Results 31 to 40 of about 278,570 (263)
Myc interacts with Max and Miz1 to repress C/EBPδ promoter activity and gene expression
Molecular Cancer, 2010 Background "Loss of function" alterations in CCAAT/Enhancer Binding Proteinδ (C/EBPδ) have been reported in a number of human cancers including breast, prostate and cervical cancer, hepatocellular carcinoma and acute myeloid leukemia.
Yu Xueyan +3 more
doaj +1 more source
c-MYC Copy-Number Gain Is an Independent Prognostic Factor in Patients with Colorectal Cancer. [PDF]
PLoS ONE, 2015 The aim of this study was to determine the incidence and clinicopathological significance of c-MYC gene copy-number (GCN) gain in patients with primary colorectal cancer (CRC).The c-MYC GCN was investigated in 367 consecutive CRC patients (cohort 1) by ...
Kyu Sang Lee +7 more
doaj +1 more source
Expression of proto-oncogene c-Myc in patients with urinary bladder transitional cell carcinoma
Current Urology, 2021 . Background:. c-Myc is a proto-oncogene located on human chromosome 8. It encodes a transcriptional factor which regulates the expression of approximately 10% to 15% of human genes, playing a crucial role in cell growth, differentiation, cellular ...
Charalampos Fragkoulis +7 more
doaj +1 more source
Neoplasia: An International Journal for Oncology Research, 2006 BACKGROUND: Deregulation of c-myc plays a major role in the carcinogenesis of human malignancies. We investigated the amplification of the c-myc gene in a surgical series of Barrett cancers. METHODS: Primary resected esophageal (Barrett) adenocarcinomas (
Burkhard H.A. von Rahden +3 more
doaj +1 more source
Integration of genome and chromatin structure with gene expression profiles to predict c-MYC recognition site binding and function. [PDF]
PLoS Computational Biology, 2007 The MYC genes encode nuclear sequence specific-binding DNA-binding proteins that are pleiotropic regulators of cellular function, and the c-MYC proto-oncogene is deregulated and/or mutated in most human cancers. Experimental studies of MYC binding to the
Yili Chen +5 more
doaj +1 more source
The polyoma virus large T binding protein p150 is a transcriptional repressor of c-MYC. [PDF]
PLoS ONE, 2012 p150, product of the SALL2 gene, is a binding partner of the polyoma virus large T antigen and a putative tumor suppressor. p150 binds to the nuclease hypersensitive element of the c-MYC promoter and represses c-MYC transcription.
Chang Kyoo Sung +8 more
doaj +1 more source
Stem Cell Research & Therapy, 2019 Background Mesenchymal stromal cells isolated from bone marrow (MSC) represent an attractive source of adult stem cells for regenerative medicine. However, thorough research is required into their clinical application safety issues concerning a risk of ...
Svitlana Melnik +6 more
doaj +1 more source
Frontiers in Pharmacology, 2021 Background: Identifying patients with de novo acute myeloid leukemia (AML) who will probably respond to the “7 + 3” induction regimen remains an unsolved clinical challenge.
Tzu-Hung Hsiao +15 more
doaj +1 more source
c-Myc and Cancer Metabolism [PDF]
Clinical Cancer Research, 2012 Abstract The processes of cellular growth regulation and cellular metabolism are closely interrelated. The c-Myc oncogene is a “master regulator” which controls many aspects of both of these processes. The metabolic changes which occur in transformed cells, many of which are driven by c-Myc overexpression, are necessary to support the ...
Donald M, Miller +4 more
openaire +2 more sources
c-Myc Suppression of DNA Double-strand Break Repair
Neoplasia: An International Journal for Oncology Research, 2012 c-Myc is a transcriptional factor that functions as a central regulator of cell growth, proliferation, and apoptosis. Overexpression of c-Myc also enhances DNA double-strand breaks (DSBs), genetic instability, and tumorigenesis. However, the mechanism(s)
Zhaozhong Li +8 more
doaj +1 more source