Randhawa P S, Pietrzak B, Nalesnik M A, Demetris A J, Locker J
Department of Pathology, University of Pittsburgh Medical Center, PA 15213, USA.
Hematol Oncol. 1997 Feb;15(1):39-46. doi: 10.1002/(sici)1099-1069(199702)15:1<39::aid-hon596>3.0.co;2-#.
The tumorigenic potential of six post-transplant B-cell lymphoproliferative disease (PTLD) lesions was evaluated in SCID mice. Three animals developed local subcutaneous B cell tumours, two of which contained Epstein-Barr virus (EBV) DNA. Two animals developed CD3 positive thymic neoplasms, and one mouse developed an uncharacterized spontaneously regressing subcutaneous tumour. Immunoglobulin gene rearrangements studies with a JH probe, and EBV clonality studies with a Bam NJ fused terminal probe, showed only one mouse tumour to be genealogically related to the corresponding clinical lesion. It is concluded that lymphoid clones which constitute human PTLD are not autonomous, but sustained by host-derived growth stimuli distinct from those operating in the SCID mouse mileu.
在严重联合免疫缺陷(SCID)小鼠中评估了六种移植后B细胞淋巴组织增生性疾病(PTLD)病变的致瘤潜力。三只动物发生了局部皮下B细胞肿瘤,其中两只含有爱泼斯坦-巴尔病毒(EBV)DNA。两只动物发生了CD3阳性胸腺肿瘤,一只小鼠发生了一种未明确的自发消退的皮下肿瘤。用JH探针进行的免疫球蛋白基因重排研究以及用Bam NJ融合末端探针进行的EBV克隆性研究表明,只有一只小鼠肿瘤与相应的临床病变存在谱系关系。得出的结论是,构成人类PTLD的淋巴样克隆不是自主的,而是由宿主来源的生长刺激维持的,这些刺激不同于在SCID小鼠环境中起作用的刺激。