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Targeted alpha-particle therapy (or TAT) is an in-development method of targeted radionuclide therapy of various cancers. It employs radioactive substances which undergo alpha decay to treat diseased tissue at close proximity. [1] It has the potential to provide highly targeted treatment, especially to microscopic tumour cells.
The research combined diverse techniques ranging from genomics, computational biology, tumour imaging, in vitro and in vivo functional models to study biological and clinical phenotypes. The proteins produced by these genes may serve as targets for novel chemotherapy drugs and other cancer treatments, or imaging scans.
An alpha privative or, rarely, [1] privative a (from Latin alpha prīvātīvum, from Ancient Greek α στερητικόν) is the prefix a-or an-(before vowels) that is used in Indo-European languages such as Sanskrit and Greek and in words borrowed therefrom to express negation or absence, for example the English words of Greek origin atypical, anesthetic, and analgesic.
Laboratory research suggests AHCC may have immunostimulatory effects. AHCC has been proposed as a treatment for cancer, but research into its effectiveness has produced only uncertain and inconclusive evidence. [1] Detailed research is needed into the pharmacology of AHCC before any recommendation of its use as an adjuvant therapy can be made.
Another form of targeted therapy involves the use of nanoengineered enzymes to bind to a tumor cell such that the body's natural cell degradation process can digest the cell, effectively eliminating it from the body. Targeted cancer therapies are expected to be more effective than older forms of treatments and less harmful to normal cells.
A main target of PEA is proposed to be the peroxisome proliferator-activated receptor alpha (PPAR-α). [3] [4] PEA also has affinity to cannabinoid-like G-coupled receptors GPR55 and GPR119. [5] PEA cannot strictly be considered a classic endocannabinoid because it lacks affinity for the cannabinoid receptors CB1 and CB2. [6]
The resulting decay reaction yields high-energy alpha particles that kill the cancer cells that have taken up enough 10 B. All clinical experience with NCT to date is with boron-10; hence this method is known as boron neutron capture therapy ( BNCT ). [ 1 ]
The phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha (the HUGO-approved official symbol = PIK3CA; HGNC ID, HGNC:8975), also called p110α protein, is a class I PI 3-kinase catalytic subunit. The human p110α protein is encoded by the PIK3CA gene. [5] Its role was uncovered by molecular pathological epidemiology (MPE). [6]