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Characteristics, Events, and Stages in Tumorigenesis
Published in Franklyn De Silva, Jane Alcorn, The Elusive Road Towards Effective Cancer Prevention and Treatment, 2023
Franklyn De Silva, Jane Alcorn
Interleukin 1 (IL1), IL12, retinoic acid, metalloproteinase inhibitors, endostatin, angiostatin, and interferons are examples for naturally occurring angiogenesis inhibitors [1076]. Various factors like VEGF, platelet-derived growth factor (PDGF), hepatocyte growth factor (HGF), basic fibroblast growth factor (FGF), hypoxia inducible factor 1 (HIF1), monocyte chemoattractant protein 1 (MCP1), macrophage inflammatory protein 1β (MIP1β), IL8, IL6, regulated on activation-normal T-cell expressed and secreted (RANTES), angiogenin, tumor necrosis factor alpha (TNFα), granulocyte colony-stimulating factor (G-CSF), placental growth factor (PGF), epidermal growth factor (EGF), transforming growth factor alpha (TGFα), TGFβ, amphiregulin, artemin, coagulation factor III, among others have been identified to be proangiogenic in many solid tumors [1076, 1077, 1087–1090]. This abundance of angiogenic factors and the redundancies that exist in the angiogenic process likely explain the suboptimal effectiveness or resistance of cancer to treatment with single antiangiogenic agents [1076].
Peripheral Mechanisms of Pain
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Nociceptors that express neurotrophic factors include nerve growth factor (NGF), neurotrophin 3 and 4, and glial-cell-derived neurotrophic factors such as artemin and neuturin. NGF is released from inflammatory and resident cells by tissue damage. It binds to nociceptive afferent nerves via its receptor, TrkA, and triggers release of nociceptive mediators from inflammatory cells.
Multiple Endocrine Neoplasia
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
The RET (rearranged during transfection) gene on chromosome 10q11.21 spans 53 kb with 21 exons and encodes a 1,114 aa, 124 kDa protein (transmembrane tyrosine kinase), which is composed of an extracellular portion (including signal peptide, cadherin-like domain, and cysteine-rich region), a single transmembrane region, and an intracellular portion (including two tyrosine kinase domains, TK1 and TK2). Interaction with ligands such as glial cell line-derived neurotrophic factor (GDNF), neurturin (TNT), artemin, or persephin stimulates RET dimerization, cross-autophosphorylation, and subsequent phosphorylation of intracellular substrates, leading to activation of downstream signaling pathways involved in cell differentiation, growth, migration, and survival [10].
An updated patent review of rearranged during transfection (RET) kinase inhibitors (2016–present)
Published in Expert Opinion on Therapeutic Patents, 2022
Rearranged during transfection (RET) is a transmembrane receptor tyrosine kinase encoded by the RET proto-oncogene located on chromosome 10. RET is integral for the development of kidneys and the enteric nervous system during embryogenesis.1 RET is expressed in neural cells and is required for proliferation, differentiation, and survival of these cells[1]. In addition, RET signaling is known to contribute to the regulation and function of hematopoietic cells and spermatogenesis [2,3]. The structure of RET (Figure 1) is similar to other receptor tyrosine kinases, and consists of an intracellular tyrosine kinase domain, a transmembrane domain, and an extracellular domain with four cadherin-like domains and a conserved cysteine region (C609, C611, C618, C620, C630, and C640)[4]. This cysteine region plays a key role in protein conformation and ligand binding [5,6]. RET activating ligands belong to the glial-cell derived neurotrophic factor (GDNF) family of ligands (GFLs) and include GDNF, neurturin, artemin, and persephin[7]. Ligands binds to the GDNF family receptor-α (GFR-α), which then causes dimerization of RET (Figure 1) and subsequent activation through autophosphorylation of the intracellular tyrosine kinase domain (Y687, Y752, Y806, Y809, Y826, Y900, Y905, Y928, Y981, Y1015, Y1062, and Y1062). Following autophosphorylation, multiple signaling pathways (such as PI3K, MAPK, JAK/STAT, and PKC pathways) are activated that regulate survival, differentiation, and proliferation[7].
The association between urinary polycyclic aromatic hydrocarbon metabolites and atopic triad by age and body weight in the US population
Published in Journal of Dermatological Treatment, 2022
Sooyoung Kim, Kathryn A. Carson, Anna L. Chien
The underlying mechanisms for the association between PAHs and atopic diseases have been investigated. On a cellular level, PAHs are potent ligands for the aryl hydrocarbon receptor (AhR), a transcription factor expressed in keratinocytes and melanocytes. In an experimental study, epicutaneous application of diesel exhaust particles activates AhR in keratinocytes and upregulate Artn expression, whose product is a neurotrophic factor artemin that is responsible for epidermal hyper-innervation that leads to hypersensitivity and pruritus in atopic dermatitis-like phenotype mice (46). In addition, atopic dermatitis-related genes, Tslp and IL-33, were upregulated after exposure to benzopyrene via AhR activation (46). Studies have shown that PAHs from diesel emission induce a cascade of oxidative stress and mitochondrial damage (47). The exposure to PAHs skewed immune responses toward a Th2 profile, which favors B-cell production of IgE and eosinophils that promote allergic inflammation (48–51). In a study of 256 atopic children (with asthma and/or allergic rhinitis), ambient PAH exposure increased total IgE level, induced epigenetic modifications in FoxP3, a key atopy-related gene, and impaired regulatory T cell function (52).
The effects of blue spaces on mental health and associated biomarkers
Published in International Journal of Mental Health, 2022
Andrew Hermanski, Jean McClelland, Jennifer Pearce-Walker, John Ruiz, Marc Verhougstraete
The specific search terms for the blue spaces were: blue space, bluespace, beach, bathing beach, ocean, oceanic, sea, shore, coast, lake, and recreational water. The specific search terms for mental health were: depressed, depressive, depression, anxiety, anxious, GAD, and stress. The specific search terms for biomarkers were: HPA axis, hypothalamic pituitary adrenal axis, proinflammatory, pro-inflammatory, IL-6, interleukin-6, CRP, c-reactive protein, neurotrophic factor, BDNF, brain-derived neurotrophic factor, 5-HT1A, 5-HT, 5-hydroxytryptamine, metabolic abnormality, cortisol, alpha-amylase, blood pressure, heart rate, adrenocorticotrophin, adrenocorticotropic hormone, corticotrophin releasing hormone, hypertension, catecholamine, serotonin, artemin, interleukin, a-melanocyte-stimulating hormone, and a-MSII.