ReviewBlood cancer journal2016
Cytogenetic and molecular abnormalities in chronic myelomonocytic leukemia.
Review in Blood cancer journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 134 citations in OpenAlex.
- Trial
- Chronic Myelomonocytic Leukemia: History, Pathobiology, Diagnostic Controversies, and Evolving Classification.Current hematologic malignancy reports · 2026Review
- IsolatedHaematologica · 2026Article
- Comorbidities and mutations including single- and multihit TET2 mutations in relation to outcome in chronic myelomonocytic leukaemia-A population-based study.British journal of haematology · 2026Article
- Article
- Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026Review
- Array comparative genomic hybridisation in haematological malignancies: A comprehensive review.African journal of laboratory medicine · 2026Review
- Solving Riddles Through Sequencing (SIRIUS): unlocking hematologic diagnoses by whole genome and transcriptome sequencing.Leukemia · 2026Article
- Impact of Epigenetic Mutations in Chronic Myelomonocytic Leukemia.Current hematologic malignancy reports · 2025Review
- Contemporary CMML Risk Stratification and Management.Current hematologic malignancy reports · 2025Review
- Myeloid neoplasms with PHF6 mutations: context-dependent genomic and prognostic characterization in 176 informative cases.Blood cancer journal · 2025Article
- A multifactorial risk scoring system for the prediction of early relapse in CMML patients with allo-HSCT: a nationwide representative multicenter study.Bone marrow transplantation · 2025Article
- AML typical mutations (CEBPA, FLT3, NPM1) identify a high-risk chronic myelomonocytic leukemia independent of CPSS molecular.Blood advances · 2025Article
- Clinical perception and novel insights of chronic myelomonocytic leukemia: a 10-year multi-center retrospective study.Frontiers in medicine · 2025Article
- Effective requesting method to detect fusion transcripts in chronic myelomonocytic leukemia RNA-seq.NAR genomics and bioinformatics · 2024Article
- A mitochondrial surveillance mechanism activated bybioRxiv : the preprint server for biology · 2024Article
- Article
- Infrequent Presentations of ChronicCancers · 2024Review
- U2AF1 in various neoplastic diseases and relevant targeted therapies for malignant cancers with complex mutations (Review).Oncology reports · 2024Review
- Molecular genetics and management of world health organization defined atypical chronic myeloid leukemia.Annals of hematology · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic myelomonocytic leukemia (CMML) is a clonal stem cell disorder associated with peripheral blood monocytosis and an inherent tendency to transform to acute myeloid leukemia. CMML has overlapping features of myelodysplastic syndromes and myeloproliferative neoplasms. Clonal cytogenetic changes are seen in ~30%, whereas gene mutations are seen in >90% of patients. Common cytogenetic abnormalities include; trisomy 8, -Y, -7/del(7q), trisomy 21 and del(20q), with the Mayo-French risk stratification effectively risk stratifying patients based on cytogenetic abnormalities. Gene mutations frequently involve epigenetic regulators (TET2 ~60%), modulators of chromatin (ASXL1 ~40%), spliceosome components (SRSF2 ~50%), transcription factors (RUNX1 ~15%) and signal pathways (RAS ~30%, CBL ~15%). Of these, thus far, only nonsense and frameshift ASXL1 mutations have been shown to negatively impact overall survival. This has resulted in the development of contemporary, molecularly integrated (inclusive of ASXL1 mutations) CMML prognostic models, including Molecular Mayo Model and the Groupe Français des Myélodysplasies model. Better understanding of the prevalent genetic and epigenetic dysregulation has resulted in emerging targeted treatment options for some patients. The development of an integrated (cytogenetic and molecular) prognostic model along with CMML-specific response assessment criteria are much needed future goals.
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.