Researchers from Rhode Island Hospital in the United States have discovered that some special chondrocytes in mice lack the Shp-2 enzyme, which can lead to the formation of multiple benign cartilage tumors. This mouse model repeats a rare tumor syndrome in humans: mixed chondromatosis (metachondromatosis).
Shp2 enzyme can regulate the activity of other proteins and signaling pathways in cells. Mice lacking Shp2 will develop two types of tumors: endogenous chondroma (enchondromas) and osteochondroma (osteochondroma). In addition, mice also develop joint deformities.
The lead author of the paper, Dr. Wentian Yang, of the Department of Orthopedics, Rhode Island Hospital, said: "The mouse model of transgenic human disease provides us with a powerful tool for better understanding the disease process and testing new therapies. Some of these benign tumors will progress to malignant chondromas called chondrosarcomas (chondrosarcomas), because the latter can spread to spread the disease more seriously, and even fatal. "
Dr. Wentian Yang said: "Because each cell type has its own weaknesses, understanding the origin of tumor formation can help develop new treatments. Our research has found a new type of cartilage stem / progenitor cell population, which is in the bone The first type of cancer stem cells found in. We confirmed that these cells are the origin cells of the tumor in our model, thus identifying a potential treatment for this rare disease. In the future, our model can also be used for certain forms of Chondrosarcoma has developed new therapies. "
It has long been speculated that damage to the cartilage growth plate is the cause of osteochondroma. Osteochondroma looks like a cartilage growth plate that has grown out in the wrong direction. New research shows that one of the causes of osteochondroma is that the enzymes in a small group of cells near the growth plate have molecular abnormalities, leading to the growth of large tumors in the bones. These tumors are very common in children.
Yang Wentian said: "These findings allow us to further understand the formation mechanism of these tumors. Next, we intend to develop a method to prevent the growth of tumors in the early stages of the disease, so that they do not need to be surgically removed."
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