Two unrelated cell-derived sequences in the genome of avian leukemia and carcinoma inducing retrovirus MH2.

Jansen, H W; Rückert, Beate; Bister, Klaus

doi:10.1002/j.1460-2075.1983.tb01686.x

Cited by 114 publications

(70 citation statements)

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“…In contrast, transforming oncogenes induced anchorage-independent growth and abrogated contact inhibition. Cooperation of oncogenes was also observed in the study of viruses such as avian MH2 (17) or erythroblastosis (18) retroviruses. These experiments paved the way for the multistep theory of oncogenesis (10).…”

Section: Multistep Oncogenesis In Experimental Models: Cooperation Ofmentioning

confidence: 83%

A cell cycle hypothesis of cooperative oncogenesis (Review)

Delaval

Birnbaum²

2007

Int J Oncol

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Abstract. The development of cancer is a multistep process. To understand oncogenesis and adapt appropriate treatments it is important to have a better definition of a number of factors, including the number and order of oncogenic steps, the identity of the targeted cells and deregulated cellular components, and the genes and pathways altered at each step. We propose here a hypothesis of oncogenesis based on the targeting of the cell cycle in two major steps. Oncogenic hits may occur in two sequences: in one scenario a first oncogenic hit alters the regulation of the G1 phase of the cell cycle leading to a proliferative, premalignant syndrome; oncogenesis is completed when a second oncogenic hit relieves the checkpoints of the late phases of the cell cycle. Alternatively, a genetic alteration may hit the late phases first; this leads to a premalignant disease with signs of senescence. In this scenario, the second hit targets the G1 phase. In the two sequences, oncogenesis is based on the cooperation of two hits targeting different phases of the cell cycle and relieving major checkpoints. Stem cells and progenitor cells of various tissues may be variably sensitive to these hits.

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Section: Multistep Oncogenesis In Experimental Models: Cooperation Ofmentioning

confidence: 83%

A cell cycle hypothesis of cooperative oncogenesis (Review)

Delaval

Birnbaum²

2007

Int J Oncol

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“…It was designated v-raf because of the ability of the virus to induce rapidly growing fibrosarcomas in mice (Rapp et al, 1983). Around the same time, chicken Raf was cloned from an avian virus (Mill-Hill No 2) and termed v-mil (Jansen et al, 1983(Jansen et al, , 1984. Cloning of human CRAF, ARAF and BRAF followed shortly afterwards (Bonner et al, 1985;Huebner et al, 1986;Beck et al, 1987;Ikawa et al, 1988;reviewed in Wellbrock et al, 2004).…”

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confidence: 99%

BRAFE600 in benign and malignant human tumours

et al. 2007

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Of the RAF family of protein kinases, BRAF is the only member to be frequently activated by mutation in cancer. A single amino acid substitution (V600E) accounts for the vast majority and results in constitutive activation of BRAF kinase function. Its expression is required to maintain the proliferative and oncogenic characteristics of BRAF E600 -expressing human tumour cells. Although BRAF E600 acts as an oncogene in the context of additional genetic lesions, in primary cells it appears to be associated rather with transient stimulation of proliferation. Eventually, BRAF E600 signalling triggers cell cycle arrest with the hallmarks of cellular senescence, as is illustrated by several recent studies in cultured cells, animal models and benign human lesions. In this review, we will discuss recent advances in our understanding of the role of BRAF E600 in benign and malignant human tumours and the implications for therapeutic intervention.

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“…2 MH2 was found to carry a second potential oncogene in addition to vmyc, which was termed v-mil, whereas its cellular counterpart was called c-mil. 3 Already a hybridization analysis and the gross comparison of restriction maps of v-raf and v-mil pointed at sequence homologies between these 2 genes. 4 By direct sequencing of both genes it was finally proven that 3611-MSV and MH2 have integrated orthologues of the same gene into their genomes.…”

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confidence: 99%

Raf kinases: Oncogenesis and drug discovery

Schreck

Rapp

2006

Intl Journal of Cancer

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Raf kinase signaling has been thoroughly investigated over the last 20 years. A-Raf, B-Raf and C-Raf, the 3 mammalian members of the Raf family, are involved in a variety of cellular processes such as growth, proliferation, survival, differentiation and transformation. The detection of B-RAF mutations in a wide variety of human cancers, the description of wildtype and mutant B-RAF as tumor antigens in melanoma and the promising outcome of clinical trials evaluating the Raf inhibitor Nexavar 1 (Sorafenib, BAY 43-9006) have sparked a broad interest in the scientific community. After a short historical detour and an introduction into Raf kinase signaling, we are going to discuss here recent outcomes of Raf kinase research with respect to tumor formation and give an overview on current efforts to develop anticancer therapies interfering with aberrant Raf kinase signaling. ' 2006 Wiley-Liss, Inc.Key words: cancer; clinical trials; transformation; drug delivery; signal transduction; mitogenic cascade; Raf kinases Raf kinases: The historyIn 1983, the cloning of the acutely transforming replication-defective mouse type C virus 3611-MSV and characterization of its acquired oncogene was reported. 1 Since 3611-MSV induces rapidly growing f ibrosarcoma in mice, the transduced oncogene was called v-raf, whereas its cellular homologue was named c-raf. 1 Shortly thereafter, Bister and coworkers described the cloning of the avian acute leukemia retrovirus Mil Hill No. 2 (MH2). 2 MH2 was found to carry a second potential oncogene in addition to vmyc, which was termed v-mil, whereas its cellular counterpart was called c-mil. 3 Already a hybridization analysis and the gross comparison of restriction maps of v-raf and v-mil pointed at sequence homologies between these 2 genes. 4 By direct sequencing of both genes it was finally proven that 3611-MSV and MH2 have integrated orthologues of the same gene into their genomes. 5 In the following we are going to use the nomenclature for Raf kinases as proposed in a recent review from Wellbrock et al. 6 In contrast to all other oncogene kinases known at that time, no tyrosine kinase activity was detected in C-Raf. 7 Indeed, it was found that C-Raf is a serine/threonine kinase. 8,9 This and the observation that Raf coexists with the Myc oncogene in retroviruses 10 led to two novel concepts: (i) There is a tyrosine to serine phosphorylation switch as the growth factor signal enters the cell, and (ii) the mechanistic basis for cooperation between nuclear and cytoplasmic oncogenes as well as for signal transduction from cell surface receptors to the nucleus is the phosphorylation of transcription factor class oncogenes such as Myc. 11-13 Growth factor abrogation and oncogene cooperation studies were performed to corroborate this signaling scheme. 14-17 Additional important early findings were (i) the cooperation between Raf and Myc in growth factor independent proliferation, immortalization and tumor induction, 14,18,19 leading to the Raf-Myc balance model, 20 and (ii) the cell lineage-switch ...

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Two unrelated cell-derived sequences in the genome of avian leukemia and carcinoma inducing retrovirus MH2.

Cited by 114 publications

References 41 publications

A cell cycle hypothesis of cooperative oncogenesis (Review)

A cell cycle hypothesis of cooperative oncogenesis (Review)

BRAFE600 in benign and malignant human tumours

Raf kinases: Oncogenesis and drug discovery

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