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Fahim Ahmad¹, Margaret White², Kazutoshi Yamamoto³

¹Molecular Imaging Branch, NCI/NIH, Bethesda, MD 20892, United States; Radiation Biology Branch, NCI/NIH, Bethesda, MD 20892, United States; Laboratory of Genitourinary Cancer Pathogenesis, NCI/NIH, Bethesda, MD 20892, United States.

Neoplasia (New York, N.Y.)

|October 8, 2025

概括

前列腺癌中RB1和TP53的丧失改变了细胞代谢,增加了葡萄糖的使用和乳酸的产生,但不一定是18FDG的吸收. 这种代谢转变会影响瘤的特征和治疗预后.

科学领域:

在瘤学瘤学.
分子生物学分子生物学
医疗成像医学成像

背景情况:

使用AR抑制剂治疗晚期前列腺癌导致抵抗性和割耐性前列腺癌 (CRPC).
在CRPC中失去RB1和TP53与疾病进展和神经内分泌前列腺癌 (NEPC) 的发展有关.
在渐进的CRPC中增加的18FDG-PETSUVmax表明代谢变化,但RB1/TP53失活的作用尚不清楚.

研究的目的:

调查前列腺癌中RB1和/或TP53失活的代谢影响.
为了确定RB1/TP53损失是否导致CRPC中葡萄糖吸收增加.
探索多式成像用于特征前列腺癌表型的实用性.

主要方法:

使用患者衍生异种移植 (PDX) 衍生CRPC器官和割敏感的前列腺癌模型.
进行了18FDG-PET成像,PSMA蛋白水平分析和13C超极化磁共振光谱.
进行了RB1/TP53的淘汰实验,以评估代谢途径的改变.

主要成果:

仅通过18FDG摄入量无法区分NEPC和腺癌;PSMA水平与表型或18FDG摄入量没有相关性.
耐化的模型表现出较高的18FDG吸收,但比对化的敏感模型更低的酸盐转化为乳酸盐.
RB1 / TP53敲击增加了基底呼吸和糖溶性活性,其联合耗尽导致葡萄糖转向糖生成,反映在乳酸脱酶流量中.

结论:

失去RB1/TP53会改变前列腺癌细胞的新陈代谢,增加糖解和乳酸生产,但不一定增加18FDG的吸收.
前列腺癌的新陈代谢异质性表明,多式成像对于准确的瘤表征至关重要.
通过多式成像改善瘤特征可能会导致更好的患者预后和治疗策略.

关键词:

德国联邦财政部-PET 代谢重编程是一种代谢重编程.代谢过程中的代谢.前列腺癌是什么意思前列腺癌是什么意思 RB1 RB1 是一个字母.这就是TP53的特点.

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