Yue Q, Yulong G, Liting Q, Shuai Y, Delong L, Yubao L, Lili J, Sidang L, Xiaomei W
Division of Avian infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, Heilongjiang, P.R. China College of Animal Husbandry and Veterinary, Liao Ning Medical University, P.R. China College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Taian, P.R. China Liaocheng Vocational and Technical College, Liaocheng, P.R. China.
Division of Avian infectious Diseases, State Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Harbin, Heilongjiang, P.R. China.
Vet Pathol. 2015 Nov;52(6):1052-6. doi: 10.1177/0300985814560232. Epub 2014 Dec 1.
To investigate the molecular mechanisms of the oncogenic effects of avian leukosis virus subgroup J (ALV-J), we examined mutations in and the expression of p53 in the myelocytomas distributed in the liver, spleen, trachea, and bone marrow, as well as in fibrosarcomas in the abdominal cavity and hemangiomas in skin from chickens that were naturally or experimentally infected with ALV-J. Two types of mutations in the p53 gene were detected in myelocytomas of both the experimentally infected and the naturally infected chickens and included point mutations and deletions. Two of the point mutations have not been reported previously. Partial complementary DNA clones with a 122-bp deletion in the p53 gene ORF and a 15-bp deletion in the C-terminus were identified in the myelocytomas. In addition, moderate expression of the mutant p53 protein was detected in the myelocytomas that were distributed in the liver, trachea, spleen, and bone marrow. Mutant p53 protein was not detected in the subcutaneous hemangiomas or in the abdominal fibrosarcomas associated with natural and experimental ALV-J infection, respectively. These results identify mutations associated with abnormal expression of p53 in ALV-J-associated myelocytomas, suggesting a role in tumorigenesis.
为了研究禽白血病病毒J亚群(ALV-J)致癌作用的分子机制,我们检测了自然或实验感染ALV-J的鸡的肝脏、脾脏、气管和骨髓中的髓细胞瘤,以及腹腔纤维肉瘤和皮肤血管瘤中p53的突变情况和表达水平。在实验感染和自然感染鸡的髓细胞瘤中均检测到p53基因的两种突变类型,包括点突变和缺失。其中两个点突变此前未见报道。在髓细胞瘤中鉴定出p53基因开放阅读框有122 bp缺失、C末端有15 bp缺失的部分互补DNA克隆。此外,在分布于肝脏、气管、脾脏和骨髓的髓细胞瘤中检测到突变型p53蛋白的适度表达。在分别与自然和实验性ALV-J感染相关的皮下血管瘤或腹腔纤维肉瘤中未检测到突变型p53蛋白。这些结果确定了与ALV-J相关髓细胞瘤中p53异常表达相关的突变,提示其在肿瘤发生中起作用。