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At least 307 records · Page 17Linked to original sources
PubMed1997

L-Myc overexpression and detection of auto-antibodies against L-Myc in both the serum and pleural effusion from a patient with non-small cell lung cancer.

Non-small cell lung cancer patient was found to have auto-antibodies against L-Myc in both the serum and pleural effusion. The titer of anti-L-Myc antibodies was higher in the pleural effusion than in the serum. Overexpression of L-Myc without DNA amplification was observed in the tumor cells. L-Myc antigen was not detected in either the serum or the pleural effusion. Anti-nuclear antibodies were also detected in both the serum and pleural effusion, although this patient did not have collagen-vascular disease.

Aged↗
PubMed1991

Derivation of mixed phenotype cell lines with ras-myc- and raf-myc-containing retroviral vectors after infection of murine long-term bone marrow cultures.

Murine long-term bone marrow cultures were infected with retroviral vectors expressing the viral ras, raf, and myc oncogenes, alone and in combination. Stably transformed clonal cell lines were obtained after infection with ras-myc and raf-myc retroviruses but not by vectors expressing ras, myc, or raf alone. Northern blot analysis demonstrated that the two clonal cell lines expressed high levels of vector-specific transcripts. Phenotypic analysis of the cell lines by flow microfluorimetry and histochemical staining suggested that both cell lines expressed markers associated with cells of the megakaryocyte differentiation pathway. Histochemical staining demonstrated that these cell lines also expressed cytoplasmic enzymes associated with granulocytes and/or monocytes/macrophages. These cell lines, despite their clonal origin, are therefore of a mixed phenotype.

Acetylcholinesterase↗
PubMedDate not supplied

C-myc, N-myc, N-ras, and c-erb-B: lack of amplification or rearrangement in human medullary thyroid carcinoma and a derivative cell line.

We investigated the copy number and possible rearrangement of the four protooncogenes, c-myc, N-myc, N-ras, and c-erb-B, in DNA from seven untreated primary cancers or metastases of medullary thyroid carcinoma and an established human medullary thyroid carcinoma cell line, TT, using the Southern blotting technique. The purpose of this study was two-fold: 1) to examine whether protooncogene perturbations in medullary thyroid carcinoma could be considered as a prognostic marker; and 2) to determine whether the protooncogenes could have a possible role in medullary thyroid tumorigenesis. Neither amplification nor rearrangement of the protooncogenes was detectable in the DNA from any tumor samples or in the cell line. Our results suggest that DNA-evident amplification and rearrangement of the c-myc, N-myc, N-ras, and c-erb-B oncogenes may not be mechanisms through which these oncogenes become activated in this malignancy.

Carcinoma↗
PubMedDate not supplied

Immortalization by truncated myc or ras genes and synergism between myc and ras genes in cell transformation.

Human c-myc and normal or mutant T24 H-ras1 genes either linked to the regulatory sequences of the human metallothionein IIa gene or unlinked have been employed individually or in combination to transfect early passage Chinese hamster lung cells. Since the c-myc and H-ras1 genes are present in recombinant plasmids carrying the aminoglycoside phosphotransferase (aph), gene transfectants were selected in the presence of geneticin. A synergistic effect has been observed between myc and H-ras1 genes in measurement of both the number of geneticin resistant colonies obtained and the parameters of morphological transformation and anchorage independence. Out study also demonstrates the ability of truncated myc and ras genes to induce immortalization of hamster cells.

Animals↗
PubMedDate not supplied

Reduction of cisplatin cytotoxicity on human lung cancer cell lines with N-myc amplification by pretreatment with N-myc antisense oligodeoxynucleotides.

Effect of N-myc antisense oligodeoxynucleotide (ODN) on the proliferation of tumor cells and its combined antitumor effect with cisplatin were examined in vitro on human lung cancer cell lines with N-myc amplification. The N-myc oligomer containing the sequence complementary to the ATG initiation codon exhibited a stronger antiproliferative effect on tumor cells than did the oligomer not containing the sequence. A significant difference in the anti-proliferative effect between antisense ODN and sense ODN treatment was observed only on tumor cells with N-myc amplification. Pretreatment with antisense ODN showed a tendency to reduce rather than enhance cisplatin cytotoxicity. Posttreatment with antisense ODN also showed no beneficial effects on cisplatin cytotoxicity. This study suggests that pretreatment with antisense ODN may not be beneficial when combined with chemotherapy.

Base Sequence↗
PubMed1997

Expression and subcellular localization of the Myc superfamily proteins: c-Myc, Max, Mad1 and Mxi1 in the epiphyseal plate cartilage chondrocytes of growing rats.

