ReviewInternational journal of hematology2001
Molecular biology of chronic myeloid leukemia.
Review in International journal of hematology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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
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
15 citing papers in PubMed, 53 citations in OpenAlex.
- Potential signaling pathways, biomarkers, natural drugs, and chronic myeloid leukemia therapeutics.Frontiers in pharmacology · 2025Review
- CRISPR/Cas9-Directed Gene Trap Constitutes a Selection System for CorrectedInternational journal of molecular sciences · 2022Article
- Molecular biology of chronic myeloid leukemia.Cancer science · 2012Review
- Fyn is not essential for Bcr-Abl-induced leukemogenesis in mouse bone marrow transplantation models.International journal of hematology · 2012Article
- PTP1B suppresses prolactin activation of Stat5 in breast cancer cells.The American journal of pathology · 2010Article
- Multiple roles and therapeutic implications of Akt signaling in cancer.OncoTargets and therapy · 2009Article
- Hematopoietic stem cell quiescence is maintained by compound contributions of the retinoblastoma gene family.Cell stem cell · 2008Article
- Fusion transcripts and transcribed retrotransposed loci discovered through comprehensive transcriptome analysis using Paired-End diTags (PETs).Genome research · 2007Article
- Effects of the tyrosine kinase inhibitor imatinib mesylate on a Bcr-Abl-positive cell line: suppression of autonomous cell growth but no effect on decreased adhesive property and morphological changes.International journal of hematology · 2003Article
- IL-3 receptor signaling is dispensable for BCR-ABL-induced myeloproliferative disease.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells.The EMBO journal · 2002Article
- Article
- Bcr-Abl is a "molecular switch" for the decision for growth and differentiation in hematopoietic stem cells.International journal of hematology · 2002Review
- Article
- Acute lymphoblastic leukemia with t(1;9;22)(q32;q34;q11).International journal of hematology · 2002Article
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
Multistep carcinogenesis is exemplified by chronic myeloid leukemia with clinical manifestation consisting of a chronic phase and blast crisis. Pathological generation of BCR-ABL (breakpoint cluster region-Abelson) results in growth promotion, differentiation, resistance to apoptosis, and defect in DNA repair in targeted blood cells. Domains in BCR and ABL sequences work in concert to elicit a variety of leukemogenic signals including Ras, STAT5 (signal transducer and activator of transcription-5), Myc, cyclin D1, P13 (phosphatidylinositol 3-kinase), RIN1 (Ras interaction/interference), and activation of actin cytoskeleton. However, the mechanism of differentiation of transformed cells is poorly understood. A mutator phenotype of BCR-ABL could explain the transformation to blast crisis. The aim of this review is to integrate molecular and biological information on BCR, ABL, and BCR-ABL and to focus on how signaling from those molecules mirrors the biological phenotypes of chronic myeloid leukemia.
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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.