ArticleBlood2017
Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed.
- Evaluating upfront high-dose consolidation after R-CHOP for follicular lymphoma by clinical and genetic risk models.Blood advances · 2020Trial
- Mouse models of B cell lymphomas on the basis of genetic features.Frontiers in immunology · 2026Review
- Clinicopathological characteristics, genetic aberrations, and optimized treatment strategies in double-hit and triple-hit lymphoma: a multi-center cohort study.Molecular biomedicine · 2025Article
- Missense Mutations in the KAT Domain ofInternational journal of molecular sciences · 2025Article
- Article
- Enhancer reprogramming: critical roles in cancer and promising therapeutic strategies.Cell death discovery · 2025Review
- Review
- Tumor Biology Hides Novel Therapeutic Approaches to Diffuse Large B-Cell Lymphoma: A Narrative Review.International journal of molecular sciences · 2024Review
- Multi-omics profiling of longitudinal samples reveals early genomic changes in follicular lymphoma.Blood cancer journal · 2024Article
- Targeting AURKA to induce synthetic lethality in CREBBP-deficient B-cell malignancies via attenuation of MYC expression.Oncogene · 2024Article
- Loss of CREBBP and KMT2D cooperate to accelerate lymphomagenesis and shape the lymphoma immune microenvironment.Nature communications · 2024Article
- Comparison of whole-genome and immunoglobulin-based circulating tumor DNA assays in diffuse large B-cell lymphoma.HemaSphere · 2024Article
- Pathogenic Variants Associated with Epigenetic Control and the NOTCH Pathway Are Frequent in Classic Hodgkin Lymphoma.International journal of molecular sciences · 2024Article
- Epigenetic profiles of elevated cell free circulating H3.1 nucleosomes as potential biomarkers for non-Hodgkin lymphoma.Scientific reports · 2023Article
- Genetic subdivisions of follicular lymphoma defined by distinct coding and noncoding mutation patterns.Blood · 2023Article
- An AID to follicular lymphoma transformation.Blood · 2023Article
- Tracing Founder Mutations in Circulating and Tissue-Resident Follicular Lymphoma Precursors.Cancer discovery · 2023Article
- Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.Signal transduction and targeted therapy · 2023Review
- The Role of CREBBP/EP300 and Its Therapeutic Implications in Hematological Malignancies.Cancers · 2023Review
- Disease-Defining Molecular Features of Primary Cutaneous B-Cell Lymphomas: Implications for Classification and Treatment.The Journal of investigative dermatology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
27 authors.
Funding
Abstract
CREBBP is targeted by inactivating mutations in follicular lymphoma (FL) and diffuse large B-cell lymphoma (DLBCL). Here, we provide evidence from transgenic mouse models that Crebbp deletion results in deficits in B-cell development and can cooperate with Bcl2 overexpression to promote B-cell lymphoma. Through transcriptional and epigenetic profiling of these B cells, we found that Crebbp inactivation was associated with broad transcriptional alterations, but no changes in the patterns of histone acetylation at the proximal regulatory regions of these genes. However, B cells with Crebbp inactivation showed high expression of Myc and patterns of altered histone acetylation that were localized to intragenic regions, enriched for Myc DNA binding motifs, and showed Myc binding. Through the analysis of CREBBP mutations from a large cohort of primary human FL and DLBCL, we show a significant difference in the spectrum of CREBBP mutations in these 2 diseases, with higher frequencies of nonsense/frameshift mutations in DLBCL compared with FL. Together, our data therefore provide important links between Crebbp inactivation and Bcl2 dependence and show a role for Crebbp inactivation in the induction of Myc expression. We suggest this may parallel the role of CREBBP frameshift/nonsense mutations in DLBCL that result in loss of the protein, but may contrast the role of missense mutations in the lysine acetyltransferase domain that are more frequently observed in FL and yield an inactive protein.
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.