ArticleLeukemia2016
Longitudinal copy number, whole exome and targeted deep sequencing of 'good risk' IGHV-mutated CLL patients with progressive disease.
Article in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 45 citations in OpenAlex.
- Proteomic and phosphoproteomic signatures of disease progression in unmutated IGHV chronic lymphocytic leukemia.Clinical proteomics · 2026Article
- Longitudinal Whole-Exome Sequencing Identifies Clonal Hematopoiesis and Genomic Heterogeneity as a Predictor of Treatment Outcome in Patients with Newly Diagnosed, Elderly Chronic Lymphocytic Leukemia.International journal of molecular sciences · 2026Article
- The Chronic Lymphocytic Leukemia Epigenome: A Powerful and Stable Framework for Understanding Biological and Clinical Heterogeneity.Hematology/oncology clinics of North America · 2025Review
- Article
- HATCHet2: clone- and haplotype-specific copy number inference from bulk tumor sequencing data.Genome biology · 2024Article
- HATCHet2: clone- and haplotype-specific copy number inference from bulk tumor sequencing data.bioRxiv : the preprint server for biology · 2023Article
- Whole-genome sequencing of chronic lymphocytic leukemia identifies subgroups with distinct biological and clinical features.Nature genetics · 2022Article
- Immunological and genetic kinetics from diagnosis to clinical progression in chronic lymphocytic leukemia.Biomarker research · 2021Article
- Clonal dynamics in a composite chronic lymphocytic leukemia and hairy cell leukemia-variant.Genes, chromosomes & cancer · 2021Article
- Chronic Lymphocytic Leukemia.Cold Spring Harbor perspectives in medicine · 2021Review
- In Vitro Modeling of Non-Solid Tumors: How Far Can Tissue Engineering Go?International journal of molecular sciences · 2020Review
- Nfkbie-deficiency leads to increased susceptibility to develop B-cell lymphoproliferative disorders in aged mice.Blood cancer journal · 2020Article
- Genetic dynamics in untreated CLL patients with either stable or progressive disease: a longitudinal study.Journal of hematology & oncology · 2019Article
- Article
- CALDER: Inferring Phylogenetic Trees from Longitudinal Tumor Samples.Cell systems · 2019Article
- Article
- Role of long non-coding RNAs in disease progression of early stage unmutated chronic lymphocytic leukemia.Oncotarget · 2019Article
- Overview of non-coding mutations in chronic lymphocytic leukemia.Molecular oncology · 2019Review
- Highly similar genomic landscapes in monoclonal B-cell lymphocytosis and ultra-stable chronic lymphocytic leukemia with low frequency of driver mutations.Haematologica · 2018Article
- Genetic landscape of ultra-stable chronic lymphocytic leukemia patients.Annals of oncology : official journal of the European Society for Medical Oncology · 2018Article
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 4 institutions in 2 countries.
Funding
Abstract
The biological features of IGHV-M chronic lymphocytic leukemia responsible for disease progression are still poorly understood. We undertook a longitudinal study close to diagnosis, pre-treatment and post relapse in 13 patients presenting with cMBL or Stage A disease and good-risk biomarkers (IGHV-M genes, no del(17p) or del(11q) and low CD38 expression) who nevertheless developed progressive disease, of whom 10 have required therapy. Using cytogenetics, fluorescence in situ hybridisation, genome-wide DNA methylation and copy number analysis together with whole exome, targeted deep- and Sanger sequencing at diagnosis, we identified mutations in established chronic lymphocytic leukemia driver genes in nine patients (69%), non-coding mutations (PAX5 enhancer region) in three patients and genomic complexity in two patients. Branching evolutionary trajectories predominated (n=9/13), revealing intra-tumoural epi- and genetic heterogeneity and sub-clonal competition before therapy. Of the patients subsequently requiring treatment, two had sub-clonal TP53 mutations that would not be detected by standard methodologies, three qualified for the very-low-risk category defined by integrated mutational and cytogenetic analysis and yet had established or putative driver mutations and one patient developed progressive, therapy-refractory disease associated with the emergence of an IGHV-U clone. These data suggest that extended genomic and immunogenetic screening may have clinical utility in patients with apparent good-risk disease.
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.