Subcutaneous Adipose Tissue FDG Uptake is Associated with Systemic Inflammatory Indices Independent of Primary-Tumor Metabolic Burden in Breast Cancer.

IF 2.5 4区 医学 Q2 RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING
Mehmet Tarık Tatoğlu, İlker Nihat Ökten, Ebru İbişoğlu, Tuçe Akkurt Söylemez, Hatice Uslu, Ferda Yerdelen Tatoğlu
{"title":"Subcutaneous Adipose Tissue FDG Uptake is Associated with Systemic Inflammatory Indices Independent of Primary-Tumor Metabolic Burden in Breast Cancer.","authors":"Mehmet Tarık Tatoğlu, İlker Nihat Ökten, Ebru İbişoğlu, Tuçe Akkurt Söylemez, Hatice Uslu, Ferda Yerdelen Tatoğlu","doi":"10.1007/s11307-026-02138-0","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Adipose tissue may contribute to systemic inflammation in breast cancer. This study evaluated whether visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) [18F]fluorodeoxyglucose ([18F]FDG) uptakes on positron emission tomography/computed tomography (PET/CT) are associated with inflammatory indices after adjustment for PET-derived tumor metabolic burden and whether metastatic status modifies these associations.</p><p><strong>Materials and methods: </strong>In this retrospective single-center cohort (n = 358) undergoing baseline [18F]FDG PET/CT, metastatic status was defined using an internal three-level clinical stage grouping: early-stage or locally advanced disease was classified as M0 and metastatic disease was classified as MET. VAT and SAT FDG uptakes were quantified as z-scored mean standardized uptake values normalized to lean body mass (SULmean) using the James lean body mass equation. Inflammatory indices from complete blood counts were log-transformed. Prespecified linear regression models with heteroskedasticity-consistent type 3 (HC3) robust standard errors were adjusted for age, body mass index (BMI), fasting glucose, stage, molecular subtype, and PET-derived primary-tumor metabolic burden metrics. Effect modification was tested via exposure × MET interaction. Sensitivity analyses used total-body tumor burden metrics in MET and recalculated SUL using the Janmahasatian lean body mass equation; overall survival (OS) was explored with Cox models.</p><p><strong>Results: </strong>Of 358 patients, 284 (79.3%) were M0 and 74 (20.7%) were MET. In M0 (complete-case n = 267), higher SAT uptake was independently associated with higher log-transformed neutrophil-to-lymphocyte ratio (log(NLR)) (β = 0.0798; 95% confidence interval (CI) 0.0130-0.1466; p = 0.019). In pooled interaction models (n = 323), SAT remained associated with log(NLR) (β = 0.0892; 95% CI 0.0196-0.1588; p = 0.012; ≈9% higher NLR per 1-standard deviation (SD)), with no evidence of effect modification by metastatic status (SAT × MET interaction p = 0.594). Results were consistent after total-body tumor-burden adjustment in MET and after recalculation of SUL using the Janmahasatian lean body mass equation. SAT was not significantly associated with OS (adjusted hazard ratio (HR) = 1.086; 95% CI 0.864-1.364; p = 0.481; n = 346).</p><p><strong>Conclusions: </strong>Higher SAT FDG uptake was modestly associated with higher NLR independent of tumor metabolic burden, with no evidence of heterogeneity by metastatic status. These findings suggest a potential tissue-specific imaging correlate of host inflammatory phenotype rather than a stand-alone clinical biomarker. Sensitivity and survival analyses remain hypothesis-generating and require external validation.</p>","PeriodicalId":18760,"journal":{"name":"Molecular Imaging and Biology","volume":" ","pages":""},"PeriodicalIF":2.5000,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular Imaging and Biology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s11307-026-02138-0","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING","Score":null,"Total":0}
引用次数: 0

Abstract

Purpose: Adipose tissue may contribute to systemic inflammation in breast cancer. This study evaluated whether visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) [18F]fluorodeoxyglucose ([18F]FDG) uptakes on positron emission tomography/computed tomography (PET/CT) are associated with inflammatory indices after adjustment for PET-derived tumor metabolic burden and whether metastatic status modifies these associations.

Materials and methods: In this retrospective single-center cohort (n = 358) undergoing baseline [18F]FDG PET/CT, metastatic status was defined using an internal three-level clinical stage grouping: early-stage or locally advanced disease was classified as M0 and metastatic disease was classified as MET. VAT and SAT FDG uptakes were quantified as z-scored mean standardized uptake values normalized to lean body mass (SULmean) using the James lean body mass equation. Inflammatory indices from complete blood counts were log-transformed. Prespecified linear regression models with heteroskedasticity-consistent type 3 (HC3) robust standard errors were adjusted for age, body mass index (BMI), fasting glucose, stage, molecular subtype, and PET-derived primary-tumor metabolic burden metrics. Effect modification was tested via exposure × MET interaction. Sensitivity analyses used total-body tumor burden metrics in MET and recalculated SUL using the Janmahasatian lean body mass equation; overall survival (OS) was explored with Cox models.

