疾病动物模型,基因修饰黑素瘤模型 z-bio 2021-03-15 288

　　[Modeling mechanism] The mechanism of melanoma transgenic animal models is similar to that of other transgenic animal models.

　　[Model Features] Ultraviolet-responsive mouse melanoma model. It expresses the anterior region of SV40 under the control of the melanocyte-specific tyrosinase enhancer. There are hyposensitivity mice that can be induced. Skin melanoma develops and newborn mice are irradiated. Using ultraviolet light (UVB), about 20% of them will develop into melanoma. Even after exposure to UVB radiation in in vitro experiments, melanocytes in transgenic mice have malignant characteristics. MT/ret skin melanosis in transgenic mice, benign melanoma lesions and melanoma occur sequentially. This change is very similar to the evolution of human congenital melanocytic nevus to melanoma, and this disease continues. The activities of protein kinases and matrix metalloproteinases activated by Mightgen gradually increase. HGF/SFt transgenic mouse melanocytes exist at the junction of epidermis, dermis and epidermis, and their performance is similar to that of human skin. Exposing newborn HGF/SF transgenic mice to a single dose of moderate-intensity UVB radiation for less than 3 hours can induce melanoma. Similar to human melanoma, the pathological changes of HGF/SF transgenic mice include various degrees of progression, from abnormal growth of precancerous nevus cells to radioactive vertical growth, and finally to a metastatic phenotype. Other transgenic animal models include ras transgenic mice, Tyr-SV40E transgenic mice and TG-3 transgenic mice.

　　[Model evaluation and application] Transgenic animal models help researchers understand the origin and development of skin malignant melanoma, including the environment (such as ultraviolet radiation) and genetic factors and common causes of melanoma, and lay the foundation for exploring reasonable treatment methods Revealed specific genes.