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| Extracorporeal Shock Wave Therapy - Underwater / Focused Shock Wave Treatment Recommended Abbreviation: ESWT Alternative Names: Extracorporeal shock waves, ESW, shock wave therapy, underwater shock waves, focused shock wave therapy Type: Physical therapy / acoustic-mechanical intervention / experimental anticancer treatment Function: Extracorporeal shock waves are high-pressure acoustic pulses transmitted through a material medium into biological tissue. Shock waves produce rapid mechanical stress, pressure gradients, cavitation-related effects, and transient increases in cell-membrane permeability. Depending on energy and treatment parameters, these effects can alter cellular signaling, drug uptake, vascular responses, apoptosis, and tissue remodeling. Cancer: Preclinical studies demonstrate direct cytotoxic and pro-apoptotic effects in multiple cancer models and increased tumor-cell permeability to anticancer drugs and other therapeutic molecules. Shock waves can enhance the cytotoxic activity of agents including cisplatin, doxorubicin, bleomycin, and paclitaxel and have been investigated for drug delivery and sonodynamic approaches. Direct shock-wave treatment of malignant tumors remains experimental and is not an established standard cancer therapy. Clinical Status: Established extracorporeal shock wave therapy is primarily used for musculoskeletal and rehabilitation indications. Active malignant tissue within the treatment field is generally considered a contraindication for routine clinical ESWT, despite experimental research investigating direct antitumor applications. |
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| Peroxisome proliferator-activated receptor gamma (PPAR-γ) is a type of nuclear receptor that plays a crucial role in regulating various biological processes, including glucose metabolism, lipid metabolism, and inflammation. It is primarily expressed in adipose tissue, but it is also found in other tissues, including the colon, breast, and prostate. PPAR-γ has been shown to have both tumor-suppressive and tumor-promoting effects, depending on the type of cancer and the context. In some cancers, activation of PPAR-γ can inhibit cell proliferation and induce apoptosis, while in others, it may promote tumor growth. PPARγ – Plays a central role in adipogenesis, lipid storage, and insulin sensitivity. – Widely expressed in adipose tissue, but also present in colon, breast, and immune cells. – In addition to metabolic functions, PPARγ regulates cell differentiation, apoptosis, and has anti-inflammatory effects. – Ligand binding (such as endogenous fatty acids or synthetic agonists like thiazolidinediones) alters transcriptional programs impacting cell cycle and survival. – In many cases, PPARγ is expressed in tumor cells, and its activation has been linked to induction of differentiation and growth arrest. – However, expression levels can differ based on tumor subtype, with some studies reporting elevated levels while others note reductions in aggressive tumors. – Crosstalk with other signaling pathways (e.g., Wnt/β-catenin, MAPK) can alter PPARγ's net effect in cancer cells. |
| 7687- | iod, | ESWT, | Shock Wave Application Increases the Antineoplastic Effect of Molecular Iodine Supplement in Breast Cancer Xenografts |
| - | in-vivo, | BC, | MDA-MB-231 |
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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