The changes in the expressions of the protooncogene protein c-Myc, its dimerization partner Max and the competitive inhibitors Mad1 and Mxi1 during the terminal differentiation of chondrocytes in vivo were investigated by immunocytochemistry. The four immunoreactivity patterns in the epiphyseal plate cartilage of growing rats, as they appeared under the light microscope, showed differences in protein expression level and intracellular distribution, with the chondrocyte developmental stage. c-Myc immunoreactivity was intense and mainly in the nuclei of proliferative chondrocytes. It decreased in the nuclei of mature chondrocytes and appeared in the cytoplasm. c-Myc immunoreactivity increased in the fully-differentiated hypertrophic chondrocytes. Immunoreactivity of the c-Myc dimerization partner Max was mainly in the nucleus of proliferative chondrocytes and decreased as the chondrocytes matured. Mad1 immunoreactivity was also concentrated in the nucleus of proliferative chondrocytes, but was mainly in the cytoplasm of mature chondrocytes and almost lost from the hypertrophic chondrocytes. Lastly, there was Mxi1 immunoreactivity in the nucleus and cytoplasm of proliferative, mature and early hypertrophic chondrocytes and the cytoplasm staining was more sustained than in the nucleus. There was little labeling in late hypertrophic chondrocytes. The electron microscope pictures corroborated these findings and showed the subcellular distributions of the immunolabelings. The gold particles reflecting Mad1 frequently formed patches and those for Mxi1 appeared to accumulate within the mitochondria of all chondrocytes. The variations in immuno-patterns and intracellular distributions suggest that each protooncogene protein has specific roles in the functional changes in the chondrocytes at each step of their terminal differentiation.

Animals↗
PubMed1984

Immunological analysis of v-myc gene products using antibodies against a myc-specific synthetic peptide.

Rabbit antisera were prepared against a synthetic peptide corresponding to the carboxyterminal amino acid sequences of the transforming protein p110gag-myc of avian oncovirus MC29. Analysis of immunoprecipitates formed with these sera (anti-mycC) demonstrated that the gag-myc hybrid proteins encoded by the avian leukemia viruses MC29, CMII, and OK10 were recognized by the anti-peptide sera, but not the gag or pol precursor proteins of helper viruses or the MH2-encoded p100gag-mil protein. In cells transformed by OK10 or MH2, putative v-myc proteins of 60K (OK10) and 59/61K (MH2) were also precipitated by anti-mycC. In addition, the anti-peptide sera reacted specifically with the gag-myc proteins encoded by three partially transformation-defective mutants of MC29, td10A, td10C, and td10H, and by MC29 variant HBI.

Amino Acid Sequence↗
PubMed1984

Biological activities of v-myc and rearranged c-myc oncogenes in rat fibroblast cells in culture.

Two distinct forms of the myc oncogene were assayed for their ability to induce, in cultured rat fibroblast cells, the alterations of cellular growth controls observed upon transfer of the gene of polyoma virus encoding only the large T protein (plt). Both of these rearranged myc genes and the plt gene had been previously shown to cooperate with ras oncogenes for transformation of rat embryo fibroblasts (REF) and were thought to induce the same early step ("immortalization") of the tumoral transformation pathway. We now report that these two different oncogenes elicite the same response in the following biological assays: (i) reduction of the requirements in serum factors for growth in culture of cells of the established FR3T3 line; (ii) expression of transformed properties in low serum medium after transfer into FR3T3 cells expressing only the middle T protein of polyoma virus (MTT lines); (iii) conferring on REF cells the ability to grow as clonal colonies after seeding at low cell density; (iv) conferring on REF cells the ability to grow continuously in cell culture. These congruent phenotypes suggest that the activities of the large T and myc proteins result in the induction of the same molecular events. These results also provide simple biological assays and selective systems for oncogenes of the myc class.

Animals↗
PubMed1986

Gene amplification of c-myc and N-myc in small cell carcinoma of the lung.

The relationship of the copy numbers of the c-myc and N-myc oncogenes to tumor formation and progression was studied in small cell carcinoma of the lung. When 96 neoplastic lesions from 45 patients were examined, these lesions could be grouped into three categories: high copy (tumors with greater than 3 copies of the N-myc or c-myc gene per haploid genome), middle copy (1.5 to 3 copies per genome), and normal copy. Fourteen of the patients had middle copy tumors, but this was almost always a result of chromosome duplication rather than the amplification of a small genetic locus. In contrast, five patients had high copy tumors, with the increased copy number in each case due to gene amplification. The amplification did not occur in a heterogeneous fashion within individual patients, since all metastatic lesions from patients with high copy lung tumors were also high copy, while none of 41 metastatic lesions from the other patients were high copy. These data suggest that gene amplification is an important step in neoplastic growth in a subset of patients with small cell carcinoma of the lung and that this genetic event occurs relatively early (before metastasis) in this subset.

