ArticleProceedings of the National Academy of Sciences of the United States of America1997
Ectopic expression of A-myb in transgenic mice causes follicular hyperplasia and enhanced B lymphocyte proliferation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
10 citing papers in PubMed, 26 citations in OpenAlex.
- Article
- A-MYB substitutes for B-MYB in activating cell cycle genes and in stimulating proliferation.Nucleic acids research · 2024Article
- Gene expression-based risk score in diffuse large B-cell lymphoma.Oncotarget · 2012Article
- Myb proteins: angels and demons in normal and transformed cells.Frontiers in bioscience (Landmark edition) · 2011Review
- A high throughput embryonic stem cell screen identifies Oct-2 as a bifunctional regulator of neuronal differentiation.Genes & development · 2009Article
- Dominant negative retinoic acid receptor initiates tumor formation in mice.Molecular cancer · 2006Article
- Making better transgenic models: conditional, temporal, and spatial approaches.Molecular biotechnology · 2005Review
- Molecular definition of the germinal centre stage of B-cell differentiation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2001Review
- Isolation and characterization of the human A-myb promoter: regulation by NF-Y and Sp1.Oncogene · 2000Article
- Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The A-myb gene is a transcription factor that shares structural and functional similarities with the v-myb oncogene. To date, v-myb is the only myb gene directly implicated in tumorigenesis, a property attributed to its transactivating ability. Recent studies have demonstrated that A-myb, like v-myb, is a potent transcriptional activator, raising the possibility that A-myb may also participate in oncogenesis. To test this hypothesis, we generated fusion constructs that contained the human A-myb cDNA under control of the mouse metallothionein promoter and the mouse mammary tumor virus long terminal repeat. These constructs were inserted into the germ line of mice, and the functional consequences of ectopic A-myb expression were examined. Although transgene expression was detected in a wide range of tissues, abnormalities were confined primarily to hematopoietic tissues. After a 9-month latency, A-myb transgenic mice developed hyperplasia of the spleen and lymph nodes. Enlarged tissues contained a polyclonally expanded B lymphocyte population that expressed a germinal center-cell phenotype. Transgenic B lymphocytes showed increased DNA synthesis in response to low dose mitogen stimulation, suggesting that A-myb may contribute to hyperplasia by increasing the rate of B cell proliferation.
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What OpenQuestion holds
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.