Researchers performed experiments on mice to confirm whether they could feasibly create a therapeutic drug as well as whether or not the cancer was stopped. They found that they were able to stop the growth of the tumors in mice who were deficient in two chemicals Pten and p19Arf these chemicals usually suppress cancer growth but are deficient in most kinds of human cancer.By deactivating the Skp2 they were able to stop cancer in mice with both deficiencies even though it was previously thought to only be able to stop cancer in p19Arf-deficeint models. Further testing on mice showed that not only can the Skp2 halt tumors taking advantage of faulty tumor suppressor chemicals it also emits oncogenic activity all by itself so its permanent removal reduces likelihood of cancer in the future.
Although the deactivation of the Skp2 gene will be revolutionary break through the application and usage still is flawed. In most forms of senescence the DNA is destroyed thus halting growth. But with Skp2 when the cells stop dividing they release proteins which protect their DNA. These proteins however cause inflammation and damage to their surrounding tissue. This damage has been proven to accelerated aging as well as lead to age related diseases including cancer (irony).
Hui-Khan-Lin lead researcher, said that the researchers would try to find out if the Skp2 or other genes can cause senescence in HER2-decient model to determine whether the Skp2 "is globally required for an oncogenic event."
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