Carcinoma, Small Cell↗
PubMed1986

Differential responsiveness of myc- and ras-transfected cells to growth factors: selective stimulation of myc-transfected cells by epidermal growth factor.

To identify functional relationships between oncogenes and growth factors, we compared the effects of transfected myc and ras oncogenes on the responsiveness of Fischer rat 3T3 cells to three growth factors: epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and transforming growth factor-beta (TGF-beta). Control cells did not grow in soft agar under any conditions. ras-Transfected cells grew in soft agar under all conditions tested and were insensitive to the stimulatory effects of exogenous growth factors. These cells secreted elevated levels of both EGF-like factors and TGF-beta, suggesting that the lack of responsiveness of these cells to exogenous growth factors arose from autocrine stimulation. myc-Transfected cells displayed conditional anchorage-independent growth: they formed numerous colonies in soft agar in the presence of EGF but relatively few colonies in the presence of PDGF or TGF-beta. Secretion of EGF-like factors and TGF-beta by these cells was not elevated above that of control cells. These results suggest a model for the mechanism of cooperation between myc and ras oncogenes in which ras-like genes induce growth factor production, while myc-like genes increase the responsiveness of cells to these factors.

Animals↗
PubMedDate not supplied

Analysis of the c-myc and N-ras genes in acute myelogenous leukemia cells which manifest the constitutive expression of the c-myc gene.

The "constitutive" expression of the c-myc gene was detected in leukemia cells obtained from 4 patients with an acute myeloid leukemia, 3 with chronic myeloid leukemia and 1 with a myelodysplastic syndrome. Studies were undertaken to determine whether or not the myc gene was rearranged or mutated in exon I within a 3'Pvu II region, a transcriptional attenuation site. Studies to explore the possibility of a point mutation in the N-ras gene were also conducted. No abnormalities were detected in either gene. Studies should be undertaken evaluating the possibility of a post-transcriptional mechanism, such as alteration of RNA stability, which could be responsible for the constitutive expression of c-myc gene.

Acute Disease↗
PubMed2006

Alternative splicing in protein associated with Myc (Pam) influences its binding to c-Myc.

We recently identified Pam (for protein associated with c-Myc), as a binding partner for the tuberous sclerosis complex (TSC) protein tuberin in brain. The highly conserved Pam homologs in Drosophila and C. elegans are neuron-specific proteins that regulate synaptic growth. The Pam gene contains 83 exons and encodes a 4,641-amino-acid polypeptide with a predicted molecular weight of approximately 510 kDa. In a previous study, we demonstrated that Pam is expressed as two forms, approximately 450 kDa in rat embryonic and a approximately 350 kDa in rat adult brain. Here we have extended that work to show the approximately 450 kDa form is expressed in rat embryonic kidney, heart, and lung and in rat cell lines, and the approximately 350 kDa form is expressed in adult rat tissues as well as in human and mouse brain and human and mouse cell lines. To understand the size difference, we investigated alternative splicing of Pam in brain and detected six isoforms in the Myc-binding region resulting from splicing of exon 53, and three new exons, 52A, 56, and 56A. We also demonstrate that the presence of exon 52A in Pam significantly enhances binding to Myc, suggesting functional importance of this alternative splicing. The presence of Pam in many cellular compartments, its spliced variants, as well as its multiple binding partners, including tuberin, make it a complex, yet intriguing protein in the nervous system.

Alternative Splicing↗
PubMed1989

Predisposition to lymphomagenesis in pim-1 transgenic mice: cooperation with c-myc and N-myc in murine leukemia virus-induced tumors.

Transgenic mice bearing the pim-1 gene supplemented with an upstream immunoglobulin enhancer and a downstream murine leukemia virus long terminal repeat express pim-1 mRNA at high levels in both B and T cells. Between 5% and 10% of the pim-1 transgenic mice develop clonal T cell lymphomas before 7 months of age, whereas none of the age-matched control mice do, providing direct evidence for the oncogenic potential of pim-1. Histological examination and FACS analysis revealed no abnormalities in hematopoietic tissues of disease-free pim-1 transgenic mice. When newborn pim-1 transgenic mice are infected with MuLV, T cell lymphomas develop much faster (latency 7-8 weeks) than in nontransgenic mice (latency 22 weeks). In all these T cell lymphomas either c-myc or N-myc was activated by proviral insertion, suggesting strong cooperation between pim-1 and myc in lymphomagenesis.

