Research ; Disrupt Protein Interactions to Minimize Spread of Cancer
In addition to inhibiting the spread of cancer cells , it opens a new way to develop drugs against cancer .
If the cancer cells do not metastasize , or spread to other parts in the body , many tumors that would not result in death . As stated by Professor Zhi - Ren Liu biology from Georgia State University in Atlanta .
" Usually in most cases , the tumor does not interfere with normal body functions . , But if the cancer cells metastasize , cancer that disrupt the function of various organs and that is what kills the patient , " said Professor Liu as reported Voa ( 6/1 ) .
Liu and co-researchers Jenny Yang , a biochemist at the University of Georgia , have found that they can stop the spread of cancer by interfering with the interaction of two types of proteins in cells .
The protein acts like a switch , to activate or stop the activities of the cell , including the displacement in the whole body . It is necessary for healing and activate the immune system, but when cancer cells migrate , or metastasize , the disease can be fatal .
The researchers found that two proteins , in particular - and calcium - calmodulin P68 - apparently led to the displacement of cells when they interact . With engineered peptides that make them separate , Yang and Liu discovered that proteins can significantly reduce or prevent the spread of cancer cells .
Using mice in the study of human colon cancer and breast cancer are severe , Liu said they reduced the metastasis of tumors by 90 percent beginning .
"The size of the tumor is much , much smaller ... and in some ways , we do not see at all metastases in this way , " said Liu .
Georgia 's second university researchers plan to develop drugs that block unification P68 and calmodulin , and they hope to eventually be doing human clinical trials with cancer patients . The discovery Zhi - Ren Liu and Jenny Yang on the role of two proteins in cancer metastasis is contained in an article published Nature Communications Magazine .
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