ArticleBlood2014
Genetic lesions associated with chronic lymphocytic leukemia chemo-refractoriness.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.
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
45 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Chronic lymphocytic leukemia/small lymphocytic lymphoma, version 1.2015.Journal of the National Comprehensive Cancer Network : JNCCN · 2015Guideline
- Whole-exome sequencing of primary plasma cell leukemia discloses heterogeneous mutational patterns.Oncotarget · 2015Trial
- Clonal Hematopoietic Mutations in Plasma Cell Disorders: Clinical Subgroups and Shared Pathogenesis.Genomics, proteomics & bioinformatics · 2025Article
- Pharmacoproteogenomic approach identifies on-target kinase inhibitors for cancer drug repositioning.In vitro cellular & developmental biology. Animal · 2024Article
- Multiple omics levels of chronic lymphocytic leukemia.Cell death discovery · 2024Review
- The clinical utility of plasma circulating tumor DNA in the diagnosis and disease surveillance in non-diffuse large B-cell non-Hodgkin lymphomas.Future oncology (London, England) · 2024Article
- Article
- Uncovering novel mutational signatures byCell genomics · 2022Article
- High-resolution Melting Analysis for NOTCH1 c.7541-7542delCT Mutation in Chronic Lymphocytic Leukemia: Prognostic Significance in Egyptian Patients.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2022Article
- Review
- Case report: Chronic lymphocytic leukemia/small lymphocytic lymphoma and monomorphic epitheliotropic intestinal T-cell lymphoma: A composite lymphoma.Pathology oncology research : POR · 2022Article
- Clinical utility of chromosomal microarray in establishing clonality and high risk features in patients with Richter transformation.Cancer genetics · 2022Article
- Article
- Chronic Lymphocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2021Review
- H3K27me3-rich genomic regions can function as silencers to repress gene expression via chromatin interactions.Nature communications · 2021Article
- Chronic Lymphocytic Leukemia.Cancers · 2020Article
- UGT2B17 modifies drug response in chronic lymphocytic leukaemia.British journal of cancer · 2020Article
- Chronic lymphocytic leukaemia: from genetics to treatment.Nature reviews. Clinical oncology · 2019Review
- T-cell acute lymphoblastic leukemias express a unique truncated FAT1 isoform that cooperates with NOTCH1 in leukemia development.Haematologica · 2019Article
- Mutations In Thirty Hotspot Genes In Newly Diagnosed Chinese Multiple Myeloma Patients.OncoTargets and therapy · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 6 institutions in 2 countries.
Funding
Abstract
Fludarabine refractoriness (FR) represents an unsolved clinical problem of chronic lymphocytic leukemia (CLL) management. Although next-generation sequencing studies have led to the identification of a number of genes frequently mutated in FR-CLL, a comprehensive evaluation of the FR-CLL genome has not been reported. Toward this end, we studied 10 FR-CLLs by combining whole-exome sequencing and copy number aberration (CNA) analysis, which showed an average of 16.3 somatic mutations and 4 CNAs per sample. Screening of recurrently mutated genes in 48 additional FR-CLLs revealed that ~70% of FR-CLLs carry ≥1 mutation in genes previously associated with CLL clinical course, including TP53 (27.5%), NOTCH1 (24.1%), SF3B1 (18.9%), and BIRC3 (15.5%). In addition, this analysis showed that 10.3% of FR-CLL cases display mutations of the FAT1 gene, which encodes for a cadherin-like protein that negatively regulates Wnt signaling, consistent with a tumor suppressor role. The frequency of FAT1-mutated cases was significantly higher in FR-CLL than in unselected CLLs at diagnosis (10.3% vs 1.1%, P = .004), suggesting a role in the development of a high-risk phenotype. These findings have general implications for the mechanisms leading to FR and point to Wnt signaling as a potential therapeutic target in FR-CLL.
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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.