ReviewProtein & cell2013
Molecular mechanisms for survival regulation of chronic myeloid leukemia stem cells.
Review in Protein & cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 33 citations in OpenAlex.
- YBX1 regulates the survival of chronic myeloid leukemia stem cells by modulating mCellular oncology (Dordrecht, Netherlands) · 2023Article
- MiR-125a-3p and MiR-320b Differentially Expressed in Patients with Chronic Myeloid Leukemia Treated with Allogeneic Hematopoietic Stem Cell Transplantation and Imatinib Mesylate.International journal of molecular sciences · 2021Article
- Sphingosine kinases are involved in the regulation of all-trans retinoic acid sensitivity of K562 chronic myeloid leukemia cells.Oncology letters · 2021Article
- RBFOX3 Promotes Gastric Cancer Growth and Progression by Activating HTERT Signaling.Frontiers in oncology · 2020Article
- Integrative Genomic Analysis Reveals Cancer-Associated Gene Mutations in Chronic Myeloid Leukemia Patients with Resistance or Intolerance to Tyrosine Kinase Inhibitor.OncoTargets and therapy · 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
- Targeting chronic myeloid leukemia stem cells with the hypoxia-inducible factor inhibitor acriflavine.Blood · 2017Article
- Article
- The human Smoothened inhibitor PF-04449913 induces exit from quiescence and loss of multipotent Drosophila hematopoietic progenitor cells.Oncotarget · 2016Article
- Two sides of the same coin: tyrosine kinase inhibition in cancer and neurodegeneration.Neural regeneration research · 2015Article
- Dipeptide species regulate p38MAPK-Smad3 signalling to maintain chronic myelogenous leukaemia stem cells.Nature communications · 2015Article
- Stem Cell Hierarchy and Clonal Evolution in Acute Lymphoblastic Leukemia.Stem cells international · 2015Review
- Salarin C inhibits the maintenance of chronic myeloid leukemia progenitor cells.Cell cycle (Georgetown, Tex.) · 2015Article
- Chronic myeloid leukemia transformation in a patient with paroxysmal nocturnal hemoglobinuria: a rare case report with literature review.International journal of clinical and experimental medicine · 2015Article
- Selective JAK2/ABL dual inhibition therapy effectively eliminates TKI-insensitive CML stem/progenitor cells.Oncotarget · 2014Article
- One more stem cell niche: how the sensitivity of chronic myeloid leukemia cells to imatinib mesylate is modulated within a "hypoxic" environment.Hypoxia (Auckland, N.Z.) · 2014Review
- Emerging therapeutic strategies for targeting chronic myeloid leukemia stem cells.Stem cells international · 2013Article
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
No grant is acknowledged in the PubMed record.
Abstract
Studies on chronic myeloid leukemia (CML) have served as a paradigm for cancer research and therapy. These studies involve the identification of the first cancer-associated chromosomal abnormality and the subsequent development of tyrosine kinase inhibitors (TKIs) that inhibit BCR-ABL kinase activity in CML. It becomes clear that leukemia stem cells (LSCs) in CML which are resistant to TKIs, and eradication of LSCs appears to be extremely difficult. Therefore, one of the major issues in current CML biology is to understand the biology of LSCs and to investigate why LSCs are insensitive to TKI monotherapy for developing curative therapeutic strategies. Studies from our group and others have revealed that CML LSCs form a hierarchy similar to that seen in normal hematopoiesis, in which a rare stem cell population with limitless self-renewal potential gives rise to progenies that lack such potential. LSCs also possess biological features that are different from those of normal hematopoietic stem cells (HSCs) and are critical for their malignant characteristics. In this review, we summarize the latest progress in CML field, and attempt to understand the molecular mechanisms of survival regulation of LSCs.
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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.