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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]).
Gastrointestinal Diseases
Published in Victor A. Bernstam, Pocket Guide to GENE LEVEL DIAGNOSTICS in Clinical Practice, 2019
A gene showing tumor-specific LOH in at least 50% of informative cases of colorectal carcinoma encodes the colony-stimulating factor 1 receptor, and has been mapped to 5q21–22, close to the FAP locus. Alleles of the APC locus (responsible for FAP) may be associated with susceptibility to colon cancer not necessarily accompanied by polyposis.
Angiogenesis and Roles of Adhesion Molecules in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
Asmita Hazra, Saptarshi Mandal
Sunitinib is another orally acting multikinase inhibitor for tyrosine kinases VEGFR1, 2, and 3; PDGFRα and β; colony-stimulating factor 1 receptor (CSF1R), c-kit, RET, and Flt3. It is Food and Drug Administration (FDA) approved for several cancers. In some cases, psoriasis has improved due to sunitinib use for unrelated causes, for example, renal cell carcinoma. Unlike sorafenib, full-blown psoriasis has not been precipitated by sunitinib. However, psoriasiform rashes have been reported with the use of sunitinib, which become particularly severe when in scrotal and genital or inguinal skin (Diamantis and Chon 2010). Crohn’s disease, a comorbidity of psoriasis, is also known to be occasionally paradoxically exacerbated, for example, with sunitinib (Boers-Sonderen et al. 2014).
Reprogramming the immunosuppressive microenvironment of IDH1 wild-type glioblastoma by blocking Wnt signaling between microglia and cancer cells
Published in OncoImmunology, 2021
Dandan Fan, Qi Yue, Jian Chen, Cong Wang, Ruilin Yu, Ziyi Jin, Shujie Yin, Qinyue Wang, Luo Chen, Xueling Liao, Chengyuan Peng, Jianpin Zhang, Zhonglian Cao, Ying Mao, Ruimin Huang, Liang Chen, Cong Li
Several approaches have been tested to eliminate immunosuppressive microglia.42 For example, a colony stimulating factor 1 receptor inhibitor was used to ablate microglia.43 However, no obvious therapeutic responses were reported in clinical trials.44 Additionally, completely exhausting microglia in the brain could lead to deadly consequences.45 A promising strategy for inhibiting glioma progression is rebalancing the ratio between immunostimulatory and immunosuppressive microglia. For example, Zhang et al. found that STAT3 inhibition resulted in the repolarization of microglia and abrogated glioma growth.46 Sarkar et al. indicated that amphotericin B shifted microglia toward an immunostimulatory phenotype and reduced the development of glioblastoma stem cells.47 Moreover, Kees et al showed that mediating microglial phenotypic transition led to reduced glioma cell invasiveness.48 Thus, compared to microglial depletion, rebalancing the microglial phenotype is expected to be more effective in ameliorating the immunosuppressive microenvironment in glioma.
Effect of Interleukin-34 on Secretion of Angiogenesis Cytokines by Peripheral Blood Mononuclear Cells of Rheumatoid Arthritis
Published in Immunological Investigations, 2020
Lu Lu Ding, Xin Li, Yi Meng Lei, Li Ping Xia, Jing Lu, Hui Shen
Interleukin (IL)-34 is a newly discovered inflammatory cytokine. It is a homodimeric secreted protein, and its main receptor is colony-stimulating factor 1 receptor (CSF-1R) (Lin et al., 2008). IL-34 binding to CSF-1R can enhance the activity of macrophages, induce the production of multiple cytokines, promote the proliferation and differentiation of lymphocytes, and mediate autoimmunity and inflammation. Our previous study found that IL-34 levels in serum and synovial fluid in patients with RA were significantly higher and correlated with disease activity (Tian et al., 2013). Immunohistochemical analysis revealed that IL-34 expression in synovial tissue was positively correlated with the severity of synovitis (Chemel et al., 2012). Numerous studies have shown that IL-34 can promote osteoclastogenesis and participate in the bone destruction of RA (Hwang et al., 2012). The above results suggested that IL-34 plays a crucial role in the pathogenesis of RA. However, whether IL-34 is involved in angiogenesis in RA and promotes pannus formation in RA have not been reported. One study showed that IL-34 promotes tumor progression and metastasis in osteosarcoma by inducing angiogenesis (Ségaliny et al., 2015). In vitro investigations using endothelial cell precursors and mature HUVECs revealed that IL-34 stimulated endothelial cell proliferation and vascular cord formation. Therefore, we hypothesize that IL-34 may be involved in angiogenesis and pannus formation in RA.
Targeting fundamental aging mechanisms to treat osteoporosis
Published in Expert Opinion on Therapeutic Targets, 2019
Jack Feehan, Ahmed Al Saedi, Gustavo Duque
Osteoclasts are highly specialized macrophage-like cells derived from the monocyte line with unique adaptations allowing for the resorption of mineralized bone. Osteoclast differentiation begins with the exposure of monocytes to monocyte colony-stimulating factor (mCSF), a member of the tumor necrosis factor (TNF) superfamily of cytokines. Binding of mCSF to the colony-stimulating factor 1 receptor on monocyte/macrophage progenitors triggers the formation of preosteoclasts, which then fully differentiate into mature osteoclasts after binding of RANK by the membrane-bound RANK ligand expressed by osteoblasts and osteocytes [50,51]. OPG is another TNF family membrane receptor principally expressed by mature osteoblasts which directly limits osteoclastogenesis via inhibition of RANK signaling, by acting as a decoy receptor for RANKL [50]. Once matured, the osteoclast develops unique features such as the ruffled border and multiple nuclei which are critical in allowing the resorption of bone, leading to calcium release into the serum. This resorption occurs in three phases. Firstly, the matured osteoclast adheres to the bone surface via integrins, forming a sealed zone directly beneath it in contact with the ruffled border. Once this resorption zone is established acids are released from the osteoclast, dissolving the mineral component of the bone. Finally, cathepsin K, and other proteolytic enzymes are secreted into the space and hydrolyze the bone matrix [52]. This process is accelerated in aging for a variety of reasons, an understanding of which opens a range of avenues for therapeutic exploitation.