally, seminal studies on germinal centre B-cell functions and lymphomagenesis were reported. Conclusions: This review summarizes the interactions between MYC and miRNAs through regulatory loops and circuits involving target genes in germinal centre B-cell lymphomas with MYC alterations. Moreover, we provide an overview of the understanding of the regulatory networks between MYC and miRNAs, highlighting the potential implication of this approach for the comprehension of germinal centre B-cell lymphoma pathogenesis. Therefore, circuits involving MYC, target genes and miRNAs provide novel insight into lymphomagenesis that could be useful for new improved therapeutic strategies.
APA, Harvard, Vancouver, ISO, and other styles
32

Schreiber-Agus, N., J. Horner, R. Torres, F. C. Chiu, and R. A. DePinho. "Zebra fish myc family and max genes: differential expression and oncogenic activity throughout vertebrate evolution." Molecular and Cellular Biology 13, no. 5 (May 1993): 2765–75. http://dx.doi.org/10.1128/mcb.13.5.2765.

Full text
Abstract:
To gain insight into the role of Myc family oncoproteins and their associated protein Max in vertebrate growth and development, we sought to identify homologs in the zebra fish (Brachydanio rerio). A combination of a polymerase chain reaction-based cloning strategy and low-stringency hybridization screening allowed for the isolation of zebra fish c-, N-, and L-myc and max genes; subsequent structural characterization showed a high degree of conservation in regions that encode motifs of known functional significance. On the functional level, zebra fish Max, like its mammalian counterpart, served to suppress the transformation activity of mouse c-Myc in rat embryo fibroblasts. In addition, the zebra fish c-myc gene proved capable of cooperating with an activated H-ras to effect the malignant transformation of mammalian cells, albeit with diminished potency compared with mouse c-myc. With respect to their roles in normal developing tissues, the differential temporal and spatial patterns of steady-state mRNA expression observed for each zebra fish myc family member suggest unique functions for L-myc in early embryogenesis, for N-myc in establishment and growth of early organ systems, and for c-myc in increasingly differentiated tissues. Furthermore, significant alterations in the steady-state expression of zebra fish myc family genes concomitant with relatively constant max expression support the emerging model of regulation of Myc function in cellular growth and differentiation.
APA, Harvard, Vancouver, ISO, and other styles
33

Schreiber-Agus, N., J. Horner, R. Torres, F. C. Chiu, and R. A. DePinho. "Zebra fish myc family and max genes: differential expression and oncogenic activity throughout vertebrate evolution." Molecular and Cellular Biology 13, no. 5 (May 1993): 2765–75. http://dx.doi.org/10.1128/mcb.13.5.2765-2775.1993.

Full text
Abstract:
To gain insight into the role of Myc family oncoproteins and their associated protein Max in vertebrate growth and development, we sought to identify homologs in the zebra fish (Brachydanio rerio). A combination of a polymerase chain reaction-based cloning strategy and low-stringency hybridization screening allowed for the isolation of zebra fish c-, N-, and L-myc and max genes; subsequent structural characterization showed a high degree of conservation in regions that encode motifs of known functional significance. On the functional level, zebra fish Max, like its mammalian counterpart, served to suppress the transformation activity of mouse c-Myc in rat embryo fibroblasts. In addition, the zebra fish c-myc gene proved capable of cooperating with an activated H-ras to effect the malignant transformation of mammalian cells, albeit with diminished potency compared with mouse c-myc. With respect to their roles in normal developing tissues, the differential temporal and spatial patterns of steady-state mRNA expression observed for each zebra fish myc family member suggest unique functions for L-myc in early embryogenesis, for N-myc in establishment and growth of early organ systems, and for c-myc in increasingly differentiated tissues. Furthermore, significant alterations in the steady-state expression of zebra fish myc family genes concomitant with relatively constant max expression support the emerging model of regulation of Myc function in cellular growth and differentiation.
APA, Harvard, Vancouver, ISO, and other styles
34

Yang, Rui, Wenzhe Wang, Meichen Dong, Kristen Roso, Xuhui Bao, Christopher Pirozzi, Darell Bigner, et al. "BIOL-10. DISTRIBUTION AND VULNERABILITY OF TRANSCRIPTIONAL OUTPUTS ACROSS THE GENOME IN MYC-AMPLIFIED MEDULLOBLASTOMA CELLS." Neuro-Oncology 23, Supplement_1 (June 1, 2021): i5. http://dx.doi.org/10.1093/neuonc/noab090.017.

