Myc pathways provoking cell suicide and cancer

Nilsson, Jonas A.; Cleveland, John L.

doi:10.1038/sj.onc.1207261

Cited by 410 publications

(350 citation statements)

References 299 publications

Supporting

Mentioning

336

Contrasting

Unclassified

Order By: Relevance

“…First identified as the cellular homolog to the viral oncogene of the avian myelocytomatosis virus and later as the driving oncogene in Burkitt's lymphoma, the c-Myc transcription factor is now known to be activated in about 70% of all cancers (Nilsson and Cleveland, 2003). On the molecular level, Myc functions as a transcription factor of the basic helix-loop-helix (HLH) leucine zipper (LZ) family that can either activate or repress target genes (Eisenman, 2001;Seoane et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

PML4 induces differentiation by Myc destabilization

et al. 2006

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 99%

PML4 induces differentiation by Myc destabilization

et al. 2006

View full text Add to dashboard Cite

“…It should be pointed out, though, that v-myc immortalization of these cells is compromising with respect to their potential clinical applications (Nilsson and Cleveland, 2003). Our data provide evidence that the multipotent hVMl human ventral mesencephalic stem cell line is capable of differentiating into functional neurons, although under the present in vitro conditions with relatively immature properties.…”

Section: Calcium Imagingmentioning

confidence: 62%

Functional properties of the human ventral mesencephalic neural stem cell line hVM1

Tønnesen

Seiz

Ramos

et al. 2010

Experimental Neurology

View full text Add to dashboard Cite

The human fetal ventral mesencephalon-derived stem cell line, hVTVIl, yields high number of tyrosine hydroxylase-expressing presumed dopaminergic neurons upon in vitro differentiation. Here we report that cells generated from this line differentiate into a neuronal phenotype, express electrophysiological properties of functional neurons and respond to neurotransmitters in vitro. However, the electrophysiological properties are immature and the cells require longer maturation time than possible under in vitro

show abstract

“…Furthermore, Bcl-2 cooperates to transform primary cells in concert with Myc proteins and accelerates MYC geneinduced oncogenesis (reviewed in (Nilsson and Cleveland, 2003)). Bcl-2 may be overexpressed in patient neuroblastomas concomitant with MYCN amplification (Castle et al, 1993;Poulaki et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

N-myc augments death and attenuates protective effects of Bcl-2 in trophically stressed neuroblastoma cells

et al. 2008

View full text Add to dashboard Cite

N-myc has proapoptotic functions, yet it acts as an oncogene in neuroblastoma. Thus, antiapoptotic mechanisms have to be operative in neuroblastoma cells that antagonize the proapoptotic effects of N-myc. We conditionally activated N-myc in SH-EP neuroblastoma cells subjected to the trophic stress of serum or nutrient deprivation while changing the expression of Bcl-2, survivin and FLIP L , antiapoptotic molecules often overexpressed in poor prognosis neuroblastomas. Bcl-2 protected SH-EP cells from death during nutritional deprivation by activating energetically advantageous oxidative phosphorylation. N-myc overrode the metabolic protection provided by Bcl-2-induced oxidative phosphorylation by reestablishing the glycolytic phenotype and attenuated the antiapoptotic effect of Bcl-2 during metabolic stress. Survivin partially antagonized the growth suppressive function of N-myc in SH-EP neuroblastoma cells during serum deprivation whereas FLIP L did not. These findings advance our understanding of the functions of N-myc in neuroblastoma cells.

show abstract

Myc pathways provoking cell suicide and cancer

Cited by 410 publications

References 299 publications

PML4 induces differentiation by Myc destabilization

PML4 induces differentiation by Myc destabilization

Functional properties of the human ventral mesencephalic neural stem cell line hVM1

N-myc augments death and attenuates protective effects of Bcl-2 in trophically stressed neuroblastoma cells

Contact Info

Product

Resources

About