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双阴性转移性前列腺癌的基因组和表观基因组景观

Arian Lundberg^1,2, Meng Zhang^1,2, Rahul Aggarwal^1,3

¹Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California.

Cancer research

|June 8, 2023

概括

研究人员在侵袭性前列腺癌亚型中确定了不同的分子驱动因素. 双阴性 (AR-/NE-) 转移性割抵抗性前列腺癌 (mCRPC) 亚型表现出最糟糕的预后,这是由于特定的遗传改变.

科学领域:

在瘤学瘤学.
基因组学就是基因组学.
分子生物学分子生物学

背景情况:

前列腺癌的全身疗法向雄激素信号,但耐药性导致攻击性的亚型.
转移性割抵抗性前列腺癌 (mCRPC) 可以发展神经内分泌 (NE) 或双阴性 (AR-/NE-) 特征.
攻击性AR-/NE-mCRPC亚型的分子基础仍然不太清楚.

研究的目的:

为了全面描述治疗中出现的mCRPC亚型的分子格局.
确定双阴性 (AR-/NE-) mCRPC亚型的关键分子驱动因素和独特特征.
为了发现攻击性mCRPC的潜在治疗点.

主要方法:

从210个mCRPC瘤中对匹配的RNA测序,全基因组测序和全基因组双硫酸盐测序数据的综合分析.
对不同的mCRPC亚型进行比较的分子和临床分析,包括AR-/NE-.
全基因组甲基化分析以确定调节机制和驱动因素的改变.

主要成果:

AR-/NE-mCRPC瘤在临床和分子上是不同的,与最短的存活时间有关.
在AR-/NE-瘤中发现了染色体重塑剂CHD7和PTEN损失的放大.
克鲁佩尔样因子5 (KLF5) 被提名为AR-/NE-表型的驱动因素,与RB1损失有关.

结论:

AR-/NE-亚型代表了一种具有独特分子驱动因素的高度侵略性的mCRPC形式.
了解这些驱动因素,如CHD7和KLF5,对于开发有针对性的疗法至关重要.
这项研究提供了关于mCRPC分子异质性的见解,并确定了潜在的治疗途径.

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