ArticleLeukemia2006
Gene expression profiling of CD34+ cells identifies a molecular signature of chronic myeloid leukemia blast crisis.
Article in Leukemia, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
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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
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.
- Chronic myeloid leukemia: an update of concepts and management recommendations of European LeukemiaNet.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2009Guideline
- Nilotinib-induced bone marrow CD34+/lin-Ph+ cells early clearance in newly diagnosed CP-Chronic Myeloid Leukemia: Final report of the PhilosoPhi34 study.European journal of haematology · 2021Trial
- Understanding drug resistance in chronic myeloid leukemia through the lens of leukemic stem cell states: insights from single-cell analyses.Haematologica · 2026Review
- Regulation of Tetraspanin CD63 in Chronic Myeloid Leukemia (CML): Single-Cell Analysis of Asymmetric Hematopoietic Stem Cell Division Genes.Bioengineering (Basel, Switzerland) · 2025Article
- Review
- Unravelling cancer subtype-specific driver genes in single-cell transcriptomics data with CSDGI.PLoS computational biology · 2023Article
- Arginine dependency is a therapeutically exploitable vulnerability in chronic myeloid leukaemic stem cells.EMBO reports · 2023Article
- A Nucleus-Targeting WT1 Antagonistic Peptide Encapsulated in Polymeric Nanomicelles Combats Refractory Chronic Myeloid Leukemia.Pharmaceutics · 2023Article
- Feature selection for high dimensional microarray gene expression data via weighted signal to noise ratio.PloS one · 2023Article
- Loss of G0/G1 switch gene 2 (G0S2) promotes disease progression and drug resistance in chronic myeloid leukaemia (CML) by disrupting glycerophospholipid metabolism.Clinical and translational medicine · 2022Article
- Article
- Integrating genetic and epigenetic factors in chronic myeloid leukemia risk assessment: toward gene expression-based biomarkers.Haematologica · 2022Review
- Understanding and Monitoring Chronic Myeloid Leukemia Blast Crisis: How to Better Manage Patients.Cancer management and research · 2021Review
- A Bayesian data fusion based approach for learning genome-wide transcriptional regulatory networks.BMC bioinformatics · 2020Article
- sigFeature: Novel Significant Feature Selection Method for Classification of Gene Expression Data Using Support Vector Machine andFrontiers in genetics · 2020Article
- Global gene expression profiles of hematopoietic stem and progenitor cells from patients with chronic myeloid leukemia: the effect of in vitro culture with or without imatinib.Cancer medicine · 2017Article
- Article
- The role of small adaptor proteins in the control of oncogenic signalingr driven by tyrosine kinases in human cancer.Oncotarget · 2016Review
- The Interferon Consensus Sequence Binding Protein (Icsbp/Irf8) Is Required for Termination of Emergency Granulopoiesis.The Journal of biological chemistry · 2016Article
- c-MYB is a transcriptional regulator of ESPL1/Separase in BCR-ABL-positive chronic myeloid leukemia.Biomarker research · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite recent success in the treatment of early-stage disease, blastic phase (BP) of chronic myeloid leukemia (CML) that is characterized by rapid expansion of therapy-refractory and differentiation-arrested blasts, remains a therapeutic challenge. The development of resistance upon continuous administration of imatinib mesylate is associated with poor prognosis pointing to the need for alternative therapeutic strategies and a better understanding of the molecular mechanisms underlying disease progression. To identify transcriptional signatures that may explain pathological characteristics and aggressive behavior of BP blasts, we performed comparative gene expression profiling on CD34+ Ph+ cells purified from patients with untreated newly diagnosed chronic phase CML (CP, n=11) and from patients in BP (n=9) using Affymetrix oligonucleotide arrays. Supervised microarray data analysis revealed 114 differentially expressed genes (P<10(-4)), 34 genes displaying more than two-fold transcriptional changes when comparing CP and BP groups. While 24 of these genes were downregulated, 10 genes, especially suppressor of cytokine signalling 2 (SOCS2), CAMPATH-1 antigen (CD52), and four human leukocyte antigen-related genes were strongly overexpressed in BP. Expression of selected genes was validated by real-time-polymerase chain reaction and flow cytometry. Our data suggest the existence of a common gene expression profile of CML-BP and provide new insight into the molecular phenotype of blasts associated with disease progression and high malignancy.
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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.