Full text
Abstract:
Abstract Myc plays a central role in tumorigenesis by orchestrating the expression of genes essential to numerous cellular processes. While it is well established that Myc functions by binding to its target genes to regulate their transcription, the distribution of the transcriptional output across human genome in Myc-amplified cancer cells, and the susceptibility of such transcriptional outputs to therapeutic interferences remain to be fully elucidated. Here, we analyze the distribution of transcriptional outputs in Myc-amplified medulloblastoma (MB) cells by profiling nascent total RNAs within a temporal context. This profiling reveals a major portion of transcriptional action in these cells was directed at the genes fundamental to cellular infrastructures, including rRNAs and particularly those in the mitochondrial genome (mtDNA). Notably, even when Myc protein was depleted by as much as 80%, the impact on transcriptional outputs across the genome was limited, with notable reduction mostly in genes of involved in ribosomal biosynthesis, genes residing in mtDNA or encoding mitochondria-localized proteins, and those encoding histones. In contrast to the limited direct impact of Myc depletion, we found that the global transcriptional outputs were highly dependent on the activity of Inosine Monophosphate Dehydrogenases (IMPDHs), rate limiting enzymes for de novo guanine nucleotide synthesis and whose expression in tumor cells was positively correlated with Myc’s expression. Blockage of IMPDHs attenuated the global transcriptional outputs with a particularly strong inhibitory effect on the aforementioned infrastructure genes, which was accompanied by the abrogation of MB cell’s proliferation in vitro and in vivo. Together, our findings reveal a real time action of Myc as a transcriptional factor in tumor cells, gain new insight into the pathogenic mechanism underlying Myc-driven tumorigenesis, and support IMPDHs as a therapeutic vulnerability in MB cells empowered by a high level of Myc oncoprotein.
APA, Harvard, Vancouver, ISO, and other styles
35

Liu, Xuefeng, Gary L. Disbrow, Hang Yuan, Vjekoslav Tomaić, and Richard Schlegel. "Myc and Human Papillomavirus Type 16 E7 Genes Cooperate To Immortalize Human Keratinocytes." Journal of Virology 81, no. 22 (September 5, 2007): 12689–95. http://dx.doi.org/10.1128/jvi.00669-07.

Full text
Abstract:
ABSTRACT The E6 protein of the oncogenic human papillomaviruses (HPVs), in combination with the E7 protein, is essential for the efficient immortalization of human foreskin keratinocytes (HFKs). Since we recently demonstrated that E6 activates the human telomerase reverse transcriptase (hTERT) promoter via a Myc-dependent mechanism, we speculated that overexpressed Myc might be able to substitute for E6 in cell immortalization. Myc (similar to E6) was unable to immortalize HFKs when transduced alone, despite inducing high levels of telomerase activity. However, when transduced with E7, Myc immortalized HFKs following a brief but detectable crisis period. In contrast to E6 + E7-immortalized cells, the Myc + E7-immortalized cells expressed high levels of p53 protein as well as two p53-regulated proteins, p21 and hdm-2. The increase in p21 and hdm-2 proteins correlated directly with their mRNA levels, suggesting transcriptional activation of the respective genes by the overexpressed p53 protein. Interestingly, a significant proportion of the p53 protein in the Myc + E7-immortalized cells was localized to the cytoplasm, potentially due to interactions with the overexpressed hdm-2 protein. Regardless, cell immortalization by the Myc + E7 genes occurred independently of p53 degradation. Since we have already observed high-efficiency cell immortalization with the hTERT + E7 or E6 mutant (p53 degradation-defective) + E7 genes (i.e., no crisis period) that proceeds in the presence of high levels of p53, we hypothesize that the crisis period in the Myc + E7 cells is due not to the levels of the p53 protein but rather to unique properties of the Myc protein. The common factor in cell immortalization by the three gene sets (E6 + E7, Myc + E7, and hTERT + E7 genes) is the induction of telomerase activity.
APA, Harvard, Vancouver, ISO, and other styles
36

Van Beneden, R. J., D. K. Watson, T. T. Chen, J. A. Lautenberger, and T. S. Papas. "Cellular myc (c-myc) in fish (rainbow trout): its relationship to other vertebrate myc genes and to the transforming genes of the MC29 family of viruses." Proceedings of the National Academy of Sciences 83, no. 11 (June 1, 1986): 3698–702. http://dx.doi.org/10.1073/pnas.83.11.3698.

