ArticleCancer research2012
Cyclophosphamide creates a receptive microenvironment for prostate cancer skeletal metastasis.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 72 citations in OpenAlex.
- Article
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- Mitochondrial pyruvate metabolism and glutaminolysis toggle steady-state and emergency myelopoiesis.The Journal of experimental medicine · 2023Article
- Circulating biomarkers for diagnosis and therapeutic monitoring in bone metastasis.Journal of bone and mineral metabolism · 2023Review
- Therapeutic Implications of the Drug Resistance Conferred by Extracellular Vesicles Derived from Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2023Review
- Chemokines network in bone metastasis: Vital regulators of seeding and soiling.Seminars in cancer biology · 2022Review
- Chemotherapy-Induced Changes in the Lung Microenvironment: The Role of MMP-2 in Facilitating Intravascular Arrest of Breast Cancer Cells.International journal of molecular sciences · 2021Article
- Stress-Inducible GeneInternational journal of molecular sciences · 2021Article
- The Role of Inflammation in Breast and Prostate Cancer Metastasis to Bone.International journal of molecular sciences · 2021Review
- Chemotherapy-Induced Upregulation of Small Extracellular Vesicle-Associated PTX3 Accelerates Breast Cancer Metastasis.Cancer research · 2021Article
- Cross Talk Between Macrophages and Cancer Cells in the Bone Metastatic Environment.Frontiers in endocrinology · 2021Review
- Small Molecule Soluble Epoxide Hydrolase Inhibitors in Multitarget and Combination Therapies for Inflammation and Cancer.Molecules (Basel, Switzerland) · 2020Review
- Bone Tropism in Cancer Metastases.Cold Spring Harbor perspectives in medicine · 2020Review
- Neutrophils are mediators of metastatic prostate cancer progression in bone.Cancer immunology, immunotherapy : CII · 2020Article
- The P2X7 Receptor in the Maintenance of Cancer Stem Cells, Chemoresistance and Metastasis.Stem cell reviews and reports · 2020Review
- Identification of Key Gene Signatures Associated With Bone Metastasis in Castration-Resistant Prostate Cancer Using Co-Expression Analysis.Frontiers in oncology · 2020Article
- The Monocytes That Repopulate in Mice After Cyclophosphamide Treatment Acquire a Neutrophil Precursor Gene Signature and Immunosuppressive Activity.Frontiers in immunology · 2020Article
- Rapamycin enhances growth inhibition on urothelial carcinoma cells through LKB1 deficiency-mediated mitochondrial dysregulation.Journal of cellular physiology · 2019Article
- Trabectedin Reduces Skeletal Prostate Cancer Tumor Size in Association with Effects on M2 Macrophages and Efferocytosis.Neoplasia (New York, N.Y.) · 2019Article
- Suppression of chemotherapy-induced cytokine/lipid mediator surge and ovarian cancer by a dual COX-2/sEH inhibitor.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
A number of cancers predominantly metastasize to bone, due to its complex microenvironment and multiple types of constitutive cells. Prostate cancer especially has been shown to localize preferentially to bones with higher marrow cellularity. Using an experimental prostate cancer metastasis model, we investigated the effects of cyclophosphamide, a bone marrow-suppressive chemotherapeutic drug, on the development and growth of metastatic tumors in bone. Priming the murine host with cyclophosphamide before intracardiac tumor cell inoculation was found to significantly promote tumor localization and subsequent growth in bone. Shortly after cyclophosphamide treatment, there was an abrupt expansion of myeloid lineage cells in the bone marrow and the peripheral blood, associated with increases in cytokines with myelogenic potential such as C-C chemokine ligand (CCL)2, interleukin (IL)-6, and VEGF-A. More importantly, neutralizing host-derived murine CCL2, but not IL-6, in the premetastatic murine host significantly reduced the prometastatic effects of cyclophosphamide. Together, our findings suggest that bone marrow perturbation by cytotoxic chemotherapy can contribute to bone metastasis via a transient increase in bone marrow myeloid cells and myelogenic cytokines. These changes can be reversed by inhibition of CCL2.
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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.