Results 71 to 80 of about 278,570 (263)
c-Myc Inhibition Induces an Additive Effect with Cyclophosphamide in Acute Lymphoblastic Leukemia [PDF]
Background: Cellular-myelocytomatosis (c-Myc), an oncoprotein and a transcription factor, is involved in several essential cellular processes. The c-Myc expression level is highly regulated in normal cells.
Mohammad Sadeghi +8 more
doaj +1 more source
SCP1 regulates c-Myc stability and functions through dephosphorylating c-Myc Ser62 [PDF]
Serine 62 (Ser62) phosphorylation affects the c-Myc protein stability in cancer cells. However, the mechanism for dephosphorylating c-Myc is not well understood. In this study, we identified carboxyl-terminal domain RNA polymerase II polypeptide A small phosphatase 1 (SCP1) as a novel phosphatase specifically dephosphorylating c-Myc Ser62.
W, Wang +8 more
openaire +2 more sources
The proposed mechanism of action for the CDK12/13 inhibitor and cyclin K degrader, CT7439. CDK12/13 inhibition interrupts transcription elongation, leading to increased DNA damage that results in cell death. This agent is a potentially novel treatment option for patients with colorectal cancer. Created in BioRender. Cyclin‐dependent kinase (CDK) 12 and
Wylie K. Watlington +10 more
wiley +1 more source
Dysregulation of transforming growth factor-beta (TGFβ) signaling has been implicated in liver carcinogenesis with both tumor promoting and inhibiting activities.
Haichuan Wang +8 more
doaj +1 more source
Direct Activation of HSP90A Transcription by c-Myc Contributes to c-Myc-induced Transformation [PDF]
The c-myc proto-oncogene encodes a ubiquitous transcription factor involved in the control of cell growth and differentiation and implicated in inducing tumorigenesis. Understanding the function of c-Myc and its role in cancer depends upon the identification of c-Myc target genes.
Teng, Shu-Chun +6 more
openaire +2 more sources
BCL9 and BCL9L drive bladder cancer progression by enhancing β‐catenin signaling, promoting proliferation, migration, invasion, and organoid growth. Genetic depletion of BCL9(L) suppresses malignant phenotypes, while pharmacological disruption of the β‐catenin/BCL9(L) complex with ZW4864 inhibits canonical Wnt signaling and tumor‐associated cellular ...
Roland Kotolloshi +11 more
wiley +1 more source
BackgroundProto-oncogenes are abnormally activated in nearly all types of tumors. However, the epigenetic mechanism of proto-oncogene activation has not yet been well elucidated.MethodsThe present study involved the construction of a double-stranded cDNA
Xuming Hu +19 more
doaj +1 more source
ObjectivesVarious studies have investigated the prognostic value of C-MYC aberrations in diffuse large B-cell lymphoma (DLBCL). However, the role of C-MYC as an independent prognostic factor in clinical practice remains controversial. A systematic review
Kuangguo Zhou +5 more
doaj +1 more source
Nucleophosmin is essential for c-Myc nucleolar localization and c-Myc-mediated rDNA transcription [PDF]
The transcription factor c-Myc has a critical role in cell proliferation and growth. The control of ribosome biogenesis by c-Myc through the regulation of transcription mediated by all three RNA polymerases is essential for c-Myc-driven proliferation. Specifically, in the nucleolus, c-Myc has been shown to be recruited to ribosomal DNA and activate RNA
Z, Li, S R, Hann
openaire +2 more sources
From tumor‐centric to ecosystem‐based hypotheses in brain tumor research and care
Primary brain tumors, whether in adults or children, present a major challenge because of their dramatic prognosis and the ongoing lack of efficient therapeutic approaches. In recent years, a shift has occurred from tumor‐centric concepts to a more holistic view of these tumors as dynamic ecosystems.
Julie Gavard +8 more
wiley +1 more source

