ReviewOncogene1999
Transformation by v-Myb.
Review in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 120 citations in OpenAlex.
- Genome-wide investigation of MYB gene family in Areca catechu and potential roles of AcTDF in transgenic Arabidopsis.Molecular biology reports · 2024Article
- Transcription Factor MYB as Therapeutic Target: Current Developments.International journal of molecular sciences · 2024Review
- MYB: A Key Transcription Factor in the Hematopoietic System Subject to Many Levels of Control.Advances in experimental medicine and biology · 2024Review
- Genome-wide identification of myeloblastosis gene family and its response to cadmium stress inFrontiers in plant science · 2022Article
- Chromatin occupancy and target genes of the haematopoietic master transcription factor MYB.Scientific reports · 2021Article
- MYB oncoproteins: emerging players and potential therapeutic targets in human cancer.Oncogenesis · 2021Review
- Association between B-Oncology letters · 2021Review
- A long lost key opens an ancient lock:Biology open · 2020Article
- Structural insights into target DNA recognition by R2R3-MYB transcription factors.Nucleic acids research · 2020Article
- A novel cell-based screening assay for small-molecule MYB inhibitors identifies podophyllotoxins teniposide and etoposide as inhibitors of MYB activity.Scientific reports · 2018Article
- MYB - A regulatory factor in hematopoiesis.Gene · 2018Review
- Association of single-nucleotide polymorphisms of high-mobility group box 1 with susceptibility and clinicopathological characteristics of uterine cervical neoplasia in Taiwanese women.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- A unifying gene signature for adenoid cystic cancer identifies parallel MYB-dependent and MYB-independent therapeutic targets.Oncotarget · 2014Article
- Stress-induced phosphorylation of Thr486 in c-Myb by p38 mitogen-activated protein kinases attenuates conjugation of SUMO-2/3.The Journal of biological chemistry · 2013Article
- DNA released by leukemic cells contributes to the disruption of the bone marrow microenvironment.Oncogene · 2013Article
- Duplication and maintenance of the Myb genes of vertebrate animals.Biology open · 2013Article
- Inhibition of Myb-dependent gene expression by the sesquiterpene lactone mexicanin-I.Leukemia · 2012Article
- Development of safer gene delivery systems to minimize the risk of insertional mutagenesis-related malignancies: a critical issue for the field of gene therapy.ISRN oncology · 2012Article
- Animal-specific C-terminal domain links myeloblastosis oncoprotein (Myb) to an ancient repressor complex.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- The early history of tumor virology: Rous, RIF, and RAV.Proceedings of the National Academy of Sciences of the United States of America · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The v-myb oncogene of the avian myeloblastosis virus (AMV) is unique among known oncogenes in that it causes only acute leukemia in animals and transforms only hematopoietic cells in culture. AMV was discovered in the 1930s as a virus that caused a disease in chickens that is similar to acute myelogenous leukemia in humans (Hall et al., 1941). This avian retrovirus played an important role in the history of cancer research for two reasons. First, AMV was used to demonstrate that all oncogenic viruses did not contain a single cancer-causing principle. In particular, although both Rous sarcoma virus (RSV) and AMV could replicate in cultures of either embryonic fibroblasts or hematopoietic cells, RSV could transform only fibroblasts whereas AMV could transform only hematopoietic cells (Baluda, 1963; Durban and Boettiger, 1981a). Second, chickens infected with AMV develop remarkably high white counts and therefore their peripheral blood contains remarkably large quantities of viral particles (Beard, 1963). For this reason AMV was often used as a prototypic retrovirus in order to study viral assembly and later to produce large amounts of reverse transcriptase for both research and commercial purposes. Following the discovery of the v-src oncogene of RSV and the demonstration that it arose from the normal c-src proto-oncogene, a number of acute leukemia viruses were analysed by similar techniques and found to also contain viral oncogenes of cellular origin (Roussel et al., 1979). In the case of AMV, it was shown that almost the entire retroviral env gene had been replaced by a sequence of cellular origin (initially called mab or amv, but later renamed v-myb) (Duesberg et al., 1980; Souza et al., 1980). Remarkably, sequences contained in this myb oncogene were shared between AMV and the avian E26 leukemia virus, but were not contained in any other acutely transforming retroviruses. In addition, the E26 virus contained a second sequence of cellular origin (ets) that was unique. The E26 leukemia virus was first described in the 1960s and causes an acute erythroblastosis in chickens, more reminiscent of the disease caused by avian erythroblastosis virus (AEV) than by AMV (Ivanov et al., 1962).
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.