Full text
APA, Harvard, Vancouver, ISO, and other styles
37

Lewis, B. C., H. Shim, Q. Li, C. S. Wu, L. A. Lee, A. Maity, and C. V. Dang. "Identification of putative c-Myc-responsive genes: characterization of rcl, a novel growth-related gene." Molecular and Cellular Biology 17, no. 9 (September 1997): 4967–78. http://dx.doi.org/10.1128/mcb.17.9.4967.

Full text
Abstract:
The c-Myc protein is a helix-loop-helix leucine zipper oncogenic transcription factor that participates in the regulation of cell proliferation, differentiation, and apoptosis. The biochemical function of c-Myc has been well described, yet the identities of downstream effectors are just beginning to emerge. We describe the identification of a set of c-Myc-responsive genes in the Rat1a fibroblast through the application of cDNA representational difference analysis (RDA) to cDNAs isolated from nonadherent Rat1a and Rat1a-myc cells. In this system, c-Myc overexpression is sufficient to induce the transformed phenotype of anchorage-independent growth. We identified 20 differentially expressed cDNAs, several of which represent novel cDNA sequences. We further characterized one of the novel cDNAs identified in this screen, termed rcl. rcl expression is (i) directly stimulated by c-Myc; (ii) stimulated in the in vivo growth system of regenerating rat liver, as is c-myc; and (iii) elevated in human lymphoid cells that overexpress c-myc. By using an anti-Rcl antibody, immunoblot analysis, and immunofluorescence microscopy, the Rcl protein was found to be a 23-kDa nuclear protein. Ectopic expression of the protein encoded by the rcl cDNA induces anchorage-independent growth in Rat1a fibroblasts, albeit to a diminished extent compared to ectopic c-Myc expression. These data suggest a role for rcl during cellular proliferation and c-Myc-mediated transformation.
APA, Harvard, Vancouver, ISO, and other styles
38

Saksela, Kalle. "myc Genes and their deregulation in lung cancer." Journal of Cellular Biochemistry 42, no. 3 (March 1990): 153–80. http://dx.doi.org/10.1002/jcb.240420306.

Full text
APA, Harvard, Vancouver, ISO, and other styles
39

Watson, John D., Sara K. Oster, Mary Shago, Fereshteh Khosravi, and Linda Z. Penn. "Identifying Genes Regulated in a Myc-dependent Manner." Journal of Biological Chemistry 277, no. 40 (July 26, 2002): 36921–30. http://dx.doi.org/10.1074/jbc.m201493200.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

Zirin, Jonathan, Xiaochun Ni, Laura M. Sack, Donghui Yang-Zhou, Yanhui Hu, Roderick Brathwaite, Martha L. Bulyk, Stephen J. Elledge, and Norbert Perrimon. "Interspecies analysis of MYC targets identifies tRNA synthetases as mediators of growth and survival in MYC-overexpressing cells." Proceedings of the National Academy of Sciences 116, no. 29 (July 1, 2019): 14614–19. http://dx.doi.org/10.1073/pnas.1821863116.

Full text
Abstract:
Aberrant MYC oncogene activation is one of the most prevalent characteristics of cancer. By overlapping datasets of Drosophila genes that are insulin-responsive and also regulate nucleolus size, we enriched for Myc target genes required for cellular biosynthesis. Among these, we identified the aminoacyl tRNA synthetases (aaRSs) as essential mediators of Myc growth control in Drosophila and found that their pharmacologic inhibition is sufficient to kill MYC-overexpressing human cells, indicating that aaRS inhibitors might be used to selectively target MYC-driven cancers. We suggest a general principle in which oncogenic increases in cellular biosynthesis sensitize cells to disruption of protein homeostasis.
APA, Harvard, Vancouver, ISO, and other styles
41

Tokgun, Onur, Pervin E. Tokgun, Kubilay Inci, and Hakan Akca. "lncRNAs as Potential Targets in Small Cell Lung Cancer: MYC -dependent Regulation." Anti-Cancer Agents in Medicinal Chemistry 20, no. 17 (November 12, 2020): 2074–81. http://dx.doi.org/10.2174/1871520620666200721130700.

