The tumor cell specific therapy
The cancer often begins with mutations in tumor suppressor pathways. The tumor suppressor genes - such as p53 - cell growth arrest and apoptosis (programmed cell death) in response to cellular stress, such as chromosomal damage. cells with p53 mutations can escape these constraints, leading to uncontrolled growth characteristic of cancer cells immortal. Almost all types of tumors have mutations in the p53 pathway, many of them in the p53 gene itself treatments to restore the function of p53 - the selective loss of cancer cells - must be more effective than standard therapies, which indiscriminately target all dividing cells.In order to develop specific therapeutic strategies, Steven Dowdy and colleagues show that restoring p53 function eliminates in mouse models of cancer
tumors and dramatically increases the survival of the animals. Although the recent successes of the tumor suppressor function in cancer cells have focused on gene therapy, Dowdy and colleagues introduced the changes in the p53 peptides (pieces of proteins) in tumor cells. p53 acts as a transcriptional activator that binds to specific gene sequences and triggers apoptosis in response to DNA damage.A region of the p53 protein, which facilitates C-terminal domain, DNA binding. In cancer cells, synthesized peptides (called p53C) comes from this region can induce apoptosis of restoring the function of p53 proteins with mutations in the DNA-binding. For p53C peptides in tumor cells, the researchers used a technique pioneered by Dowdy offer proteins in a position within the cell.
Since the cell membrane usually limited (larger molecules generally enter through surface receptors) the passage of small molecules, this is no small matter.Testing the efficacy of peptide therapy in strains of mice, human-metastatic disease model, researchers found that mice treated with peptide p53C a significant reduction in tumor mass was found and lived six times longer than mice with a peptide or control
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