China
Africa
Explore chapters and articles related to this topic
Familial Gastrointestinal Stromal Tumor Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Mapped to chromosome 4q12, the KIT gene encodes the 145 kDa receptor tyrosine kinase c-KIT, which belongs to the type III receptor tyrosine kinase family (which also includes PDGFRA, PDGFRB, macrophage colony stimulating factor receptor [CSF1R], and FL cytokine receptor [FLT3]).
The Role of Filgrastim
Published in Howard J.A. Carp, Recurrent Pregnancy Loss, 2020
Fabio Scarpellini, Marco Sbracia
The mechanism of action of filgrastim in RPL treatment is unclear, as there is no direct evidence of the effect of filgrastim in pregnancy. However, there is indirect evidence regarding the interaction of filgrastim with the trophoblast and immune system. The effects of G-CSF on trophoblast growth and invasiveness have been reported by several studies. G-CSF and its receptor are expressed in trophoblast cells throughout the pregnancy [17–21]. The G-CSF/G-CSFR axis was described in the placenta and decidua in 1989 by Uzumaki et al. [17]. Several other authors have also shown its pivotal role in the regulation of trophoblast invasiveness and development [18–21]. Several authors have reported that granulite colony-stimulating factor receptor (G-CSFR) expressed in trophoblast cell lines activate different signal transduction pathways, such as JAK/STAT, PI3 K, and MAPKs, which in turn increase matrix metalloproteinase-2 and vascular endothelial growth factor secretion [36]. Furthermore, G-CSF upregulates β1 integrin and increases the migration of human trophoblast cell line Swan 71 [37]. G-CSF also increases the expression of mRNAs for several genes involved in the implantation processes in an in vitro model taken from endometrial biopsies [38].
Monocyte and lymphocyte membrane markers: Ontogeny and clinical significance
Published in Gabriel Virella, Medical Immunology, 2019
Scott Sugden, Damien Montamat-Sicotte, Karen K. Yam, Joseph Murphy, Bader Yassine Diab, Virginia Litwin
One of the key players of monopoiesis is the transcription factor PU.1. High expression of PU.1 will lead to the activation of different myeloid specific factors such as interferon regulatory factor-8 (IRF8), kruppel-like factor 4 (KLF-4), and Erg1. PU.1 expression is also indispensable to the expression of macrophage colony stimulating factor receptor (M-CSFR, CD115). Macrophage colony stimulating factor (M-CSF) and IL-34 are two ligands for CD155 crucial to monocyte development.
The role of microRNA in neuronal inflammation and survival in the post ischemic brain: a review
Published in Neurological Research, 2023
William A. Li, Aslan Efendizade, Yuchuan Ding
As mentioned above, infiltrated inflammatory cells produce ROS, inflammatory cytokines, and MMPs which induce neuron injury directly or indirectly by disrupting BBB integrity. Monocyte infiltration is one of the major cellular responses in stroke [51]. Thus, miRNAs that regulate monocyte differentiation, maturation, and activation are potential candidates for intervention. Using cord blood CD34+ hematopoietic progenitor cells, Fontana et al. demonstrated that miR-17-5p contributes to the differentiation and maturation of progenitor cells into monocytes through the acute myeloid leukemia-1 (AML1) and macrophage-colony stimulating factor receptor (M-CSFR) pathway [52]. miRNA 17-5p binds the AML1 mRNA 3′-UTR and cause AML1 mRNA degradation. This leads to macrophage colony-stimulating factor receptor (M-CSFR) down-regulation, subsequently enhances progenitor cell proliferation and simultaneously inhibits monocyte differentiation and maturation [52]. This inhibition of monocyte maturation in the periphery helps reduce the inflammatory response in the penumbral tissue, and thus could potentially be exerting neuroprotective properties.
Emerging clinical investigational drugs for the treatment of amyotrophic lateral sclerosis
Published in Expert Opinion on Investigational Drugs, 2023
Loreto Martinez-Gonzalez, Ana Martinez
(NCT04066244) is an orally bioavailable, potent, selective, and brain-penetrant antagonist of the macrophage colony-stimulating factor receptor (CSF-1 R or c-fms), being developed by Novartis to treat solid CNS tumors as glioblastoma. In 2022, sotuletinib obtained the orphan drug status granted by FDA to treat patients with ALS based in its ability to decrease neuroinflammation by microglia depletion [34]. Sotuletinib decrease the translocator protein (TSPO) binding in the brain, a 18 kDa protein mainly found on the outer mitochondrial membrane of microglia, reducing microglia activation [34]. The current clinical trial will evaluate safety, tolerability, and brain microglia response in 46 participants with ALS following multiple doses of Sotuletinib. In some patients from one of the study groups, TSPO ligand positron emission tomography (PET) imaging will be performed while in the remainder participants of this trial group CSF biomarker will be analyzed to look for efficacy signals.
Overview and recent advances in the targeting of medulloblastoma cancer stem cells
Published in Expert Review of Anticancer Therapy, 2021
In 2015, it was published that cancer cell lines from multiple tumor types, including medulloblastoma, contained subpopulations that demonstrated cell surface expression of the granulocyte colony stimulating factor receptor (GCSF-R, CD114) [106]. CD114 has previously been described as a possible marker of CSCs in neuroblastoma [107], as CD114 expression defined a discrete subpopulation within neuroblastoma cell lines with self-renewal, pluripotency, and enhanced tumorigenicity. This CD114+ cell subpopulation was also distinct from previously characterized tumor-initiating cell subpopulations defined by CD133 expression, neurosphere assays, and side population staining. Further studies using limiting dilution and competitive lineage-tracing assays demonstrated CD114+ cells were capable of both self-renewal and differentiation. The gene expression patterns of CD114+ cells closely resembled embryonic and induced pluripotent stem cells and were similar to premigratory neural crest cells, while the CD114- subpopulation demonstrated gene expression patterns consistent with migratory neural crest cells representing a later stage of differentiation. CD114+ cells also were treatment-resistant, and CD114+ neuroblastoma cells were enriched in post-chemotherapy patient samples, and further increased in post-chemotherapy metastases. Xenograft tumors treated with chemotherapy demonstrated similar increases in the prevalence of CD114+ cells.