ReviewCancer science2003
Pre-B lymphomas in SL/Kh mice: a multifactorial disease model.
Review in Cancer science, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 17 citations in OpenAlex.
- Testing and Confidence Intervals for High Dimensional Proportional Hazards Model.Journal of the Royal Statistical Society. Series B, Statistical methodology · 2017Article
- Review
- ZFP521 contributes to pre-B-cell lymphomagenesis through modulation of the pre-B-cell receptor signaling pathway.Oncogene · 2016Article
- A quantitative trait locus responsible for inducing B-cell lymphoblastic lymphoma is a hotspot for microsatellite instability.Cancer science · 2010Article
- Early B-cell factor-associated zinc-finger gene is a frequent target of retroviral integration in murine B-cell lymphomas.Oncogene · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pre-B lymphoma in the inbred mouse strain SL/Kh is an excellent multifactorial disease model. The endogenous murine leukemia virus provirus Emv11, genetically acquired from an AKR progenitor, is the pathogenetic agent that reintegrates to dysregulate several host genes, i.e., Stat5a, Evi3, c-Myc, N-Myc, Stat5b, and others. Constitutive activation of Stat5a either by provirus integration or by transfection of the active mutant Stat5a cDNA transforms pre-B cells in bone marrow. Genetically determined expansion of early B cells and a dominant SL/Kh MHC allele predispose the animals to succumb to pre-B lymphomas. A number of other host genetic and epigenetic factors that determine the types of lymphomas, susceptibility to lymphomas, and length of the latent period are discussed.
Indexed as
Identifiers
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.