ArticleBlood2009
CXCR4 expression and biologic activity in acute myeloid leukemia are dependent on oxygen partial pressure.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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
72 citing papers in PubMed, 131 citations in OpenAlex.
- Differential hypoxic regulation of the microRNA-146a/CXCR4 pathway in normal and leukemic monocytic cells: impact on response to chemotherapy.Haematologica · 2015Trial
- Trial
- The Role of the Bone Marrow Microenvironment in the Pathogenesis of Acute Myeloid Leukemia.Biomedicines · 2026Review
- Establishment and validation of a clinical threshold criteria for choosing PET imaging tracers for indolent non-Hodgkin's lymphoma.EJNMMI research · 2025Article
- CXCR4 as a therapeutic target in acute myeloid leukemia.Leukemia · 2024Review
- Review
- Article
- Expression of CXCL8 (IL-8) in the Pathogenesis of T-Cell Acute Lymphoblastic Leukemia Patients.Cureus · 2023Article
- Concomitant targeting of FLT3 and BTK overcomes FLT3 inhibitor resistance in acute myeloid leukemia through the inhibition of autophagy.Haematologica · 2023Article
- GPC-100, a novel CXCR4 antagonist, improves in vivo hematopoietic cell mobilization when combined with propranolol.PloS one · 2023Article
- A Novel Peptide that Disrupts the Lck-IPArchives of microbiology & immunology · 2023Article
- Bone Marrow Microenvironment as a Source of New Drug Targets for the Treatment of Acute Myeloid Leukaemia.International journal of molecular sciences · 2022Review
- The genesis and evolution of acute myeloid leukemia stem cells in the microenvironment: From biology to therapeutic targeting.Cell death discovery · 2022Review
- Hypoxic stress and hypoxia-inducible factors in leukemias.Frontiers in oncology · 2022Review
- Identification of Protein Biomarker Signatures for Acute Myeloid Leukemia (AML) Using Both Nontargeted and Targeted Approaches.Proteomes · 2021Article
- Leukaemia: a model metastatic disease.Nature reviews. Cancer · 2021Review
- Role of CXCR4 in the progression and therapy of acute leukaemia.Cell proliferation · 2021Review
- The Role of Hypoxic Bone Marrow Microenvironment in Acute Myeloid Leukemia and Future Therapeutic Opportunities.International journal of molecular sciences · 2021Review
- Far from Health: The Bone Marrow Microenvironment in AML, A Leukemia Supportive Shelter.Children (Basel, Switzerland) · 2021Review
- Abnormal dopamine receptor signaling allows selective therapeutic targeting of neoplastic progenitors in AML patients.Cell reports. Medicine · 2021Article
12 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
6 authors at 1 institution in 1 country.
Funding
Abstract
The CXCR4/SDF-1 axis has been studied extensively because of its role in development and hematopoiesis. In acute myeloid leukemia (AML), elevated expression of CXCR4 has been shown to correlate with shortened survival. Hy-poxia increases CXCR4 in several tumor models, but the impact of reduced O(2) partial pressure (pO(2)) on expression and biologic function of CXCR4 in AML is unknown. We determined pO(2) in bone marrows of AML patients as 6.1% (+/-1.7%). At this pO(2), CXCR4 surface and total expression were up-regulated within 10 hours in leukemic cell lines and patient samples as shown by Western blotting, fluorescence-activated cell sorting, and microscopy. Interestingly, hypoxic cells failed to internalize CXCR4 in response to SDF-1, and upon reoxygenation at 21% O(2), surface and total expression of CXCR4 rapidly decreased independent of adenosine triphosphate or proteasome activity. Instead, increased pO(2) led to alteration of lipid rafts by cholesterol depletion and structural changes and was associated with increased shedding of CXCR4-positive microparticles, suggesting a novel mechanism of CXCR4 regulation. Given the importance of CXCR4 in cell signaling, survival, and adhesion in leukemia, the results suggest that pO(2) be considered a critical variable in conducting and interpreting studies of CXCR4 expression and regulation in leukemias.
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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.