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p53, tumor suppression and aging
January 03, 2006In the January 1 issue of Genes & Development, Dr. Mary Ellen Perry and colleagues validate the p53 inhibitor, Mdm2, as a promising target for cancer therapies.
The p53 tumor suppressor plays a critical role in cancer formation, and many anticancer strategies aim to activate p53 in order to curb tumor formation. Mdm2 is a key inhibitor of p53 and therefore an attractive target to modulate p53 activity in cells. However, conflicting evidence exists regarding whether or not p53-mediated tumor suppression comes at the cost of accelerated aging.
To analyze the effects of reduced Mdm2 levels on tumorigenesis - as well as the potential for unwanted side effects - Dr. Perry's team used mdm2-hypomorphic mice (that express less Mdm2 protein than normal mice) which have elevated levels of wild-type p53 activity. The researchers found that even a modest decrease (about 20%) in Mdm2 effectively prevents tumor formation and does not lead to premature aging.
Dr. Perry emphasizes that "many people develop cancer at a young age due to increased expression of Mdm2. The possibility that inhibitors of Mdm2 could delay cancer in such people without causing detrimental side effects is bolstered by our demonstration that mice expressing 30-80% the normal level of Mdm2 develop fewer tumors than wild type mice, yet age normally."
Cold Spring Harbor Laboratory
Dr. Perry emphasizes that "many people develop cancer at a young age due to increased expression of Mdm2. The possibility that inhibitors of Mdm2 could delay cancer in such people without causing detrimental side effects is bolstered by our demonstration that mice expressing 30-80% the normal level of Mdm2 develop fewer tumors than wild type mice, yet age normally."
Cold Spring Harbor Laboratory
P53 Current Events and P53 News RSSCornell researchers identify a weak link in cancer cell armor
The seeming invincibility of cancerous tumors may be crumbling, thanks to a promising new gene therapy that eliminates the ability of certain cells to repair themselves.
CSHL study shows that some malignant tumors can be shut down after all
Oncologists have had their hands tied because more than half of all human cancers have mutations that disable a protein called p53.
October 15, 2009 Loss of Tumor-Suppressor and DNA-Maintenance Proteins Causes Tissue Demise, Penn Study Finds
A study published in the October issue of Nature Genetics demonstrates that loss of the tumor-suppressor protein p53, coupled with elimination of the DNA-maintenance protein ATR, severely disrupts tissue maintenance in mice. As a result, tissues deteriorate rapidly, which is generally fatal in these animals. In addition, the study provides supportive evidence for the use of inhibitors of ATR in cancer therapy.
Roles of S100A2 and p63 in the carcinogenesis of esophageal squamous cell carcinoma
As a member of the S100 family, S100A2 is considered a candidate tumor-suppressor gene. Recently, p63 gene, a new member of the p53 gene family, has been studied in the fields of tumorigenesis, cell apoptosis and tissue growth.
Lung cancer suppresses miR-200 to invade and spread
Primary lung cancer shifts to metastatic disease by suppressing a family of small molecules that normally locks the tumor in a noninvasive state, researchers at The University of Texas M. D. Anderson Cancer Center report in the Sept. 15 edition of Genes and Development.
Tumor suppressor pulls double shift as reprogramming watchdog
A collaborative study by researchers at the Salk Institute for Biological Studies uncovered that the tumor suppressor p53, which made its name as "guardian of the genome", not only stops cells that could become cancerous in their tracks but also controls somatic cell reprogramming.
Tumor mutations can predict chemo success
New work by MIT cancer biologists shows that the interplay between two key genes that are often defective in tumors determines how cancer cells respond to chemotherapy.
Scientists track impact of DNA damage in the developing brain
Switching off a key DNA repair system in the developing nervous system is linked to smaller brain size as well as problems in brain structures vital to movement, memory and emotion.
Estrogen can reduce stroke damage by inactivating protein
Estrogen can halt stroke damage by inactivating a tumor-suppressing protein known to prevent many cancers, Medical College of Georgia researchers say.
Protein can help cells or cause cancer, Purdue researcher finds
A Purdue University scientist has discovered a key process in cell growth that can lead to the formation of tumors.
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