ArticleLeukemia2011
High levels of the adhesion molecule CD44 on leukemic cells generate acute myeloid leukemia relapse after withdrawal of the initial transforming event.
Article in Leukemia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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
39 citing papers in PubMed, 76 citations in OpenAlex.
- 7-Ketocholesterol Links Sterol Homeostasis to Hedgehog Signaling and Stress-Survival Responses in MSCs from Patients with Acute Myeloid Leukemia.International journal of molecular sciences · 2026Article
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- A translational perspective of the malignant hematopoietic proteoglycome.Cell & bioscience · 2025Review
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- CD44: a cancer stem cell marker and therapeutic target in leukemia treatment.Frontiers in immunology · 2024Review
- Hematopoietic and leukemic stem cells homeostasis: the role of bone marrow niche.Exploration of targeted anti-tumor therapy · 2024Review
- Hyaluronic Acid Nanoparticles for Immunogenic Chemotherapy of Leukemia and T-Cell Lymphoma.Pharmaceutics · 2022Article
- Regulation of Malignant Myeloid Leukemia by Mesenchymal Stem Cells.Frontiers in cell and developmental biology · 2022Review
- Hyaluronic Acid-Conjugated Carbon Nanomaterials for Enhanced Tumour Targeting Ability.Molecules (Basel, Switzerland) · 2021Review
- Article
- Conditionally immortalised leukaemia initiating cells co-expressing Hoxa9/Meis1 demonstrate microenvironmental adaptation properties ex vivo while maintaining myelomonocytic memory.Scientific reports · 2021Article
- A narrative review of central nervous system involvement in acute leukemias.Annals of translational medicine · 2021Review
- CNTs mediated CD44 targeting; a paradigm shift in drug delivery for breast cancer.Genes & diseases · 2020Review
- Location First: Targeting Acute Myeloid Leukemia Within Its Niche.Journal of clinical medicine · 2020Review
- Follistatin is a novel therapeutic target and biomarker in FLT3/ITD acute myeloid leukemia.EMBO molecular medicine · 2020Article
- Targeting Immunophenotypic Markers on Leukemic Stem Cells: How Lessons from Current Approaches and Advances in the Leukemia Stem Cell (LSC) Model Can Inform Better Strategies for Treating Acute Myeloid Leukemia (AML).Cold Spring Harbor perspectives in medicine · 2020Review
- Leukemia Stem Cell Release From the Stem Cell Niche to Treat Acute Myeloid Leukemia.Frontiers in cell and developmental biology · 2020Review
- Cancer Stem Cells-Origins and Biomarkers: Perspectives for Targeted Personalized Therapies.Frontiers in immunology · 2020Review
- BETP degradation simultaneously targets acute myelogenous leukemia stem cells and the microenvironment.The Journal of clinical investigation · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple genetic hits are detected in patients with acute myeloid leukemia (AML). To investigate this further, we developed a tetracycline-inducible mouse model of AML, in which the initial transforming event, overexpression of HOXA10, can be eliminated. Continuous overexpression of HOXA10 is required to generate AML in primary recipient mice, but is not essential for maintenance of the leukemia. Transplantation of AML to secondary recipients showed that in established leukemias, ∼80% of the leukemia-initiating cells (LICs) in bone marrow stopped proliferating upon withdrawal of HOXA10 overexpression. However, the population of LICs in primary recipients is heterogeneous, as ∼20% of the LICs induce leukemia in secondary recipients despite elimination of HOXA10-induced overexpression. Intrinsic genetic activation of several proto-oncogenes was observed in leukemic cells resistant to inactivation of the initial transformation event. Interestingly, high levels of the adhesion molecule CD44 on leukemic cells are essential to generate leukemia after removal of the primary event. This suggests that extrinsic niche-dependent factors are also involved in the host-dependent outgrowth of leukemias after withdrawal of HOXA10 overexpression event that initiates the leukemia.
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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.