Results 41 to 50 of about 278,661 (263)

Organoids in pediatric cancer research

open access: yesFEBS Letters, EarlyView.
Organoid technology has revolutionized cancer research, yet its application in pediatric oncology remains limited. Recent advances have enabled the development of pediatric tumor organoids, offering new insights into disease biology, treatment response, and interactions with the tumor microenvironment.
Carla Ríos Arceo, Jarno Drost
wiley   +1 more source

Mechanisms of c-myc degradation by nickel compounds and hypoxia.

open access: yesPLoS ONE, 2009
Nickel (Ni) compounds have been found to cause cancer in humans and animal models and to transform cells in culture. At least part of this effect is mediated by stabilization of hypoxia inducible factor (HIF1a) and activating its downstream signaling ...
Qin Li, Thomas Kluz, Hong Sun, Max Costa
doaj   +1 more source

siRNA directed against c-Myc inhibits proliferation and downregulates human telomerase reverse transcriptase in human colon cancer Colo 320 cells

open access: yesJournal of Experimental & Clinical Cancer Research, 2008
The c-Myc and human telomerase reverse transcriptase gene (hTERT) gene are frequently deregulated and overexpressed in malignancy. hTERT activity is induced by c-Myc and strategies designed to inhibit c-Myc expression in cancer cells may have ...
Guofu Huang   +9 more
doaj   +1 more source

Protein pyrophosphorylation by inositol pyrophosphates — detection, function, and regulation

open access: yesFEBS Letters, EarlyView.
Protein pyrophosphorylation is an unusual signaling mechanism that was discovered two decades ago. It can be driven by inositol pyrophosphate messengers and influences various cellular processes. Herein, we summarize the research progress and challenges of this field, covering pathways found to be regulated by this posttranslational modification as ...
Sarah Lampe   +3 more
wiley   +1 more source

PDCD11 Stabilizes C‐MYC Oncoprotein by Hindering C‐MYC‐SKP2 Negative Feedback Loop to Facilitate Progression of p53‐Mutant Breast and Colon Malignancies

open access: yesAdvanced Science
C‐MYC is a proto‐oncoprotein whose dysregulation triggers tumorigenesis and tumor progression in ≈70% of cancer cases. It is presently demonstrated that aberrantly upregulated MYC is caused by the overexpressed and “extra‐nucleolar” PDCD11 in p53‐mutant ...
Li Ding   +12 more
doaj   +1 more source

Inhibition of c-Myc overcomes cytotoxic drug resistance in acute myeloid leukemia cells by promoting differentiation. [PDF]

open access: yesPLoS ONE, 2014
Nowadays, drug resistance still represents a major obstacle to successful acute myeloid leukemia (AML) treatment and the underlying mechanism is not fully elucidated. Here, we found that high expression of c-Myc was one of the cytogenetic characteristics
Xiao-Na Pan   +8 more
doaj   +1 more source

Mechanisms of apoptosis by c-Myc [PDF]

open access: yesOncogene, 1999
Much recent research on c-Myc has focused on how it drives apoptosis. c-Myc is widely known as a crucial regulator of cell proliferation in normal and neoplastic cells, but until relatively recently its apoptotic properties, which appear to be intrinsic, were not fully appreciated. Its death-dealing aspects have gained wide attention in part because of
openaire   +2 more sources

ABL kinase‐dependent phosphorylation of SH proteins promotes their direct interaction with CRK family SH2 domains

open access: yesFEBS Letters, EarlyView.
CT10 regulator of kinase (CRK) and CRK‐Like (CRKL) are signaling adaptors driving cell adhesion, motility, differentiation, and proliferation. SH2‐domain containing (SH) proteins are enriched in YXXP motifs which when phosphorylated create preferred binding sites for CRK family SH2 domains.
Phoebe M. Cousens   +8 more
wiley   +1 more source

Recent advances in searching c-Myc transcriptional cofactors during tumorigenesis

open access: yesJournal of Experimental & Clinical Cancer Research, 2018
Background The mechanism by which c-Myc exerts its oncogenic functions is not completely clear and different hypotheses are still under investigation. The knowledge of the capacity of c-Myc to bind exclusively E-box sequences determined the discrepancy ...
Matteo Caforio   +5 more
doaj   +1 more source

Tumour–host interactions in Drosophila: mechanisms in the tumour micro‐ and macroenvironment

open access: yesMolecular Oncology, EarlyView.
This review examines how tumour–host crosstalk takes place at multiple levels of biological organisation, from local cell competition and immune crosstalk to organism‐wide metabolic and physiological collapse. Here, we integrate findings from Drosophila melanogaster studies that reveal conserved mechanisms through which tumours hijack host systems to ...
José Teles‐Reis, Tor Erik Rusten
wiley   +1 more source

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