Characterization of the hemopoietic target cells for the avian leukemia virus E26

Moscovici, Mișu; Jurdic, Pierre; Samarut, Jacques; Gazzolo, Louis; Mura, Casilda V.; Moscovici, C.

doi:10.1016/0042-6822(83)90396-3

Cited by 94 publications

(72 citation statements)

References 21 publications

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“…Both the v-erbA oncogene, carried by the Avian Erythroblastosis Virus (AEV), for a review, see and the p135 gag-myb-ets oncogene carried by the E26 virus (Moscovici et al, 1983;Radke et al, 1982) act through the blockade of speci®c dierentiation programs. Those two oncoproteins are derived by recombination within the viral genome of cellular genes encoding transcriptions factors and are considered to transform cells through their ability to aect the expression of genes normally regulated by their cellular counterparts (respectively c-erbAa, c-Myb and c-Ets-1).…”

Section: Introductionmentioning

confidence: 99%

Role of the different RAR isoforms in controlling the erythrocytic differentiation sequence. Interference with the v-erbA and p135gag-myb-ets nuclear oncogenes

Gandrillon

Samarut

1998

Oncogene

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Little is known as to how the nuclear oncogenes v-erbA and p135gag-myb-ets do transform cells. The elucidation of their molecular mechanisms of action requires the identi®cation of relevant target genes. We analysed the possibility for the RARb gene to represent such a target gene. We ®rst show that the RARb gene induction is a speci®c and direct process, requiring the continous presence of retinoids and under the control of the RARa isoform exclusively. We then show that the expression of either the v-erbA or the p135 gag-myb-ets oncogene is not sucient to block the RARb gene induction. We con®rmed the loss of RARb gene response in certain cell lines but we discarded the possibility that this loss might represent a necessary step for cell lines immortalization. We further show that the RARa isoform activation is necessary and sucient to induce the growth inhibition and the dierentiation stimulation characteristic for the commitment-inducing ability of retinoids in chicken erythrocytic progenitor cells. We therefore propose a model showing that RARa but not RARb is the key mediator for commitment to dierentiation and that it should control two dierent set of genes whose expression is dierentially aected by the verbA and the p135 gag-myb-ets oncogenes.

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Section: Introductionmentioning

confidence: 99%

Role of the different RAR isoforms in controlling the erythrocytic differentiation sequence. Interference with the v-erbA and p135gag-myb-ets nuclear oncogenes

Gandrillon

Samarut

1998

Oncogene

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“…Another avian leukemia virus (ALV), E26, also has been shown to contain most of the v-myb sequences and an additional nucleotide sequence derived from the c-ets protooncogene (27,41). While the target cells of AMV are of the myeloid lineage, cells of the myeloid as well as erythroid lineages are transformed by E26 (36,37,50). It appears that the myeloid leukemogenicity shared by AMV and E26 correlates with the common myb sequence.…”

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confidence: 99%

Two modes of c-myb activation in virus-induced mouse myeloid tumors.

Shen-Ong¹,

Morse²,

Potter³

et al. 1986

Mol. Cell. Biol.

