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Any of several genes encoding DNA-binding proteins that can promote the development of various cancers when present at high concentrations.


An oncogene on chromosome 8q24 of cellular (c-myc) or viral (v-myc) origin, which was first identified in the genome of a group of acutely transforming retroviruses capable of inducing avian neoplasia, possibly linked to RNA processing.

c-myc is present in normal tissues; the protein product is required for progression through the cell cycle. Myc-null cell lines show profound growth defect, with lengthening of G1 and G2 phases of the cell cycle. There is a marked reduction in cyclin D1-CDK4 and D1-CDK6 complexes during entry to S phase, with lesser reductions in cyclin E2-CDK2 and cyclin A-CDK2. Myc induces expression of cyclins D1 and D2.

Oncogenic expression of c-myc involves mutations on exon 2, which occur in more than 50% of Burkitt's lymphomas. The typical translocation in Burkitt’s lymphoma is t(8;14)(q24;q23), juxtaposing the c-myc and the immunoglobulin heavy-chain genes. Variant translocations are to 2p11 or 22q11, juxtaposing kappa or lambda light-chain genes respectively. FISH performed with dual probes can demonstrate the IgH/c-myc translocation. Tricolour with a probe against the centromere of chromosome 8 will control c-myc amplification or loss of the derivative chromosome 8; dual colour break-apart probes will show splitting of the gene.
References in periodicals archive ?
c-Myc is required for the glucose-mediated induction of metabolic enzyme genes.
Sorrento will contribute key small molecule programs (lead inhibitors of the proto-oncogenes c-Myc, and the master metabolism regulator HIF-1 alpha, and an inducer of the tumor suppressor cytokine TRAIL) to the joint venture which will be 60% owned by NantBioScience and 40% owned by Sorrento, and funded accordingly.
Cytogenetic analysis was performed with fluorescence in situ hybridization to reveal gene rearrangements of BCL-2 (18q21), BCL-6 (3q27), and c-MYC (8q24) genes (Figure 3).
On the other hand, the transcriptions of the PDFG signalling pathway-influencing genes were upregulated (ITPR1, c-MYC and SRGAP3; Table 2).
Using the chemotherapy drug, cisplatin (which is commonly used as a first-line therapy for various cancers) to design a set of experiments, the research team found that the c-MYC oncoprotein increases cisplatin resistance by decreasing production of a c-MYC inhibitor called BIN1.
Each tumor was assessed by the average and the maximum numbers of copies of C-MYC and HER2 genes per cell and the average ratio of C-MYC and HER2 genes to chromosomes 8 and 17 copy numbers.
Novus Biologicals provides THAP11-related products, such as c-Myc antibodies, OCT4 antibodies, and Nanog antibodies, as well as other THAP-11 antibodies.
The other topics are polyunsaturated fatty acid deficiency, the correlation between vascular endothelial growth factor and proto-oncogene c-fos and c-myc, and the expression of neural cell adhesion molecules and osteonectin.
Furthermore, it was shown that the target RNA, from the c-myc gene, one of the main causes of restenosis, was effectively inhibited by the antisense compound AVI-5126 developed by Cook Medical's partner AVI BioPharma, Inc.
Common to all Burkitt lymphomas, endemic or sporadic, are distinctive chromosomal translocations that reactivate expression of the c-myc protooncogene and comprise the primary oncogenic mechanism.
Monoclonal antibodies against [alpha]-fetoprotein (sc-8399), K-ras (sc-30), c-myc (sc-42), estrogen receptor (ER)-[alpha] (sc-8002), [beta]-actin (sc-1616) and polyclonal antibodies against cyclin DI (sc-753), cdk4 (sc-601), and endothelial growth factor receptor (EGFR, sc-03) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA).
C-myc is believed to regulate the many downstream genes that produce the pathology of restenosis, including cell migration and adhesion, collagen formation, secretion of extra-cellular matrix, and cell proliferation.