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| Mild Hyperthermia (Approximately 39°C to 41°C Pathways and Effects: -Heat Shock Protein (HSP) Induction: Mild heat stress triggers the production of HSPs (e.g., HSP70, HSP90) that help cells cope with stress, which can sometimes provide a transient protective effect. However, these proteins can also act as immunomodulators. -Modulation of the Immune System: Mild hyperthermia can enhance dendritic cell activation and improve antigen presentation, leading to the stimulation of anti-tumor immune responses. -Vasodilation: Increased blood flow and improved oxygenation can sensitize tumors to radiation therapy and certain chemotherapeutics. Moderate Hyperthermia (Approximately 41°C to 43°C) Pathways and Effects: -Enhanced Cytotoxicity: At temperatures in this range, tumor cells become more vulnerable to radiation and some chemotherapeutic agents. This is partly due to the inhibition of DNA repair pathways. -Increased Permeability: Moderate heat can increase the permeability of cellular membranes, aiding in drug delivery and the uptake of chemotherapeutic agents. -Induction of Apoptosis: Elevated temperatures can trigger apoptotic signaling pathways in cancer cells, sometimes in conjunction with other therapies. High Hyperthermia / Thermal Ablation (Approximately 43°C to 50°C and above) Pathways and Effects: -Direct Cytotoxicity: High temperatures can lead to protein denaturation, membrane disruption, and direct cell death. -Coagulative Necrosis: Sustained high temperatures cause irreversible cell injury leading to necrosis of tumor tissues. -Vascular Damage: Hyperthermia in this range can damage tumor vasculature, reducing blood supply and indirectly causing tumor cell death. -Enhanced Immune Response: Although high temperatures can cause immediate cell death, the release of tumor antigens and damage-associated molecular patterns (DAMPs) can stimulate an anti-tumor immune response
Time-Scale Flag (TSF): P / R / G
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| In all eukaryotic cells, intracellular Ca2+ levels are maintained at low resting concentrations (approximately 100 nM) by the activity of the major Ca2+ extrusion system, the plasma membrane Ca2+-ATPase (PMCA), which exchanges extracellular protons (H+) for cytosolic Ca2+. Indeed, sustained elevation of [Ca2+]C in the form of overload, saturating all Ca2+-dependent effectors, prolonged decrease in [Ca2+]ER, causing ER stress response, and high [Ca2+]M, inducing mitochondrial permeability transition (MPT), are considered to be pro-death factors. In cancer the Ca2+-handling toolkit undergoes profound remodelling (figure 1) to favour activation of Ca2+-dependent transcription factors, such as the nuclear factor of activated T cells (NFAT), c-Myc, c-Jun, c-Fos that promote hypertrophic growth via induction of the expression of the G1 and G1/S phase transition cyclins (D and E) and associated cyclin-dependent kinases (CDK4 and CDK2). Thus, cancer cells may evade apoptosis through decreasing calcium influx into the cytoplasm. This can be achieved by either downregulation of the expression of plasma membrane Ca2+-permeable ion channels or by reducing the effectiveness of the signalling pathways that activate these channels. Such protective measures would largely diminish the possibility of Ca2+ overload in response to pro-apoptotic stimuli, thereby impairing the effectiveness of mitochondrial and cytoplasmic apoptotic pathways. Voltage-Gated Calcium Channels (VGCCs): Overexpression of VGCCs has been associated with increased tumor growth and metastasis in various cancers, including breast and prostate cancer. Store-Operated Calcium Entry (SOCE): SOCE mechanisms, such as STIM1 and ORAI1, are often upregulated in cancer cells, contributing to enhanced cell survival and proliferation. High intracellular calcium levels are associated with increased cell proliferation and migration, leading to a poorer prognosis. Calcium signaling can also influence hormone receptor status, affecting treatment responses. Increased Ca²⁺ signaling is associated with advanced disease and metastasis. Patients with higher CaSR expression may have a worse prognosis due to enhanced tumor growth and resistance to apoptosis. -Ca2+ is an important regulator of the electric charge distribution of bio-membranes. |
| 5052- | HPT, | Hyperthermia Induces Apoptosis through Endoplasmic Reticulum and Reactive Oxygen Species in Human Osteosarcoma Cells |
| - | in-vitro, | OS, | U2OS |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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