ReviewBlood2009
Molecular biology of bcr-abl1-positive chronic myeloid leukemia.
Review in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 315 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
315 citing papers in PubMed, 746 citations in OpenAlex.
- Trial
- Dasatinib Plus Intensive Chemotherapy in Children, Adolescents, and Young Adults With Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia: Results of Children's Oncology Group Trial AALL0622.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2018Trial
- Article
- Translocation-induced enhancer rewiring reveals cryptic oncogenic circuits in multiple myeloma.Science advances · 2026Article
- Identification of new dasatinib analogues targeting mutated BCR-ABL1: virtual screening, molecular docking, and dynamics simulations studies.Molecular diversity · 2026Article
- From fatal disease to functional cure: 25 years of tyrosine kinase inhibition in chronic myeloid leukemia.Leukemia · 2026Review
- HIRA-SETDB1-H3K9me3 axis regulates chromatin architecture in leukemia cells.The Journal of biological chemistry · 2026Article
- BCR-ABL1 Drives Transcriptional Reprogramming of Chronic Myeloid Leukemia Cells for Immune Evasion Through C/EBPβ.MedComm · 2026Article
- Article
- Clinico-Metabolic Profiling Unraveled Key Metabolic Alterations Underlying the Pathophysiology of Chronic Myeloid Leukemia.ACS omega · 2026Article
- Population-scale interpretation of RNA isoform diversity enabled by Isopedia.bioRxiv : the preprint server for biology · 2026Article
- IFDlong: a model-based isoform and fusion detector for accurate annotation and quantification of long-read RNA-seq data.Genome biology · 2026Article
- Chronic Myeloid Leukemia: Historical Perspective, Pathophysiology, and Treatment Advances.Acta haematologica · 2026Review
- Detection of known gene fusions in cancer cell lines using whole-genome bisulfite sequencing data.Scientific reports · 2026Article
- Evolving Therapeutic Algorithms in Chronic Myeloid Leukemia: Integrating Efficacy, Safety, and Survivorship.Biomedicines · 2026Review
- Phosphoinositide-dependent kinase 1 (PDK1) in cancer: molecular insights and therapeutic strategies.Frontiers in chemistry · 2026Review
- From the bench of molecular understanding to the bedside of optimal therapy forEJC paediatric oncology · 2025Article
- Cracking the resistance code: The molecular reclassification of cancer and precision therapy strategies.Seminars in cancer biology · 2025Review
- Genes-first and phenotypes-first paths to treatment resistance in hematological malignancies.Cell death & disease · 2025Review
- A Flexible End-to-End Automated Sample Preparation Workflow Enables Standardized and Scalable Bottom-up Proteomics.Analytical chemistry · 2025Article
255 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 myeloid leukemia (CML) has been regarded as the paradigmatic example of a malignancy defined by a unique molecular event, the BCR-ABL1 oncogene. Decades of research zeroing in on the role of BCR-ABL1 kinase in the pathogenesis of CML have culminated in the development of highly efficacious therapeutics that, like imatinib mesylate, target the oncogenic kinase activity of BCR-ABL1. In recent years, most research efforts in CML have been devoted to developing novel tyrosine kinase inhibitors (TKIs) as well as to elucidating the mechanisms of resistance to imatinib and other TKIs. Nonetheless, primordial aspects of the pathogenesis of CML, such as the mechanisms responsible for the transition from chronic phase to blast crisis, the causes of genomic instability and faulty DNA repair, the phenomenon of stem cell quiescence, the role of tumor suppressors in TKI resistance and CML progression, or the cross-talk between BCR-ABL1 and other oncogenic signaling pathways, still remain poorly understood. Herein, we synthesize the most relevant and current knowledge on such areas of the pathogenesis of CML.
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.