This writer obviously hasn't heard about Kevetrin.
Eight big questions in cancer research
6. Will p53 ever realize its promise?
The gene that encodes for the p53 protein is among the most frequently mutated genes in cancer. The normal activity of p53 prevents cancer, and there are several different types of p53 mutations that cause tumor growth and aggressiveness. This has tantalized researchers because p53 represented a possible therapeutic target that could have a wide impact across many cancers. Unfortunately, the protein complexity proved to be more challenging than researchers anticipated.
"Ten years ago the function of p53 seemed clear, in that it activated cell cycle arrest and apoptosis in nascent tumor cells, thus preventing cancer development," says Karen Vousden, Director of the Cancer Research UK Beatson Institute. "However, over the past 10 years we have come to appreciate the many and diverse functions of p53—from roles in stem cell reprogramming to the control of the metabolism and the immune response."
These complexities give researchers many more options to harness its functions for therapy, she adds. Current drugs work to turn p53 back on in cancer cells. The drugs can work very well, but they are associated with toxic side effects and drug resistance. Future approaches could focus more on targeting vulnerabilities that lead to p53 loss of function in the first place.
Source: "Karen Vousden: Guardian of the Genome" http://www.cell.com/trends/cancer/abstract/S2...15)00018-7
http://medicalxpress.com/news/2015-09-big-cancer.html
Eight big questions in cancer research
6. Will p53 ever realize its promise?
The gene that encodes for the p53 protein is among the most frequently mutated genes in cancer. The normal activity of p53 prevents cancer, and there are several different types of p53 mutations that cause tumor growth and aggressiveness. This has tantalized researchers because p53 represented a possible therapeutic target that could have a wide impact across many cancers. Unfortunately, the protein complexity proved to be more challenging than researchers anticipated.
"Ten years ago the function of p53 seemed clear, in that it activated cell cycle arrest and apoptosis in nascent tumor cells, thus preventing cancer development," says Karen Vousden, Director of the Cancer Research UK Beatson Institute. "However, over the past 10 years we have come to appreciate the many and diverse functions of p53—from roles in stem cell reprogramming to the control of the metabolism and the immune response."
These complexities give researchers many more options to harness its functions for therapy, she adds. Current drugs work to turn p53 back on in cancer cells. The drugs can work very well, but they are associated with toxic side effects and drug resistance. Future approaches could focus more on targeting vulnerabilities that lead to p53 loss of function in the first place.
Source: "Karen Vousden: Guardian of the Genome" http://www.cell.com/trends/cancer/abstract/S2...15)00018-7
http://medicalxpress.com/news/2015-09-big-cancer.html
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