Results 21 to 30 of about 23,377,083 (210)

Myc interacts with Max and Miz1 to repress C/EBPδ promoter activity and gene expression

open access: yesMolecular 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

MYC is a metastasis gene for non-small-cell lung cancer. [PDF]

open access: yes, 2009
Metastasis is a process by which cancer cells learn to form satellite tumors in distant organs and represents the principle cause of death of patients with solid tumors. NSCLC is the most lethal human cancer due to its high rate of metastasis.
Christian Korn   +25 more
core   +2 more sources

c-myc Amplification Is Frequent in Esophageal Adenocarcinoma and Correlated with the Upregulation of VEGF-A Expression

open access: yesNeoplasia: 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]

open access: yesPLoS 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

Molecular and functional characterization of the interaction between c-Myc and the MCM helicase [PDF]

open access: yes, 2006
The Myc genes (c-myc, n-myc, l-myc, s-myc) encode a family of protein that share structural an biological features and are conserved across all Metazoans.
Ruggiero, Luca
core   +1 more source

Expression of proto-oncogene c-Myc in patients with urinary bladder transitional cell carcinoma

open access: yesCurrent 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

MYC and N-MYC are overexpressed in MYC-ER and N-MYC-ER-expressing cells, and naturally overexpressed MYC controls circadian gene expression.

open access: yes, 2023
A.MYCN was determined in parental SKNAS, SKNAS N-MYC-ER, or SHEP N-MYC-ER by qPCR in n = 3 replicates by quantitative PCR (qPCR), normalized to β2M. MYCN overexpression is shown relative to parental SKNAS, since SHEP do not express MYCN. B.
Brian J. Altman (16819407)   +12 more
core   +1 more source

Impact of c-MYC expression on proliferation, differentiation, and risk of neoplastic transformation of human mesenchymal stromal cells

open access: yesStem 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

The polyoma virus large T binding protein p150 is a transcriptional repressor of c-MYC. [PDF]

open access: yesPLoS 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

c-Myc and Cancer Metabolism [PDF]

open access: yesClinical 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

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