Full text
Abstract:
Background: Small Cell Lung Cancer (SCLC) is a highly aggressive malignancy. MYC family oncogenes are amplified and overexpressed in 20% of SCLCs, showing that MYC oncogenes and MYC regulated genes are strong candidates as therapeutic targets for SCLC. c-MYC plays a fundamental role in cancer stem cell properties and malignant transformation. Several targets have been identified by the activation/repression of MYC. Deregulated expression levels of lncRNAs have also been observed in many cancers. Objective: The aim of the present study is to investigate the lncRNA profiles which depend on MYC expression levels in SCLC. Methods: Firstly, we constructed lentiviral vectors for MYC overexpression/inhibition. MYC expression is suppressed by lentiviral shRNA vector in MYC amplified H82 and N417 cells, and overexpressed by lentiviral inducible overexpression vector in MYC non-amplified H345 cells. LncRNA cDNA is transcribed from total RNA samples, and 91 lncRNAs are evaluated by qRT-PCR. Results: We observed that N417, H82 and H345 cells require MYC for their growth. Besides, MYC is not only found to regulate the expressions of genes related to invasion, stem cell properties, apoptosis and cell cycle (p21, Bcl2, cyclinD1, Sox2, Aldh1a1, and N-Cadherin), but also found to regulate lncRNAs. With this respect, expressions of AK23948, ANRIL, E2F4AS, GAS5, MEG3, H19, L1PA16, SFMBT2, ZEB2NAT, HOTAIR, Sox2OT, PVT1, and BC200 were observed to be in parallel with MYC expression, whereas expressions of Malat1, PTENP1, Neat1, UCA1, SNHG3, and SNHG6 were inversely correlated. Conclusion: Targeting MYC-regulated genes as a therapeutic strategy can be important for SCLC therapy. This study indicated the importance of identifying MYC-regulated lncRNAs and that these can be utilized to develop a therapeutic strategy for SCLC.
APA, Harvard, Vancouver, ISO, and other styles
42

Nedeljković, Milica, Nikola Tanić, Tatjana Dramićanin, Zorka Milovanović, Snežana Šušnjar, Vedrana Milinković, Ivana Vujović, Mirjana Prvanović, and Nasta Tanić. "Importance of Copy Number Alterations of FGFR1 and C-MYC Genes in Triple Negative Breast Cancer." Journal of Medical Biochemistry 38, no. 1 (March 1, 2019): 63–70. http://dx.doi.org/10.2478/jomb-2018-0012.

Full text
Abstract:
Summary Background: Triple negative breast cancer (TNBC) is characterized by aggressive clinical course and is unresponsive to anti-HER2 and endocrine therapy. TNBC is difficult to treat and is often lethal. Given the need to find new targets for therapy we explored clinicopathological significance of copy number gain of FGFR1 and c-MYC. Our aim was to determine the impact of FGFR1 and c-MYC copy number gain on clinical course and outcome of TNBC. Methods: FGFR1 and c-MYC gene copy number alterations were evaluated in 78 archive TNBC samples using TaqMan based quantitative real time PCR assays. Results: 50% of samples had increased c-MYC copy number. c-MYC copy number gain was associated with TNBC in contrast to ER positive cancers. Our results showed significant correlation between c-MYC copy number gain and high grade of TNBCs. This suggests that c-MYC copy number could be an useful prognostic marker for TNBC patients. c-MYC copy number gain was associated with high pTNM stage as well as lobular and medullary tumor subtypes. 43% of samples had increased FGFR1 copy number. No correlations between FGFR1 copy number gain and clinicopathological variables were observed. Conclusions: We identified c-MYC copy number gain as a prognostic marker for TNBC. Our results indicate that c- MYC may contribute to TNBC progression. We observed no significant association between c-MYC and/or FGFR1 copy number status and patient survival.
APA, Harvard, Vancouver, ISO, and other styles
43

Kim, So Hee, Bokyung Kim, Jung Hak Kim, Dong-Hoon Kim, Seung Hoon Lee, Dong-Seok Lee, and Hong J. Lee. "L-myc Gene Expression in Canine Fetal Fibroblasts Promotes Self-Renewal Capacity but Not Tumor Formation." Cells 10, no. 8 (August 4, 2021): 1980. http://dx.doi.org/10.3390/cells10081980.

