...
首页> 外文期刊>癌と化学療法 >Acquired tumor 'robustness' in the case of prostate cancer
【24h】

Acquired tumor 'robustness' in the case of prostate cancer

机译:在前列腺癌的情况下获得性肿瘤的“坚固性”

获取原文
获取原文并翻译 | 示例

摘要

Tumors are highly robust and maintain their proliferative potential against both a wide range of host-defense mechanisms and anticancer therapies. In this study, we investigated the levels of human leukocyte antigen (HLA) class I, multi-drug resistance 1 (MDR1), and androgen receptor (AR) expressions in untreated prostate cancers harvested by radical prostectomy. The mean percentages of cancer cells expressing HLA class I, MDR1, and AR among the 10 cancer samples were 41, 35, and 74%, respectively. In addition, double-staining of HLA class I and MDR1 revealed the four definite populations (HLA class I(+)/MDR(+), HLA class I(+)/MDR(-), HLA class I (-)/MDR(+), and HLA class I(-)/MDR(-)) in cancer tissues from the majority of cancer patients tested, and the mean percentages of cells expressing these combinations were 13, 29, 22, and 38%, respectively. Similar results were obtained by double staining of HLA class I and AR, except for 2 cases in which HLA class I(-)/AR (+) cancer cells predominated. These results indicated that untreated prostate cancer cells acquired a wide range of genomic mutation, which may have been caused by internal host pressure to eliminate malignant cells, and would provide evidence of the robustness of untreated prostate cancer.
机译:肿瘤具有很强的鲁棒性,并且在广泛的宿主防御机制和抗癌疗法中均保持其增殖潜力。在这项研究中,我们调查了未经根治性前列腺切除术治疗的未治疗前列腺癌中人类白细胞抗原(HLA)I类,多药耐药性1(MDR1)和雄激素受体(AR)的表达水平。在10个癌症样本中,表达I类HLA,MDR1和AR的癌细胞的平均百分比分别为41%,35%和74%。此外,对HLA I类和MDR1进行双重染色显示了四个确定的种群(HLA I类(+)/ MDR(+),HLA I类(+)/ MDR(-),HLA I类(-)/ MDR (+)和HLA I类(-)/ MDR(-)在大多数测试过的癌症患者的癌组织中,表达这些组合的细胞的平均百分比分别为13%,29%,22%和38%。通过对HLA I类和AR双重染色获得了相似的结果,除了2例HLA I类(-)/ AR(+)癌细胞为主。这些结果表明未治疗的前列腺癌细胞获得了广泛的基因组突变,这可能是由于内部宿主消除恶性细胞的压力所致,并且将提供未经治疗的前列腺癌的鲁棒性证据。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号