子宫内膜癌症治疗后的生物驱动监测：整合复发表型的分子临床框架
Toward Biology-Driven Surveillance After Endometrial Cancer Treatment: A Molecular-Clinical Framework Integrating Recurrence Phenotype.
摘要(中文译文)
当前子宫内膜癌的治疗后监测策略主要依赖临床分期和组织学分级，尚未整合分子肿瘤生物学。分子分型揭示了子宫内膜癌各亚型之间存在深刻的生物学异质性，包括复发模式、预后和治疗反应性的差异，然而监测策略尚未系统性地调整以反映这种异质性。旨在提出一种以生物学为驱动的子宫内膜癌监测框架，整合分子亚型、临床病理危险因素和复发表型。本叙述性综述和概念框架综合了队列研究、分子分型分析、国际指南以及探讨子宫内膜癌各分子亚型复发模式和治疗反应性的文献证据。我们提出一种三层监测模型，将患者分为低危、中危和高危组。该框架将分子亚型与临床病理修饰因素及预期复发表型相结合。在无特定分子谱（NSMP）亚型中，CTNNB1突变状态被纳入作为主要修饰因素，将CTNNB1突变型肿瘤归入中危组，无论雌激素受体（ER）状态如何。在CTNNB1野生型NSMP肿瘤中，ER表达作为次要修饰因素，可识别出一个生物学低危亚组。L1CAM表达被视为NSMP内的高危修饰因素。该框架还考虑了复发治疗可修饰性的差异，包括免疫治疗在错配修复缺陷肿瘤中的作用。统一的治疗后监测不能反映子宫内膜癌的生物学多样性。所提出的框架提供了一种以生物学为基础的监测方法，使随访强度与复发表型和治疗机会相匹配。该模型可作为评估子宫内膜癌个体化监测策略的前瞻性研究的概念基础。
Abstract
Current post-treatment surveillance strategies for endometrial cancer rely predominantly on clinical stage and histological grade, without integration of molecular tumor biology. Molecular classification has revealed profound biological heterogeneity across endometrial cancer subtypes, including differences in recurrence patterns, prognosis, and treatment responsiveness, yet surveillance strategies have not been systematically adapted to reflect this heterogeneity. To propose a biology-driven surveillance framework for endometrial cancer that integrates molecular subtype, clinicopathological risk factors, and recurrence phenotype. This narrative review and conceptual framework synthesizes evidence from cohort studies, molecular classification analyses, international guidelines, and the literature addressing recurrence patterns and treatment responsiveness across molecular subtypes of endometrial cancer. We propose a three-tier surveillance model stratifying patients into low-, intermediate-, and high-risk groups. The framework integrates molecular subtype with clinicopathological modifiers and expected recurrence phenotype. Within the no specific molecular profile (NSMP) subtype, CTNNB1 mutation status is incorporated as a primary modifier, assigning CTNNB1-mutated tumors to the intermediate-risk group regardless of estrogen receptor (ER) status. In CTNNB1 wild-type NSMP tumors, ER expression functions as a secondary modifier, allowing identification of a biologically low-risk subgroup. L1CAM expression is considered a high-risk modifier within NSMP. The framework also accounts for differences in the therapeutic modifiability of recurrence, including the role of immunotherapy in mismatch repair-deficient tumors. Uniform post-treatment surveillance does not reflect the biological diversity of endometrial cancer. The proposed framework provides a biologically grounded approach to surveillance that aligns follow-up intensity with recurrence phenotype and therapeutic opportunities. This model may serve as a conceptual basis for prospective studies evaluating personalized surveillance strategies in endometrial cancer.
如何引用
AMA
Wiktor Szatkowski, Izabela Glanowska-Nawrat. Toward Biology-Driven Surveillance After Endometrial Cancer Treatment: A Molecular-Clinical Framework Integrating Recurrence Phenotype.. Cancers. 2026; doi:10.3390/cancers18091443.
APA
Wiktor Szatkowski, Izabela Glanowska-Nawrat (2026). Toward Biology-Driven Surveillance After Endometrial Cancer Treatment: A Molecular-Clinical Framework Integrating Recurrence Phenotype.. Cancers. https://doi.org/10.3390/cancers18091443
GB/T 7714
Wiktor Szatkowski, Izabela Glanowska-Nawrat. Toward Biology-Driven Surveillance After Endometrial Cancer Treatment: A Molecular-Clinical Framework Integrating Recurrence Phenotype.[J]. Cancers, 2026 doi:10.3390/cancers18091443.
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