ArticleCancer research2008
Sequential transcription factor targeting for diffuse large B-cell lymphomas.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 30 citations in OpenAlex.
- Expression of p21 protein predicts clinical outcome in DLBCL patients older than 60 years treated with R-CHOP but not CHOP: a prospective ECOG and Southwest Oncology Group correlative study on E4494.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Trial
- Developmental cell death of cortical projection neurons is controlled by a Bcl11a/Bcl6-dependent pathway.EMBO reports · 2022Article
- iRGD-modified exosomes-delivered BCL6 siRNA inhibit the progression of diffuse large B-cell lymphoma.Frontiers in oncology · 2022Article
- Progress toward B-Cell Lymphoma 6 BTB Domain Inhibitors for the Treatment of Diffuse Large B-Cell Lymphoma and Beyond.Journal of medicinal chemistry · 2021Article
- Article
- Biomarkers and novel therapeutic approaches for diffuse large B-cell lymphoma in the era of precision medicine.Oncotarget · 2020Review
- Identification of Thiourea-Based Inhibitors of the B-Cell Lymphoma 6 BTB Domain via NMR-Based Fragment Screening and Computer-Aided Drug Design.Journal of medicinal chemistry · 2018Article
- BCL6 Antagonizes NOTCH2 to Maintain Survival of Human Follicular Lymphoma Cells.Cancer discovery · 2017Article
- The Expanding Role of the BCL6 Oncoprotein as a Cancer Therapeutic Target.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Review
- Selective targeting of BCL6 induces oncogene addiction switching to BCL2 in B-cell lymphoma.Oncotarget · 2016Article
- Integrin-specific hydrogels as adaptable tumor organoids for malignant B and T cells.Biomaterials · 2015Article
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- Breaking bad in the germinal center: how deregulation of BCL6 contributes to lymphomagenesis.Trends in molecular medicine · 2014Review
- Mechanism-based epigenetic chemosensitization therapy of diffuse large B-cell lymphoma.Cancer discovery · 2013Article
- Targeting BCL6 in diffuse large B-cell lymphoma: what does this mean for the future treatment?Expert review of hematology · 2013Article
- Lineage-specific functions of Bcl-6 in immunity and inflammation are mediated by distinct biochemical mechanisms.Nature immunology · 2013Article
- Pathogenesis of human B cell lymphomas.Annual review of immunology · 2012Review
- BCL6 repression of EP300 in human diffuse large B cell lymphoma cells provides a basis for rational combinatorial therapy.The Journal of clinical investigation · 2010Article
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Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Transcription factors play a central role in malignant transformation by activating or repressing waves of downstream target genes. Therapeutic targeting of transcription factors can reprogram cancer cells to lose their advantages in growth and survival. The BCL6 transcriptional repressor plays a central role in the pathogenesis of diffuse large B-cell lymphomas (DLBCL) and controls downstream checkpoints, including the p53 tumor suppressor gene. We report that a specific inhibitor of BCL6 called BPI can trigger a p53 response in DLBCL cells. This was partially due to induction of p53 activity and partially due to relief of direct repression by BCL6 of p53 target genes. BPI could thus induce a p53-like response even in the presence of mutant p53. Moreover, sequential BCL6 peptide inhibitors followed by p53 peptide or small-molecule activators provided a more powerful antilymphoma effect than either treatment alone by maximally restoring p53 target gene expression. Therefore, tandem targeting of the overlapping BCL6 and p53 transcriptional programs can correct aberrant survival pathways in DLBCL and might provide an effective therapeutic approach to lymphoma therapy.
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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.