CELL-POPULATION KINETICS OF THE RHABDOMYOSARCOMA R1H OF THE RAT AFTER SINGLE DOSES OF X-RAYS
CELL-POPULATION KINETICS OF THE RHABDOMYOSARCOMA R1H OF THE RAT AFTER SINGLE DOSES OF X-RAYS
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DOI：
10.1080/09553009014552701
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发表时间：
1990-03-01
影响因子：
2.6
通讯作者：
BECKBORNHOLDT, HP
中科院分区：
文献类型：
--
作者：
JUNG, H;KRUGER, HJ;BECKBORNHOLDT, HP
研究了在用单次亚治愈X射线剂量7戈伊、15 Gy和30 Gy局部照射后，大鼠的实体可移植横纹肌肉瘤R1 H的去增殖和再增殖的动力学。在照射后4周的时间间隔内连续测量几个参数：通过流式细胞术测定肿瘤与宿主细胞的数量比，以及肿瘤和宿主细胞的细胞DNA含量;通过生物化学测定每克肿瘤组织的DNA量;从体外集落测定获得肿瘤细胞的克隆形成分数;并通过原位卡尺测量评估肿瘤体积。由每克的DNA量和每个细胞的平均DNA含量，获得每克肿瘤组织的细胞总数。从这个和其他测量的参数，克隆性肿瘤细胞，非克隆性肿瘤细胞和有核宿主细胞的数量，每个肿瘤，以及它们随时间和剂量的变化，可以得出。结果表明，在种群减少之前有一个滞后期，其数量为3 ± 8。1.4，1.cntdot.4.+-. 0.8或0 ±。分别以7戈伊、15或30 Gy照射0.7天。非克隆原性肿瘤细胞的减少率随剂量增加而增加;非克隆原性肿瘤细胞的减半时间为4 ± 7。1.cntdot.8，2.cntdot.6.+-. 0.cnt.7或2.cnt.1.+-。对于所施用的三个剂量为0 ± 4天。没有迹象表明，注定细胞的增殖有助于显着照射后肿瘤的生长。在与去种群之前的时间长度相似的滞后期之后，观察到宿主细胞的大量迁移。在某些条件下，经辐照的肿瘤中97%以上的细胞被发现来自宿主。在克隆源性肿瘤细胞的再增殖开始之前有一个滞后期，其长度从2 ± 7增加。0.cnt.7至5.cnt.0.+-。0.8或6.cntdot.3.+-。分别为7.5、15或30 Gy，持续1天。再增殖的初始速率随辐射剂量而增加;在滞后期结束后，克隆源性肿瘤细胞的倍增时间（在对照组中为3 ± 7。0·2天）为3·1·±。0.cntdot.1，2.cntdot.1.+-. 0.cntdot.1和1.cntdot.1.+-。对于所施用的三个剂量为0 ≤ 1天。然而，所有的再增殖曲线都可以用一个特定的Gompertz函数来描述（其参数也很好地拟合了未受干扰的肿瘤的体积生长），这表明再增殖的速率对应于未处理的肿瘤的生长速率，所述未处理的肿瘤含有与辐照肿瘤中留下的相当数量的克隆原。
The kinetics of depopulation and repopulation of the solid transplantable rhabdomyosarcoma R1H of the rat following local irradiation with single subcurative X-ray doses of 7.cntdot.5, 15 and 30 Gy was studied. Several parameters were sequentially measured over a time interval of 4 weeks after irradiation: the ratio of the number of tumour to host cells, and the cellular DNA content of tumour and host cells, were determined by flow cytometry; the amount of DNA per gram of tumour tissue was determined biochemically; the clonogenic fraction of tumour cells was obtained from in vitro colony assay; and the tumour volume was assessed by in situ caliper measurements. From the amount of DNA per gram and the average DNA content per cell, the total number of cells per gram of tumour tissue was obtained. From this and the other parameters measured, the number of clonogenic tumour cells, non-clonogenic tumour cells and nucleated host cells per tumour, as well as their variation with time and dose, could be derived. The results showed that there was a lag period prior to depopulation amounting to 3.cntdot.8 .+-. 1.4, 1.cntdot.4 .+-. 0.cntdot.8 or 0 .+-. 0.cntdot.7 days for 7.cntdot.5, 15 or 30 Gy, respectively. The rate of depopulation of non-clonogenic tumour cells increased with dose; the halving times of non-clonogens were 4.cntdot.7 .+-. 1.cntdot.8, 2.cntdot.6 .+-. 0.cntdot.7 or 2.cntdot.1 .+-. 0.cntdot.4 days for the three doses applied. There were no indications that proliferation of doomed cells contributed significantly to tumour growth after irradiation. After lag periods that were similar in length to those prior to depopulation, a massive immigration of host cells was observed. Under certain conditions more than 97 per cent of the cells present in irradiated tumours were found to be of host origin. There was a lag period before the onset of repopulation by clonogenic tumour cells, the length of which increased from 2.cntdot.7 .+-. 0.cntdot.7 to 5.cntdot.0 .+-. 0.8 or 6.cntdot.3 .+-. 1.cntdot.0 days for 7.5, 15 or 30 Gy, respectively. The initial rate of repopulation increased with radiation dose; after the end of the lag period the doubling time of clonogenic tumour cells (in controls amounting to 3.cntdot.7 .+-. 0.cntdot.2 days) was 3.cntdot.1 .+-. 0.cntdot.1, 2.cntdot.1 .+-. 0.cntdot.1 and 1.cntdot.1 .+-. 0.cntdot.1 days for the three doses applied. Nevertheless, all repopulation curves could be described by one particular Gompertz function (whose parameters also give a good fit to the volume growth of the undisturbed tumour), indicating that the rate of repopulation corresponds to the growth rate of untreated tumours that contain a comparable number of clonogens as are left in the irradiated tumours.