ArticleBlood2009
Mouse models of non-Hodgkin lymphoma reveal Syk as an important therapeutic target.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 117 citations in OpenAlex.
- An Open-label, Phase II Trial of Entospletinib (GS-9973), a Selective Spleen Tyrosine Kinase Inhibitor, in Diffuse Large B-cell Lymphoma.Clinical lymphoma, myeloma & leukemia · 2018Trial
- Trial
- Antithrombotic Effects of Fostamatinib in Combination with Conventional Antiplatelet Drugs.International journal of molecular sciences · 2022Article
- Regulation of B-Cell Receptor Signaling and Its Therapeutic Relevance in Aggressive B-Cell Lymphomas.Cancers · 2022Review
- Immunotherapies of retinoblastoma: Effective methods for preserving vision in the future.Frontiers in oncology · 2022Review
- An Overview on Diffuse Large B-Cell Lymphoma Models: Towards a Functional Genomics Approach.Cancers · 2021Review
- Gain-of-function variants in SYK cause immune dysregulation and systemic inflammation in humans and mice.Nature genetics · 2021Article
- Review
- Forward and Reverse Genetics of B Cell Malignancies: From Insertional Mutagenesis to CRISPR-Cas.Frontiers in immunology · 2021Review
- Inhibition of the deubiquitinase USP10 induces degradation of SYK.British journal of cancer · 2020Article
- Pathogenic B-cell receptor signaling in lymphoid malignancies: New insights to improve treatment.Immunological reviews · 2019Review
- SYK Inhibition Potentiates the Effect of Chemotherapeutic Drugs on Neuroblastoma Cells in Vitro.Cancers · 2019Article
- Inhibition of ovarian tumor cell invasiveness by targeting SYK in the tyrosine kinase signaling pathway.Oncogene · 2018Article
- SYK-targeted dendritic cell-mediated cytotoxic T lymphocytes enhance the effect of immunotherapy on retinoblastoma.Journal of cancer research and clinical oncology · 2018Article
- A novel orally available Syk/Src/Jak2 inhibitor, SKLB-850, showed potent anti-tumor activities in B cell lymphoma (BCL) models.Oncotarget · 2017Article
- Article
- Aberrant SYK Kinase Signaling Is Essential for Tumorigenesis Induced by TSC2 Inactivation.Cancer research · 2017Article
- Overview of the Use of Murine Models in Leukemia and Lymphoma Research.Frontiers in oncology · 2017Review
- Targeting B-cell receptor signaling in leukemia and lymphoma: how and why?International journal of hematologic oncology · 2016Review
- Calling in SYK: SYK's dual role as a tumor promoter and tumor suppressor in cancer.Biochimica et biophysica acta · 2015Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on bySyk to death.2009
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
We have generated mouse models of non-Hodgkin lymphoma (NHL) that rely on the cooperation between MYC overexpression and B-cell antigen receptor (BCR) signaling for the initiation and maintenance of B-cell lymphomas. Using these mouse models of NHL, we have focused on the identification of BCR-derived signal effectors that are important for the maintenance of NHL tumors. In the present study, we concentrate on Spleen tyrosine kinase (Syk), a nonreceptor tyrosine kinase required to transduce BCR-dependent signals. Using a genetic approach, we showed that Syk expression is required for the survival of murine NHL-like tumors in vitro and that tumor cells deficient in Syk fail to expand in vivo. In addition, a pharmacologic inhibitor of Syk was able to induce apoptosis of transformed B cells in vitro and led to tumor regression in vivo. Finally, we show that genetic or pharmacologic inhibition of Syk activity in human NHL cell lines are generally consistent with results found in the mouse models, suggesting that targeting Syk may be a viable therapeutic strategy.
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.