首页> 美国卫生研究院文献>Cancer Medicine >Killer immunoglobulin‐like receptor genotypes and chronic myeloid leukemia outcomes after imatinib cessation for treatment‐free remission
【2h】

Killer immunoglobulin‐like receptor genotypes and chronic myeloid leukemia outcomes after imatinib cessation for treatment‐free remission

机译:伊马替尼停药后无治疗缓解的杀伤性免疫球蛋白样受体基因型和慢性粒细胞白血病预后

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

>Background Natural Killer (NK) cells are innate lymphoid cells that can be cytotoxic toward a large panel of solid tumors and hematological malignancies including chronic myeloid leukemia (CML). Such a cytotoxicity depends on various receptors. Killer immunoglobulin‐like receptors (KIR) belong to these receptors and are involved in maturation process, then in the activation abilities of NK cells. Methods: We investigated the prognostic impact of the KIR2DL5B genotype in 240 CML patients included in two clinical trials investigating tyrosine kinase inhibitors (TKI) discontinuation: STIM and STIM2. Results: After adjustment for standard risk factors in CML, we found that the inhibitory receptor KIR2DL5B‐positive genotype was independently related to a delayed second deep molecular remission (HR 0.54, 95% CI [0.32‐0.91], P = 0.02) after TKI rechallenge but not to time to first deep molecular remission or treatment‐free remission rates. Conclusion: These results suggest that KIR2DL5B could carry a role in lymphocyte‐mediated control of leukemic residual disease control in patient with CML relapse.
机译:>背景天然杀伤(NK)细胞是先天性淋巴样细胞,对大量实体瘤和血液系统恶性肿瘤(包括慢性髓样白血病(CML))具有细胞毒性。这种细胞毒性取决于各种受体。杀伤性免疫球蛋白样受体(KIR)属于这些受体,参与成熟过程,然后参与NK细胞的激活能力。方法:我们调查了KIR2DL5B基因型对240例CML患者的预后影响,该研究包括两项研究酪氨酸激酶抑制剂(TKI)停用的临床试验:STIM和STIM2。结果:在调整了CML中的标准危险因素后,我们发现抑制受体KIR2DL5B阳性基因型与TKI后延迟的第二次深层分子缓解(HR 0.54,95%CI [0.32-0.91],P = 0.02)独立相关再次挑战,但不宜尝试首次达到深部分子缓解或无治疗的缓解率。结论:这些结果表明,KIR2DL5B可能在CML复发患者的淋巴细胞介导的白血病残留疾病控制中发挥作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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