Full text
Abstract:
Canines are useful in mammalian preclinical studies because they are larger than rodents and share many diseases with humans. Canine fetal fibroblast cells (CFFs) are an easily accessible source of somatic cells. However, they are easily driven to senescence and become unusable with continuous in vitro culture. Therefore, to overcome these deficiencies, we investigated whether tetracycline-inducible L-myc gene expression promotes self-renewal activity and tumorigenicity in the production of induced conditional self-renewing fibroblast cells (iCSFCs). Here, we describe the characterization of a new iCSFC line immortalized by transduction with L-myc that displays in vitro self-renewal ability without tumorigenic capacity. We established conditionally inducible self-renewing fibroblast cells by transducing CFF-3 cells with L-myc under the tetracycline-inducible gene expression system. In the absence of doxycycline, the cells did not express L-myc or undergo self-renewal. The iCSFCs had a fibroblast-like morphology, normal chromosome pattern, and expressed fibroblast-specific genes and markers. However, the iCSFCs did not form tumors in a soft agar colony-forming assay. We observed higher expression of three ES modules (core pluripotency genes, polycomb repressive complex genes (PRC), and MYC-related genes) in the iCSFCs than in the CFF-3 cells; in particular, the core pluripotency genes (OCT4, SOX2, and NANOG) were markedly up-regulated compared with the PRC and MYC module genes. These results demonstrated that, in canine fetal fibroblasts, L-myc tetracycline-inducible promoter-driven gene expression induces self-renewal capacity but not tumor formation. This study suggests that L-myc gene-induced conditional self-renewing fibroblast cells can be used as an in vitro tool in a variety of biomedical studies related to drug screening.
APA, Harvard, Vancouver, ISO, and other styles
44

Schreiber-Agus, N., R. Torres, J. Horner, A. Lau, M. Jamrich, and R. A. DePinho. "Comparative analysis of the expression and oncogenic activities of Xenopus c-, N-, and L-myc homologs." Molecular and Cellular Biology 13, no. 4 (April 1993): 2456–68. http://dx.doi.org/10.1128/mcb.13.4.2456.

Full text
Abstract:
A polymerase chain reaction-based cloning strategy allowed for the isolation of two distinct Xenopus L-myc genes, as well as previously isolated xc- and xN-myc genes, thus demonstrating that these three well-defined members of the mammalian myc gene family are present in lower vertebrates as well. Comparison of the Xenopus and mammalian Myc families revealed a high degree of structural relatedness at the gene and protein levels; this homology was consistent with the ability of the xc-myc1 and xN-myc1 genes to function as oncogenes in primary mammalian cells. In contrast, the xL-myc1 gene was found to be incapable of transforming rat embryo fibroblast cells, and this inactivity may relate to localized but significant differences in its putative transactivation domain. Analysis of xc-, xN-, and xL-myc gene expression demonstrated that (i) all three genes were highly expressed during oogenesis and their transcripts accumulated as abundant maternal mRNAs, (ii) each gene exhibited a distinctive pattern of expression during embryogenesis and in adult tissues, and (iii) the xL-myc1 and xL-myc2 genes were coordinately expressed in the maternal and zygotic genomes. The markedly high expression of the Xenopus myc gene family in differentiated tissues, such as the central nervous system and kidney, contrasts sharply with the low levels observed in mammalian adult tissues. These differences may reflect unique functions of the Myc family proteins in processes specific to amphibians, such as tissue regeneration.
APA, Harvard, Vancouver, ISO, and other styles
45

Schreiber-Agus, N., R. Torres, J. Horner, A. Lau, M. Jamrich, and R. A. DePinho. "Comparative analysis of the expression and oncogenic activities of Xenopus c-, N-, and L-myc homologs." Molecular and Cellular Biology 13, no. 4 (April 1993): 2456–68. http://dx.doi.org/10.1128/mcb.13.4.2456-2468.1993.

