ArticleThe Journal of experimental medicine2013
Pten loss in the bone marrow leads to G-CSF-mediated HSC mobilization.
Article in The Journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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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.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Hesperidin/Salinomycin Combination; a Natural Product for Deactivation of the PI3K/Akt Signaling Pathway and Anti-Apoptotic Factors in KG1a Cells.Journal of fluorescence · 2025Article
- Loss of Dnmt3a impairs hematopoietic homeostasis and myeloid cell skewing via the PI3Kinase pathway.JCI insight · 2023Article
- Investigating increased hematopoietic stem cell fitness in a novel mouse model.Small GTPases · 2022Article
- PTEN in Regulating Hematopoiesis and Leukemogenesis.Cold Spring Harbor perspectives in medicine · 2020Review
- Deregulation of tumor suppressive ASXL1-PTEN/AKT axis in myeloid malignancies.Journal of molecular cell biology · 2020Article
- The role of granulocyte colony‑stimulating factor in breast cancer development: A review.Molecular medicine reports · 2020Review
- Formaldehyde induces the apoptosis of BMCs of BALB/c mice via the PTEN/PI3K/Akt signal transduction pathway.Molecular medicine reports · 2019Article
- The Key Roles of PTEN in T-Cell Acute Lymphoblastic Leukemia Development, Progression, and Therapeutic Response.Cancers · 2019Review
- Oncogenic PTEN functions and models in T-cell malignancies.Oncogene · 2016Review
- Article
- Pten Cell Autonomously Modulates the Hematopoietic Stem Cell Response to Inflammatory Cytokines.Stem cell reports · 2016Article
- DNA Damage Response in Hematopoietic Stem Cell Ageing.Genomics, proteomics & bioinformatics · 2016Review
- Article
- PTEN opposes negative selection and enables oncogenic transformation of pre-B cells.Nature medicine · 2016Article
- Modeling the Pro-inflammatory Tumor Microenvironment in Acute Lymphoblastic Leukemia Predicts a Breakdown of Hematopoietic-Mesenchymal Communication Networks.Frontiers in physiology · 2016Article
- The Role of PTEN in Myeloid Malignancies.Hematology reports · 2015Review
- A PI3K p110β-Rac signalling loop mediates Pten-loss-induced perturbation of haematopoiesis and leukaemogenesis.Nature communications · 2015Article
- Prognostic value of the expression of phosphatase and tensin homolog and CD44 in elderly patients with refractory acute myeloid leukemia.Oncology letters · 2015Article
- Article
- Hematopoietic stem cell quiescence and function are controlled by the CYLD-TRAF2-p38MAPK pathway.The Journal of experimental medicine · 2015Article
Corrections and comments
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Authors and funding
8 authors at 6 institutions in 3 countries.
Funding
Abstract
The phosphatase and tumor suppressor PTEN inhibits the phosphoinositol-3-kinase (PI3K) signaling pathway and plays a key role in cell growth, proliferation, survival, and migration. Pten conditional deletion using MxCre or Scl-CreER(T) leads to splenomegaly and leukemia formation, which occurs after the relocation of normal hematopoietic stem cells (HSCs) from the bone marrow to the spleen. Unexpectedly, dormant HSCs in the bone marrow do not enter the cell cycle upon Pten loss, they do not lose self-renewal activity, and they are not exhausted. Instead, Pten deficiency causes an up-regulation of the PI3K pathway in myeloid cells, but not in HSCs. Strikingly, myeloid cells secrete high levels of G-CSF upon Pten loss, leading to the mobilization of HSCs from the bone marrow and accumulation in the spleen. After deletion of Pten in mice lacking G-CSF, the splenomegaly, myeloproliferative disease, and splenic HSC accumulation are rescued. Our data show that although PTEN has little if any role in normal HSCs, it is essential to prevent overt G-CSF production by myeloid and stromal cells which otherwise causes HSCs to relocate to the spleen followed by lethal leukemia initiation.
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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.