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对清细胞细胞癌的第一线治疗产生原发性和获得性耐药性

Serena Astore¹, Giulia Baciarello¹, Linda Cerbone¹

¹Medical Oncology, San Camillo Forlanini Hospital, Rome 00152, Italy.

Cancer drug resistance (Alhambra, Calif.)

|October 16, 2023

概括

第一线治疗改善了转移性细胞癌 (mRCC) 的结果,但耐药性很常见. 整合遗传和免疫标志物可以预测反应,并克服对免疫检查点抑制剂 (ICI) 和VEGFR向的氨酸激酶抑制剂 (TKI) 等疗法的耐药性.

科学领域:

在瘤学瘤学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

转移性细胞癌 (mRCC) 治疗已经通过一线组合取得了进展,但内在或获得的耐药性仍然是一个挑战.
抵抗机制是多因素的,涉及血管新生,瘤免疫微环境 (TIME) 和缺氧,所有这些都导致了RCC的异质性.
了解这些复杂的相互作用对于改善患者治疗结果至关重要.

研究的目的:

审查目前对mRCC中免疫检查点抑制剂 (ICI) 和血管内皮生长因子受体 (VEGFR) 向的氨酸激酶抑制剂 (TKI) 的原发性和获得性耐药性机制的研究.
探索血管新生,时间和缺氧在RCC病原和耐药性之间的联系.
确定潜在的生物标志物来预测治疗反应,并制定克服耐药性的策略.

主要方法:

关于mRCC中ICI和TKI耐药机制的最新研究的文献综述.
在RCC中分析血管生成,TIME和缺氧之间的相互作用.
对基因和免疫学标记的探索,以预测治疗反应.

主要成果:

对mRCC疗法的耐药性,包括ICI和针对VEGFR的TKIs,是一个重要的临床障碍.
血管新生,时间和缺氧是相互关联的因素,影响RCC异质性和治疗反应.
整合瘤遗传和免疫学标记显示出预测治疗反应和理解耐药性的前景.

结论:

需要进一步研究将遗传和免疫学标记结合起来,以预测治疗反应并克服mRCC的耐药性.
了解ccRCC的进化方法可能有助于患者选择和治疗策略的制定.
针对抗性机制是改善mRCC患者长期治疗结果的关键.

关键词:

细胞癌是细胞癌.检查点抑制剂检查点抑制剂电阻的阻力可以针对性治疗的目标治疗.瘤微环境是一个微环境.

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