Animals↗
PubMed1991

Novel zinc finger gene implicated as myc collaborator by retrovirally accelerated lymphomagenesis in E mu-myc transgenic mice.

To search for genes that can collaborate with myc in lymphomagenesis, we exploited retroviral insertional mutagenesis in E mu-myc transgenic mice. Moloney murine leukemia virus accelerated development of B lymphoid tumors. Three quarters contained a provirus within the known pim-1 or pim-2 loci, new loci bmi-1 and emi-1, or combinations of these. bmi-1 insertions predominated, occurring in half the tumors, and resulted in elevated bmi-1 mRNA levels. Significantly, the bmi-1 gene, which is expressed in diverse normal cells, encodes a Cys/His metal-binding motif (C3HC4) that resembles those in several DNA-binding proteins and defines a new category of zinc finger gene. Thus, myc-induced lymphomagenesis can entail the concerted action of several genes, including the presumptive nuclear regulator bmi-1.

Amino Acid Sequence↗
PubMed1989

Ribonucleoprotein and protein factors bind to an H-DNA-forming c-myc DNA element: possible regulators of the c-myc gene.

We have located a positive, cis-acting DNA sequence element within the 5' flanking DNA of the c-myc gene (-125 base pairs). This DNA sequence element has a large purine-pyrimidine strand asymmetry and can assume the H-DNA conformation. A factor with the properties of a ribonucleoprotein (RNP) interacts with this DNA region. The interaction of the c-myc DNA sequence element and the RNP involves an RNase H-sensitive mechanism and, therefore, may involve an RNA.DNA hybrid. In addition, a protein factor(s) binds to this DNA sequence element. DNA footprinting and mutant oligonucleotide binding/competition assays implicate a punctate, poly(G.C) recognition/binding sequence for the RNP factor, whereas the major protein factor requires two ACCCT sequence motifs for maximal binding. These results suggest that RNP and protein factors act as positive transcriptional regulators of the c-myc gene, perhaps by altering DNA topology.

Base Sequence↗
PubMed2006

Transforming growth factor-beta1 sensitivity is altered in Abl-Myc- and Raf-Myc-induced mouse pre-B-cell tumors.

Understanding the mechanisms leading to transformation of early B-lineage precursors is an important step leading to rational design of new treatments for precursor (pre)-B-cell leukemia. We used normal mouse pre-B cells to determine if and how transforming growth factor (TGF)-beta1 affects these precursors to the B-cell lineage and whether transformed pre-B cells respond to TGF-beta1. We found that normal pre-B cells proliferating in the presence of interleukin (IL)-7 enter cell-cycle arrest after exposure to TGF-beta1. However, clonally related IL-7-independent tumors induced by oncogenes abl + myc or raf + myc have reduced sensitivity to TGF-beta1. In contrast, tumor cells induced by myc alone remain sensitive to TGF-beta1 growth suppression. These results suggest that lesions in different molecular signaling pathways can lead to loss of TGF-beta1 sensitivity in a single cell type. The approach of using normal pre-B-cell lines and transformation by overexpression of different oncogenes provides a system to compare and contrast molecular pathways that lead to full malignancy.

Animals↗
PubMed1989

Chromosomal location of N-myc and L-myc genes in the mouse.

The myc family of proto-oncogenes consists of at least three members, whose expression is tightly and co-ordinately regulated. The genes are nevertheless dispersed to three distinct chromosomal sites in humans. We have now used somatic cell genetics and the analysis of restriction fragment length polymorphisms (RFLPs) to identify and chromosomally map two mouse N-myc loci, to chromosomes 12 and 5, and two L-myc loci, provisionally to chromosomes 4 and 12. The second locus in each pair may be a pseudogene.

Animals↗
PubMedDate not supplied

Translocation joins c-myc and immunoglobulin gamma 1 genes in a Burkitt lymphoma revealing a third exon in the c-myc oncogene.

Recombinant DNA clones have been used to directly demonstrate that the Burkitt lymphoma cell line Raji, t(8;14) (q24;q32), has a rearranged copy of the c-myc gene adjacent to the gamma 1 constant region gene of the human immunoglobulin heavy-chain locus; the genes are arranged in the opposite direction for transcription. At least one further 5' exon has been detected in the normal c-myc gene by analysis of RNA transcripts, and the occurrence of high levels of two c-myc mRNA size classes, both apparently initiating in this exon, is described.

Burkitt Lymphoma↗