Results: Of 358 patients, 284 (79.3%) were M0 and 74 (20.7%) were MET. In M0 (complete-case n = 267), higher SAT uptake was independently associated with higher log-transformed neutrophil-to-lymphocyte ratio (log(NLR)) (β = 0.0798; 95% confidence interval (CI) 0.0130-0.1466; p = 0.019). In pooled interaction models (n = 323), SAT remained associated with log(NLR) (β = 0.0892; 95% CI 0.0196-0.1588; p = 0.012; ≈9% higher NLR per 1-standard deviation (SD)), with no evidence of effect modification by metastatic status (SAT × MET interaction p = 0.594). Results were consistent after total-body tumor-burden adjustment in MET and after recalculation of SUL using the Janmahasatian lean body mass equation. SAT was not significantly associated with OS (adjusted hazard ratio (HR) = 1.086; 95% CI 0.864-1.364; p = 0.481; n = 346).

Conclusions: Higher SAT FDG uptake was modestly associated with higher NLR independent of tumor metabolic burden, with no evidence of heterogeneity by metastatic status. These findings suggest a potential tissue-specific imaging correlate of host inflammatory phenotype rather than a stand-alone clinical biomarker. Sensitivity and survival analyses remain hypothesis-generating and require external validation.

乳腺癌中皮下脂肪组织FDG摄取与全身炎症指数相关,与原发肿瘤代谢负荷无关。
目的:脂肪组织可能与乳腺癌的全身性炎症有关。本研究评估了内脏脂肪组织(VAT)和皮下脂肪组织(SAT) [18F]氟脱氧葡萄糖([18F]FDG)摄取正电子发射断层扫描/计算机断层扫描(PET/CT)后是否与炎症指标相关,以及转移状态是否改变了这些关联。材料和方法:在这项接受基线[18F]FDG PET/CT的回顾性单中心队列(n = 358)中,使用内部三级临床分期分组来定义转移状态:早期或局部晚期疾病被归类为M0,转移性疾病被归类为MET。VAT和SAT FDG摄取量被量化为z得分平均标准化摄取量,使用James瘦体重方程归一化为瘦体重(SULmean)。全血细胞计数的炎症指数进行对数转换。根据年龄、体重指数(BMI)、空腹血糖、分期、分子亚型和pet来源的原发性肿瘤代谢负担指标,调整具有异方差一致的3型(HC3)稳健标准误差的预先指定线性回归模型。通过暴露x MET相互作用测试效果的改变。敏感性分析采用MET的全身肿瘤负荷指标,并使用Janmahasatian瘦体重方程重新计算SUL;采用Cox模型探讨总生存期(OS)。结果:358例患者中M0 284例(79.3%),MET 74例(20.7%)。在M0(完整病例n = 267)中,较高的SAT摄取与较高的对数转化中性粒细胞与淋巴细胞比率(log(NLR))独立相关(β = 0.0798; 95%可信区间(CI) 0.0130-0.1466;p = 0.019)。在合并相互作用模型(n = 323)中,SAT仍然与log(NLR)相关(β = 0.0892; 95% CI 0.0196-0.1588; p = 0.012;每1个标准差(SD) NLR高约9%),没有证据表明转移状态改变了效果(SAT × MET相互作用p = 0.594)。在MET的全身肿瘤负荷调整和使用Janmahasatian瘦体重方程重新计算SUL后,结果是一致的。SAT与OS无显著相关(校正风险比(HR) = 1.086;95% ci 0.864-1.364;p = 0.481;n = 346)。结论:较高的SAT FDG摄取与较高的NLR有一定的相关性,独立于肿瘤代谢负荷,没有证据表明转移状态具有异质性。这些发现表明宿主炎症表型的潜在组织特异性成像相关,而不是一个独立的临床生物标志物。敏感性和生存分析仍然是假设生成的,需要外部验证。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
6.90
自引率
3.20%
发文量
95
审稿时长
3 months
期刊介绍: Molecular Imaging and Biology (MIB) invites original contributions (research articles, review articles, commentaries, etc.) on the utilization of molecular imaging (i.e., nuclear imaging, optical imaging, autoradiography and pathology, MRI, MPI, ultrasound imaging, radiomics/genomics etc.) to investigate questions related to biology and health. The objective of MIB is to provide a forum to the discovery of molecular mechanisms of disease through the use of imaging techniques. We aim to investigate the biological nature of disease in patients and establish new molecular imaging diagnostic and therapy procedures. Some areas that are covered are: Preclinical and clinical imaging of macromolecular targets (e.g., genes, receptors, enzymes) involved in significant biological processes. The design, characterization, and study of new molecular imaging probes and contrast agents for the functional interrogation of macromolecular targets. Development and evaluation of imaging systems including instrumentation, image reconstruction algorithms, image analysis, and display. Development of molecular assay approaches leading to quantification of the biological information obtained in molecular imaging. Study of in vivo animal models of disease for the development of new molecular diagnostics and therapeutics. Extension of in vitro and in vivo discoveries using disease models, into well designed clinical research investigations. Clinical molecular imaging involving clinical investigations, clinical trials and medical management or cost-effectiveness studies.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书