Results 91 to 100 of about 18,976,803 (305)

C-MYC aberrations as prognostic factors in diffuse large B-cell lymphoma: a meta-analysis of epidemiological studies.

PLoS ONE, 2014
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, Danmei Xu, Yang Cao, Jue Wang, Yunfan Yang, Mei Huang   +5 more
doaj   +1 more source

c-Myc oncoprotein function

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, 1991
Genetic alterations of the c-myc locus in various malignancies and the ability of c-myc to transform cultured cells and induce tumors in transgenic animals attest to its central role in many neoplasms. By dissecting the c-Myc protein, a number of critical functional domains of c-Myc have been identified and characterized; these findings suggest a model
openaire   +2 more sources

Nucleophosmin is essential for c-Myc nucleolar localization and c-Myc-mediated rDNA transcription [PDF]

Oncogene, 2012
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

Inhibition of cyclin‐dependent kinases 12/13 using CT7439 as a treatment for colorectal cancer with CDK12 upregulation

Molecular Oncology, EarlyView.
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, Divya L. Dayanidhi, Mohammad Zokaasadi, John B. Mantyh, Pelumi D. Olawuni, Gabrielle Rupprecht, Jeremy M. Force, Shannon McCall, Ashwani K. Bahl, David S. Hsu, Jason A. Somarelli   +10 more
wiley   +1 more source

LINC01963 promotes pancreatic ductal adenocarcinoma proliferation via METTL3/IGF2BP2 axis-mediated m⁶A modification of c-Myc

Journal of Experimental & Clinical Cancer Research
Background C-Myc overexpression is an important molecular hallmark of pancreatic ductal adenocarcinoma (PDAC), but directly targeting c-Myc is extremely challenging.
Qixian Liu, Ruiyu Li, Bohan Liu, Hangqi Liu, Xuqing Shi, Xianglin Yin, Xinping Ju, Sichong Zhang, Jun Wang, Yuhan Zhang, Xiaoding Liu, Dongmei Li, Longyun Chen, Yamei Niu, Huanwen Wu, Zhiyong Liang   +15 more
doaj   +1 more source

Domain-specific c-Myc ubiquitylation controls c-Myc transcriptional and apoptotic activity [PDF]

Proceedings of the National Academy of Sciences, 2012
The oncogenic transcription factor c-Myc causes transformation and tumorigenesis, but it can also induce apoptotic cell death. Although tumor suppressors are necessary for c-Myc to induce apoptosis, the pathways and mechanisms are unclear.
Qin, Zhang, Erick, Spears, David N, Boone, Zhaoliang, Li, Mark A, Gregory, Stephen R, Hann   +5 more
openaire   +2 more sources

Targeting transcription factors associated with hemoglobinopathies: Lessons from successful interventions and implications for cancer

Molecular Oncology, EarlyView.
This review summarizes the transcription factors, repressive chromatin‐modifying complexes, and epigenetic mechanisms that control fetal hemoglobin repression. Notably, many regulators of γ‐globin silencing also function in transcriptional and epigenetic networks that drive cancer, highlighting opportunities to translate advances in hemoglobinopathy ...
Meigen Yu, Puspa Das, Xing Zhang, Xiaodong Cheng   +3 more
wiley   +1 more source

Glutathione Depletion Induced by c-Myc Downregulation Triggers Apoptosis on Treatment with Alkylating Agents

Neoplasia: An International Journal for Oncology Research, 2004
Here we investigate the mechanism(s) involved in the c-Myc-dependent drug response of melanoma cells. By using three M14-derived c-Myc low-expressing clones, we demonstrate that alkylating agents, cisplatin and melphalan, trigger apoptosis in the c-Myc ...
Annamaria Biroccio, Barbara Benassi, Francesco Fiorentino, Gabriella Zupi   +3 more
doaj   +1 more source

Nucleophosmin interacts directly with c-Myc and controls c-Myc-induced hyperproliferation and transformation [PDF]

Proceedings of the National Academy of Sciences, 2008
The transcription factor c-Myc is essential for cellular proliferation and is one of the most frequently activated oncogenes, but the molecular mechanism mediating its critical role in transformation is unclear. Like c-Myc, multifunctional nucleophosmin (NPM) is tightly regulated during proliferation and is overexpressed in several different types of ...
Zhaoliang, Li, David, Boone, Stephen R, Hann   +2 more
openaire   +2 more sources

Pharmacological chromatin remodeling enhances response to estrogen therapy in ER+ breast cancer

Molecular Oncology, EarlyView.
Estrogen therapy elicits clinical benefit in ~ 30% of patients with endocrine‐resistant estrogen receptor (ER)‐positive breast cancer. Based on findings that ER transcriptional activation underlies response to estrogen therapy, we tested the effects of epigenetic dysregulation via pharmacological inhibition of histone deacetylases (HDACi).
Anneka L. Johnson Thomas, Barbara Karakyriakou, Patricia C. Muskus, Alyssa M. Roberts, Justin Rendleman, Alexa Warren, Hanxu Lu, Kimberly A. Birmingham, Malone K. Friedman, Abigail E. Goen, Huijuan Yang, Owen M. Wilkins, Fred W. Kolling, Eugene Demidenko, Julie M. Jorns, Brock C. Christensen, Todd W. Miller   +16 more
wiley   +1 more source