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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.
Alpha radiation is a nuclear phenomenon in which a heavy radionuclide emits an energetic alpha particle (consisting of two protons and two neutrons) and transmutes to a different radionuclide. The emitted alpha particle has a range in tissue of only 40-90 microns, which minimizes collateral damage when used for treatment purposes.
A 2024 systematic review of the literature found that chemoradiation with 5-FU and mitomycin C, as used in the Nigro Protocol, improves outcomes like colostomy-free survival in anal cancer patients compared to alternatives like cisplatin. However, it can lead to more severe side effects, especially blood-related toxicity. [7]
A chemotherapy regimen is a regimen for chemotherapy, defining the drugs to be used, their dosage, the frequency and duration of treatments, and other considerations.In modern oncology, many regimens combine several chemotherapy drugs in combination chemotherapy.
Acute promyelocytic leukemia is characterized by a chromosomal translocation involving the retinoic acid receptor alpha (RARA) gene on chromosome 17. [3] In 95% of cases of APL, the RARA gene on chromosome 17 is involved in a reciprocal translocation with the promyelocytic leukemia gene (PML) on chromosome 15, a translocation denoted as t(15;17)(q22;q21). [3]
An important problem is the occurrence of missing data for participants in a clinical trial. This can happen when patients are lost to follow-up (for instance, by withdrawal due to adverse effects of the intervention) and no response is obtainable for these patients. However, full application of ITT analysis can only be performed where there is ...
Multimodal Therapy for Young Patients Young T-ALL patients have shown significant improvement through multimodal therapy . This involves initial induction therapy, including a glucocorticoid , vincristine , L-asparaginase , and an anthracycline for 4 to 6 weeks, followed by intensive combination therapy for 6–8 months, and finally 18–30 ...
Vinblastine is a vinca alkaloid [9] [2] [10] and a chemical analogue of vincristine. [11] [12] It binds tubulin, thereby inhibiting the assembly of microtubules. [13]Vinblastine treatment causes M phase specific cell cycle arrest by disrupting microtubule assembly and proper formation of the mitotic spindle and the kinetochore, each of which are necessary for the separation of chromosomes ...