Full text
Abstract:
A polymerase chain reaction-based cloning strategy allowed for the isolation of two distinct Xenopus L-myc genes, as well as previously isolated xc- and xN-myc genes, thus demonstrating that these three well-defined members of the mammalian myc gene family are present in lower vertebrates as well. Comparison of the Xenopus and mammalian Myc families revealed a high degree of structural relatedness at the gene and protein levels; this homology was consistent with the ability of the xc-myc1 and xN-myc1 genes to function as oncogenes in primary mammalian cells. In contrast, the xL-myc1 gene was found to be incapable of transforming rat embryo fibroblast cells, and this inactivity may relate to localized but significant differences in its putative transactivation domain. Analysis of xc-, xN-, and xL-myc gene expression demonstrated that (i) all three genes were highly expressed during oogenesis and their transcripts accumulated as abundant maternal mRNAs, (ii) each gene exhibited a distinctive pattern of expression during embryogenesis and in adult tissues, and (iii) the xL-myc1 and xL-myc2 genes were coordinately expressed in the maternal and zygotic genomes. The markedly high expression of the Xenopus myc gene family in differentiated tissues, such as the central nervous system and kidney, contrasts sharply with the low levels observed in mammalian adult tissues. These differences may reflect unique functions of the Myc family proteins in processes specific to amphibians, such as tissue regeneration.
APA, Harvard, Vancouver, ISO, and other styles
46

Bueno, María J., Marta Gómez de Cedrón, Gonzalo Gómez-López, Ignacio Pérez de Castro, Lorena Di Lisio, Santiago Montes-Moreno, Nerea Martínez, et al. "Combinatorial effects of microRNAs to suppress the Myc oncogenic pathway." Blood 117, no. 23 (June 9, 2011): 6255–66. http://dx.doi.org/10.1182/blood-2010-10-315432.

Full text
Abstract:
Abstract Many mammalian transcripts contain target sites for multiple miRNAs, although it is not clear to what extent miRNAs may coordinately regulate single genes. We have mapped the interactions between down-regulated miRNAs and overexpressed target protein-coding genes in murine and human lymphomas. Myc, one of the hallmark oncogenes in these lymphomas, stands out as the up-regulated gene with the highest number of genetic interactions with down-regulated miRNAs in mouse lymphomas. The regulation of Myc by several of these miRNAs is confirmed by cellular and reporter assays. The same approach identifies MYC and multiple Myc targets as a preferential target of down-regulated miRNAs in human Burkitt lymphoma, a pathology characterized by translocated MYC oncogenes. These results indicate that several miRNAs must be coordinately down-regulated to enhance critical oncogenes, such as Myc. Some of these Myc-targeting miRNAs are repressed by Myc, suggesting that these tumors are a consequence of the unbalanced activity of Myc versus miRNAs.
APA, Harvard, Vancouver, ISO, and other styles
47

Zimmerman, K., E. Legouy, V. Stewart, R. Depinho, and F. W. Alt. "Differential regulation of the N-myc gene in transfected cells and transgenic mice." Molecular and Cellular Biology 10, no. 5 (May 1990): 2096–103. http://dx.doi.org/10.1128/mcb.10.5.2096.

Full text
Abstract:
The N-myc gene is expressed specifically in the early developmental stages of numerous cell lineages. To assay for sequences that could potentially regulate N-myc expression, we transfected constructs that contained murine N-myc genomic sequences linked to a reporter gene and genomic clones that contained the complete human or murine N-myc genes into cell lines that either express or do not express the endogenous N-myc gene. Following either transient or stable transfection, the introduced N-myc sequences were expressed regardless of the expression status of the endogenous gene. In contrast, when the clones containing the complete human N-myc gene were introduced into the germline of transgenic mice, expression in some transgenic lines paralleled the tissue- and stage-specific expression of the endogenous murine gene. These findings demonstrate differences in the regulation of N-myc genes in recipient cells following in vitro versus in vivo introduction, suggesting that early developmental events may play a role in the regulation of N-myc expression.
APA, Harvard, Vancouver, ISO, and other styles
48

Zimmerman, K., E. Legouy, V. Stewart, R. Depinho, and F. W. Alt. "Differential regulation of the N-myc gene in transfected cells and transgenic mice." Molecular and Cellular Biology 10, no. 5 (May 1990): 2096–103. http://dx.doi.org/10.1128/mcb.10.5.2096-2103.1990.

