Kristjansen P E, Spang-Thomsen M, Quistorff B
Department of Oncology, Finsen Institute-Rigshospitalet, Copenhagen, Denmark.
Cancer Res. 1991 Oct 1;51(19):5160-4.
Two human small cell lung cancer tumor lines, maintained as solid tumor xenografts on nude mice and as in vitro cell cultures, were studied by in vivo 31P magnetic resonance spectroscopy and by biochemical analysis of extracts of solid tumors and cell cultures. The tumor lines CPH SCCL 54A and CPH SCCL 54B are subpopulations from the same tumor. In solid tumors (n = 125), the ATP/Pi ratio was greater in 54A than in 54B. This was due to a higher ATP level in 54A, whereas there was no difference in Pi, ADP, and AMP. A decrease in ATP/Pi during growth was caused by a decline in ATP, whereas Pi remained unchanged. Small amounts of phosphocreatine were found in the xenografts and in tumor extracts, but not in the cell extracts; correspondingly, there was a low creatine kinase activity in solid tumors and no activity in the cell cultures. Thus, the phosphocreatine content of the solid tumors originated from the stroma. A difference in ATP content between 54A and 54B was also found in cell cultures; hence, the metabolic difference is an intrinsic quality of the malignant cells and is not caused by the host system.
通过体内31P磁共振波谱以及实体瘤和细胞培养提取物的生化分析，对两个人类小细胞肺癌肿瘤系进行了研究。这两个肿瘤系以实体瘤异种移植的形式在裸鼠身上维持，并作为体外细胞培养物。肿瘤系CPH SCCL 54A和CPH SCCL 54B是来自同一肿瘤的亚群。在实体瘤（n = 125）中，54A的ATP/Pi比值高于54B。这是由于54A中的ATP水平较高，而Pi、ADP和AMP没有差异。生长过程中ATP/Pi的降低是由ATP的下降引起的，而Pi保持不变。在异种移植瘤和肿瘤提取物中发现了少量磷酸肌酸，但在细胞提取物中未发现；相应地，实体瘤中的肌酸激酶活性较低，而细胞培养物中没有活性。因此，实体瘤的磷酸肌酸含量源自基质。在细胞培养物中也发现了54A和54B之间ATP含量的差异；因此，代谢差异是恶性细胞的内在特性，并非由宿主系统引起。
