Involvement of Myc targets in c-myc and N-myc induced human tumors

Ben-Yosef, Tamar; Yanuka, Ofra; Halle, David; Benvenisty, Nissim

doi:10.1038/sj.onc.1201939

Cited by 80 publications

(68 citation statements)

References 42 publications

(65 reference statements)

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“…Recent results, however, indicate that the regulation of these genes by c-myc overexpression di ers among cell types, strongly suggesting an important role for tissue-speci®c co-activators or other factors (Ben-Yosef et al, 1998). The statement that di erences in target gene expression pro®les between cell lines overexpressing two di erent myc genes are due to intrinsic di erences in the myc proteins themselves is therefore complicated by this consideration (Ben-Yosef et al, 1998). We have recently compared the properties of three cell lines engineered to express c-myc, N-myc, or L-myc at equivalent levels (Nesbit et al, 1998).…”

Section: E Ects Of Myc Gene Gain-and Loss-of-function In Vivomentioning

confidence: 99%

MYC oncogenes and human neoplastic disease

1999

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c-myc, N-myc and L-myc are the three members of the myc oncoprotein family whose role in the pathogenesis of many human neoplastic diseases has received wide empirical support. In this review, we ®rst summarize data, derived mainly from non-clinical studies, indicating that these oncoproteins actually serve quite di erent roles in vivo. This concept necessarily lies at the heart of the basis for the observation that the deregulated expression of each MYC gene is reproducibly associated with only certain naturally occurring malignancies in humans and that these genes are not interchangeable with respect to their aberrant functional consequences. We also review evidence implicating each of the above MYC genes in speci®c neoplastic diseases and have attempted to identify unresolved questions which deserve further basic or clinical investigation. We have made every attempt to review those diseases for which signi®cant and con®rmatory evidence, based on studies with primary tumor material, exists to implicate MYC members in their causation and/or progression.

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Section: E Ects Of Myc Gene Gain-and Loss-of-function In Vivomentioning

confidence: 99%

MYC oncogenes and human neoplastic disease

1999

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“…Even though N-myc is able to functionally complement c-myc during development, 11,13 not all c-myc target genes are expressed in N-myc-expressing NB cells. 34 For this reason, we felt it was important to study how N-myc affected the cell cycle machinery in NB cells. Our finding that N-myc stimulated cyclin E and cyclin E-dependent kinase activity and increased E2F-1 mRNA levels were consistent with Leone et al, 35 who showed that in ras-activated cells, c-myc stimulates cyclin E-dependent kinase activity and E2F.…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid decreases targeting of p27 for degradation via an N-myc-dependent decrease in p27 phosphorylation and an N-myc-independent decrease in Skp2

et al. 2003

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Poor prognosis neuroblastoma (NB) tumors are marked by amplification and overexpression of N-myc. Retinoic acid (RA) decreases N-myc levels and induces cell cycle arrest in vitro and increases event-free survival in advanced stage NB patients. In this study, we investigated the mechanism(s) by which RA regulates cell cycle and how N-myc affects NB cell cycle progression. Constitutive N-myc overexpression stimulates increases in cyclin E-dependent kinase activity and decreases in p27 resulting in increased DNA synthesis.

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“…Ornithine decarboxylase (ODC) is perhaps the best studied target of c-Myc (BelloFernandez et al, 1993;Wagner et al, 1993a;Tobias et al, 1995;Wu et al, 1996b;Packham and Cleveland, 1997;Ben-Yosef et al, 1998). Signi®cantly, ODC has been shown to be necessary and su cient for apoptosis by c-Myc in 32D myeloid cells (Packham and Cleveland, 1994).…”

Section: Myc Target Genes and Apoptosismentioning

confidence: 99%