Full text
Abstract:
The N-myc gene is expressed specifically in the early developmental stages of numerous cell lineages. To assay for sequences that could potentially regulate N-myc expression, we transfected constructs that contained murine N-myc genomic sequences linked to a reporter gene and genomic clones that contained the complete human or murine N-myc genes into cell lines that either express or do not express the endogenous N-myc gene. Following either transient or stable transfection, the introduced N-myc sequences were expressed regardless of the expression status of the endogenous gene. In contrast, when the clones containing the complete human N-myc gene were introduced into the germline of transgenic mice, expression in some transgenic lines paralleled the tissue- and stage-specific expression of the endogenous murine gene. These findings demonstrate differences in the regulation of N-myc genes in recipient cells following in vitro versus in vivo introduction, suggesting that early developmental events may play a role in the regulation of N-myc expression.
APA, Harvard, Vancouver, ISO, and other styles
49

Scafuro, Marika, Lucia Capasso, Vincenzo Carafa, Lucia Altucci, and Angela Nebbioso. "Gene Transactivation and Transrepression in MYC-Driven Cancers." International Journal of Molecular Sciences 22, no. 7 (March 27, 2021): 3458. http://dx.doi.org/10.3390/ijms22073458.

Full text
Abstract:
MYC is a proto-oncogene regulating a large number of genes involved in a plethora of cellular functions. Its deregulation results in activation of MYC gene expression and/or an increase in MYC protein stability. MYC overexpression is a hallmark of malignant growth, inducing self-renewal of stem cells and blocking senescence and cell differentiation. This review summarizes the latest advances in our understanding of MYC-mediated molecular mechanisms responsible for its oncogenic activity. Several recent findings indicate that MYC is a regulator of cancer genome and epigenome: MYC modulates expression of target genes in a site-specific manner, by recruiting chromatin remodeling co-factors at promoter regions, and at genome-wide level, by regulating the expression of several epigenetic modifiers that alter the entire chromatin structure. We also discuss novel emerging therapeutic strategies based on both direct modulation of MYC and its epigenetic cofactors.
APA, Harvard, Vancouver, ISO, and other styles
50

Ho, Jenny S. L., Weili Ma, Daniel Y. L. Mao, and Samuel Benchimol. "p53-Dependent Transcriptional Repression of c-myc Is Required for G1 Cell Cycle Arrest." Molecular and Cellular Biology 25, no. 17 (September 1, 2005): 7423–31. http://dx.doi.org/10.1128/mcb.25.17.7423-7431.2005.

Full text
Abstract:
ABSTRACT The ability of p53 to promote apoptosis and cell cycle arrest is believed to be important for its tumor suppression function. Besides activating the expression of cell cycle arrest and proapoptotic genes, p53 also represses a number of genes. Previous studies have shown an association between p53 activation and down-regulation of c-myc expression. However, the mechanism and physiological significance of p53-mediated c-myc repression remain unclear. Here, we show that c-myc is repressed in a p53-dependent manner in various mouse and human cell lines and mouse tissues. Furthermore, c-myc repression is not dependent on the expression of p21WAF1. Abrogating the repression of c-myc by ectopic c-myc expression interferes with the ability of p53 to induce G1 cell cycle arrest and differentiation but enhances the ability of p53 to promote apoptosis. We propose that p53-dependent cell cycle arrest is dependent not only on the transactivation of cell cycle arrest genes but also on the transrepression of c-myc. Chromatin immunoprecipitation assays indicate that p53 is bound to the c-myc promoter in vivo. We report that trichostatin A, an inhibitor of histone deacetylases, abrogates the ability of p53 to repress c-myc transcription. We also show that p53-mediated transcriptional repression of c-myc is accompanied by a decrease in the level of acetylated histone H4 at the c-myc promoter and by recruitment of the corepressor mSin3a. These data suggest that p53 represses c-myc transcription through a mechanism that involves histone deacetylation.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Myc Genes' for other source types:
Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography