Myc is one of the most commonly deregulated oncogenes in human cancer, yet therapies directly targeting Myc hyperactivation are not presently available in the clinic. The evolutionarily conserved function of Myc in modulating protein synthesis control is critical to the Myc oncogenic program. Indeed, enhancing the protein synthesis capacity of cancer cells directly contributes to their survival...

MYC is a multifunctional transcription factor that is deregulated in many human cancers. MYC impacts a collaborative genetic program that orchestrates cell proliferation, metabolism, and stress responses. Although the progression of MYC-amplified tumors shows robust dependence on MYC activity, directly targeting MYC as a therapeutic method has proven to be technically difficult. Therefore, alte...

Myc oncogenic transcription factors (c-Myc, N-Myc, and L-Myc) coordinate the control of cell growth, division, and metabolism. In cancer, Myc overexpression is often associated with aggressive disease, which is in part due to the destruction of select targets by the ubiquitin-proteasome system (eg, SCF(Skp2)-directed destruction of the Cdk inhibitor p27(Kip1)). We reasoned that Myc would also r...

The myc proto-oncogene family has been implicated in multiple cellular processes, including proliferation, differentiation, and apoptosis. The Myc proteins, as heterodimers with Max protein, have been shown to function as activators of transcription through an E-box DNA-binding element, CACGTG. We have now found that the c-Myc proteins regulate transcription through another, noncanonical, DNA s...

MYC gene overexpression was identified recently as a downstream step at the end of the Wnt/APC/beta-catenin pathway dysregulation observed in colorectal cancer (T-C. He et al., Science (Washington DC), 281: 1509-1512, 1998). It thus appears that an excess of c-myc protein is a primary cause of numerous cancers. In breast cancer, MYC has been studied mostly at the DNA level because of the poor q...

Rat fibroblast cell lines with targeted disruptions of both c-myc gene copies were constructed. Although c-myc null cells are viable, their growth is significantly impaired. The absence of detectable N-myc or L-myc expression indicates that Myc function is not absolutely essential for cell viability. The c-myc null phenotype is stable and can be reverted by introduction of a c-myc transgene. Ex...

Introduction: HIV negative patients (pts) with B cell lymphoma (Ly) carrying MYC rearrangements and BCL2+/-BCL6 translocations [double hit (DHL) or triple Ly (THL)] have shown a dismal prognosis when treated standard chemotherapy. Data about the of “single hit” Ly, (SHL) are more controverse. In HIV-associated lymphomas (HIV+Ly), scanty data available on prevalence prognostic impact rearrangeme...

objective: every cell type is characterized by a specific transcriptional profile together with a unique epigenetic landscape. reprogramming factors such as oct4, klf4, sox2 and c-myc enable somatic cells to change their transcriptional profile and convert them to pluripotent cells. small molecules such as bix-01294, bay k8644, rg-108 and valproic acid (vpa) are reported as effective molecules ...

The impact of low temperature on the Korolkov Aronnik plant triggers expression CBF family transcription factors, which, in turn, activate many downstream genes that confer resistance to cold and frost. article will consider identification ICE1 gene (inducer 1 expression) by Korolkov, an upstream factor regulates during cold. A mutation wild blocks CBF3 reduces located CBFs, which leads a signi...