ReviewCancer science2012
Molecular biology of chronic myeloid leukemia.
Review in Cancer science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Frequencies of BCR::ABL1 Transcripts in Patients with Chronic Myeloid Leukemia: A Meta-Analysis.Genes · 2024Pooled it
- Advances in Drug Targeting, Drug Delivery, and Nanotechnology Applications: Therapeutic Significance in Cancer Treatment.Pharmaceutics · 2025Review
- CX‑5461 potentiates imatinib‑induced apoptosis in K562 cells by stimulatingExperimental and therapeutic medicine · 2024Article
- CFL1 is Implicated in Chronic Myeloid Leukemia Response during Imatinib Therapy.Journal of Cancer · 2024Article
- Article
- Targeting UPR signaling pathway by dasatinib as a promising therapeutic approach in chronic myeloid leukemia.Medical oncology (Northwood, London, England) · 2022Article
- Article
- Validation of the EUTOS Long-Term Survival Score in Chinese Chronic Myeloid Leukemia Patients Treated with Imatinib: A Multicenter Real-World Study.Cancer management and research · 2020Article
- Signaling pathways involved in chronic myeloid leukemia pathogenesis: The importance of targeting Musashi2-Numb signaling to eradicate leukemia stem cells.Iranian journal of basic medical sciences · 2019Review
- Hyper-activation of Aurora kinase a-polo-like kinase 1-FOXM1 axis promotes chronic myeloid leukemia resistance to tyrosine kinase inhibitors.Journal of experimental & clinical cancer research : CR · 2019Article
- Sodium butyrate and panobinostat induce apoptosis of chronic myeloid leukemia cells via multiple pathways.Molecular genetics & genomic medicine · 2019Article
- Fumarate hydratase deficiency induces chronic myeloid leukemia progression.Translational cancer research · 2019Article
- Hematological malignancies during pregnancy.Molecular and clinical oncology · 2019Review
- Paradoxical counteraction by imatinib against cell death in myeloid progenitor 32D cells expressing p210BCR-ABL.Oncotarget · 2018Article
- Bcr-Abl regulation of sphingomyelin synthase 1 reveals a novel oncogenic-driven mechanism of protein up-regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- 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
- Adhesion to stromal cells mediates imatinib resistance in chronic myeloid leukemia through ERK and BMP signaling pathways.Scientific reports · 2017Article
- In Vitro Antileukemia Activity of ZSTK474 on K562 and Multidrug Resistant K562/A02 Cells.International journal of biological sciences · 2016Article
- IGFBP-2 - taking the lead in growth, metabolism and cancer.Journal of cell communication and signaling · 2015Article
- Doxorubicin Differentially Induces Apoptosis, Expression of Mitochondrial Apoptosis-Related Genes, and Mitochondrial Potential in BCR-ABL1-Expressing Cells Sensitive and Resistant to Imatinib.BioMed research international · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Detailed information on the crystal structure of the pharmacologically targeted domains of the BCR-ABL molecule and on its intracellular signaling, which are potentially involved in growth, anti-apoptosis, metabolism and stemness, has made the study of chronic myeloid leukemia the most successful field in tumor biology. However, we now face the issue of drug resistance due to deregulation in the quality control of both DNA and protein. BCR-ABL is basically a misfolded protein with intrinsically disordered regions, which not only produces endoplasmic reticulum stress followed by unfolded protein response in some settings, but also conformational plasticity that may affect the structure of the whole molecule. The intercellular signaling derived from the leukemic cell microenvironment may influence the intracellular responses that take place in a manner both dependent on and independent of BCR-ABL tyrosine kinase activity.
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.