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Even though PUMA function is compromised in most cancer cells, it does not appear that genetic inactivation of PUMA is a direct target of cancer. [ 36 ] [ 37 ] [ 38 ] Many cancers do exhibit p53 gene mutations, making gene therapies that target this gene [ clarification needed ] impossible, but an alternate pathway may be to focus on ...
p53, also known as Tumor protein P53, cellular tumor antigen p53 (UniProt name), or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. The p53 proteins (originally thought to be, and often spoken of as, a single protein) are crucial in vertebrates , where they prevent cancer formation. [ 5 ]
For instance, the most researched immunotoxin for cancer therapy is the diphtheria toxin as it inhibits protein synthesis by inactivating elongation factor 2 (EF-2) which in turn inhibits protein translation, [6] [9] Moreover, p53 is identified to be frequently abnormal in human tumors and studies show that restoring function of p53 can cause ...
Efforts to induce this phenomenon have used cancer vaccines (derived from cancer cells or selected cancer antigens), or direct treatment with immune-stimulating factors on skin cancers. [53] Some oncolytic viruses are very immunogenic and may by infection of the tumour, elicit an anti-tumor immune response, especially viruses delivering ...
Deficient expression of DNA repair proteins due to an inherited mutation can cause increased risk of cancer. Individuals with an inherited impairment in any of 34 DNA repair genes (see article DNA repair-deficiency disorder) have an increased risk of cancer, with some defects causing up to a 100% lifetime chance of cancer (e.g. p53 mutations ...
The p53 (a tumor suppressor gene in the normal population) genome on 17p in neurofibrosarcoma patients is mutated, increasing the probability of cancer. The normal p53 gene will regulate cell growth and inhibit any uncontrollable cell growth in the healthy population; since p53 is inactivated in neurofibrosarcoma patients, they are much more ...
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