126

108

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Two modes of disruption of the protooncogene c-myb by viral insertional mutagenesis In mouse myeloid tumor cells are described. The first mode was found in six tumors in which a Moloney murine leukemia virus component had inserted in the same transcriptional orientation upstream of the 5'-most exon with v-myb homology (vEl). cDNA sequence data indicate the presence of a truncated c-myb mRNA that is initiated in the upstream 5' long terminal repeat of the integrated provirus and processed via a cryptic splice donor sequence in the gag region to the splice acceptor site in vEl of the c-myb gene, thus removing the remaining downstream viral and myb intronic sequences. Unlike most gag-onc transcripts, the gag and myb sequences in the hybrid transcript were not in the same reading frame. It is presumed that the gag sequence provides a cryptic translation initiation site for the novel amino-truncated c-myb protein. The second mode of disruption was by downstream virus insertion at the 3' side of the c-myb, which results in the synthesis of a small (-2 kilobase) myb transcript. The 5' long terminal repeat of the inserted provirus provides a TGA termination codon that results in the elimination of 240 normal c-myb amino acid residues from the carboxyl terminus of the tumor-specific myb protein. These results suggest that truncated myb proteins play a role in neoplastic transformation of myeloid cells. Avian myeloblastosis virus (AMV) is a replicationdefective retrovirus which induces myeloblastosis in vivo and transforms myelomonocytic cells in vitro (35). The viral genome contains a v-myb sequence that is homologous to the middle portion of the chicken protooncogene c-myb (1,16,22,52,58) and is thought to be essential for its oncogenic properties (11,59). Another avian leukemia virus (ALV), E26, also has been shown to contain most of the v-myb sequences and an additional nucleotide sequence derived from the c-ets protooncogene (27,41). While the target cells of AMV are of the myeloid lineage, cells of the myeloid as well as erythroid lineages are transformed by E26 (36, 37, 50). It appears that the myeloid leukemogenicity shared by AMV and E26 correlates with the common myb sequence. The p75 protein encoded by normal c-myb is 30 kilodaltons (kDa) larger than the p45 protein encoded by the AMVtransduced v-myb (23). Several lines of evidence indicate that a variety of alterations in protooncogenes can render them oncogenic (reviewed in reference 64). It is, however, currently unclear whether truncation of the c-myb protein is the abnormality responsible for the tumors induced by v-myb.The acute transforming retroviruses of mammalian and avian origin have led to the identification of nearly 20 cellular oncogenes. Retroviruses that lack oncogenes can induce a variety of tumors by insertional mutagenesis which affects both known c-onc genes and previously unidentified cellular genes (e.g., int loci) that are now implicated in tumorigenesis (reviewed in reference 3). Two modes of insertional mutagenesis which involve oncoge...

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“…The viral oncogenes v-myb and v-myc both transform myelomonocytic cells in vitro and in vivo, but they elicit characteristic and different phenotypes (3-6, 13-15, 18, 25, 27, 29, 30 (28,31), and (iii) the ability of genes such as v-myc and Ela to complement activated c-ras genes in rat embryo cell transformation (23,32).…”

Section: Discussionmentioning

confidence: 99%

Coordinate regulation of myelomonocytic phenotype by v-myb and v-myc.

Symonds¹,

Klempnauer²,

Snyder³

et al. 1986

Mol. Cell. Biol.

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Both avian myeloblastosis virus (by the action of v-myb) and avian myelocytomatosis virus MC29 (by the action of v-myc) transform cells of the myelomonocytic lineage. Whereas avian myeloblastosis virus elicits a relatively immature phenotype, cells transformed by MC29 resemble mature macrophages. When cells previously transformed by v-myb were superinfected with MC29, their phenotype was rapidly altered to that of a more mature cell. These superinfected cells expressed both v-myb (at a level similar to that found before superinfection) and v-myc. It therefore appears that the expression of v-myc can elicit certain properties of a more differentiated phenotype. In addition, unlike cells transformed by v-myb alone, the cells expressing both v-myb and v-myc could not be induced by the tumor promoter 12-0-tetradecanoylphorbol-13-acetate to differentiate to fully mature macrophages. Cells with a morphology similar to that of the superinfected cells were elicited by simultaneously infecting yolk sac macrophages with avian myeloblastosis virus and MC29. Such cells expressed both v-myb and v-myc. These results indicate that expression of v-myb and v-myc in infected cells coordinately regulates myelomonocytic phenotype and that the two viral oncogenes vary in their ability to interfere with tumor promoter-induced differentiation. Our findings also sustain previous suggestions that the oncogenes v-myb and v-myc may not transform target cells by simply blocking differentiation.

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Characterization of the hemopoietic target cells for the avian leukemia virus E26

Cited by 94 publications

References 21 publications

Role of the different RAR isoforms in controlling the erythrocytic differentiation sequence. Interference with the v-erbA and p135gag-myb-ets nuclear oncogenes

Role of the different RAR isoforms in controlling the erythrocytic differentiation sequence. Interference with the v-erbA and p135gag-myb-ets nuclear oncogenes

Two modes of c-myb activation in virus-induced mouse myeloid tumors.

Coordinate regulation of myelomonocytic phenotype by v-myb and v-myc.

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