HETEROGENEITY IN THE DEVELOPMENT OF APOPTOSIS IN IRRADIATED MURINE TUMORS OF DIFFERENT HISTOLOGIES
HETEROGENEITY IN THE DEVELOPMENT OF APOPTOSIS IN IRRADIATED MURINE TUMORS OF DIFFERENT HISTOLOGIES
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DOI：
10.1080/09553009314551801
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发表时间：
1993-11-01
影响因子：
2.6
通讯作者：
PETERS, LJ
中科院分区：
文献类型：
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作者：
MEYN, RE;STEPHENS, LC;PETERS, LJ
15个不同的小鼠肿瘤进行了评估，在体内照射后的最初几个小时内，肿瘤组织中发生的细胞凋亡的发展程度。以0、2.5、10或25戈伊照射后3或6小时处死动物。通过显微镜检查肿瘤标本的组织切片，以异常细胞核的百分比对细胞凋亡进行评分。结果表明，三个四乳腺腺癌，卵巢腺癌，淋巴瘤显示至少10%的细胞凋亡后25戈伊，而五肉瘤，三个鳞状细胞癌，肝癌没有。在那些有反应的肿瘤中，时间过程和剂量反应是相似的。当使用常规测定法分析时，将这些数据与这些相同肿瘤的已知反应进行比较。通过显著凋亡反应的肿瘤具有较长的特定生长延迟和较低的TCD50（治愈50%动物的剂量）剂量，因此表明照射后的急性凋亡反应可能是某些对照射反应良好的肿瘤的特征。此外，该分析揭示了在单个肿瘤标本内和不同肿瘤类型之间的凋亡反应的异质性。肿瘤内和肿瘤间异质性的这些观察结果与肿瘤细胞凋亡倾向受遗传调控的观点一致。
Fifteen different murine tumours were evaluated with respect to the degree of apoptosis development that occurs in the tumour tissue in the first few hours following irradiation in vivo. Animals were killed at 3 or 6 h following irradiation with 0, 2.5, 10 or 25 Gy. Apoptosis was scored as percent aberrant nuclei by microscopic examination of histological sections made from the tumour specimens. Results showed that three of four mammary adenocarcinomas, one ovarian adenocarcinoma, and one lymphoma displayed at least 10% apoptotic cells after 25 Gy, whereas five sarcomas, three squamous cell carcinomas, and a hepatocarcinoma did not. The time courses and dose responses were similar in those tumours that responded. These data were compared with the known response of these same tumours when analysed using conventional assays. The tumours that did respond by significant apoptosis had longer specific growth delays and lower TCD50 (dose to cure 50% of animals) doses, thus suggesting that an acute apoptotic response following irradiation may be a feature of certain tumours that respond well to irradiation. Additionally, this analysis revealed heterogeneity in the apoptotic response both within an individual tumour specimen and among different tumour types. These observations of intra and intertumour heterogeneity are consistent with the idea that the propensity for apoptosis in tumours is genetically regulated.