Nevertheless, no TP53-based therapy has been successfully translated into clinical cancers treatment due to the complexity of TP53 signaling. POLR2A encodes an enzyme that’s inhibited by alpha-amanatin. We found that suppression of POLR2A with low-dosage alpha-amanatin stopped tumor cell growth and decreased toxicity. We anticipate that inhibiting POLR2A is a novel therapeutic approach for human cancers harboring such common genomic alterations, stated Lu.. ADCs predicated on alpha-amanatin can help treat colorectal cancer For some right time, cancer scientists have considered the toxin, alpha-amanatin produced from death cap mushrooms, as a possible cancer treatment. However, because of its penchant for leading to liver toxicity, its potential as an effective therapy has been limited.Because of this prognostic association, a decrease in the BCR-ABL transcript level by 3 log10 products or more was described as a major molecular response.9 To improve on outcomes obtained with imatinib at a dose of 400 mg daily, various groupings have explored the use of higher doses of imatinib and combinations of imatinib with pegylated interferon alfa or cytarabine.10,11 Each of these studies offers used a cytogenetic response because the major end point. Owing to the extremely high rate of cytogenetic response with 400 mg of imatinib, it has been difficult showing compelling improvement with any of these therapies. Peginterferon alfa was the first biologic agent to cause a marked decrease in Philadelphia chromosome positivity in individuals with CML.