Wang Haiyun, Yee Douglas, Potter David, Jewett Patricia, Yau Christina, Beckwith Heather, Watson Allison, O'Grady Nicholas, Wilson Amy, Brain Susie, Pohlmann Paula, Blaes Anne
Cancer Care Associates.
University of Minnesota Department of Medicine: University of Minnesota Twin Cities Department of Medicine.
Res Sq. 2023 May 31:rs.3.rs-2588168. doi: 10.21203/rs.3.rs-2588168/v1.
Increased body mass index (BMI) has been associated with poor outcomes in women with breast cancer. We evaluated the association between BMI and pathological complete response (pCR) in the I-SPY 2 trial.
978 patientsenrolled in the I-SPY 2 trial 3/2010-11/2016 and had a recorded baseline BMI prior to treatment were included in the analysis. Tumor subtypes were defined by hormone receptor and HER2 status. Pretreatment BMI was categorized as obese (BMI≥30 kg/m2), overweight (25≤BMI < 30 kg/m2), and normal/underweight (< 25 kg/m2). pCR was defined as elimination of detectable invasive cancer in the breast and lymph nodes (ypT0/Tis and ypN0) at the time of surgery. Logistic regression analysis was used to determine associations between BMI and pCR. Event-free survival (EFS) and overall survival (OS) between different BMI categories were examined using Cox proportional hazards regression.
The median age in the study population was 49 years. pCR rates were 32.8% in normal/underweight, 31.4% in overweight, and 32.5% in obese patients. In univariable analysis, there was no significant difference in pCR with BMI. In multivariable analysis adjusted for race/ethnicity, age, menopausal status, breast cancer subtype, and clinical stage, there was no significant difference in pCR after neoadjuvant chemotherapy for obese compared with normal/underweight patients (OR = 1.1, 95% CI: 0.68-1.63, p = 0.83), and for overweight compared with normal/underweight (OR = 1, 95% CI: 0.64-1.47, p = 0.88). We tested for potential interaction between BMI and breast cancer subtype; however, the interaction was not significant in the multivariable model (p = 0.09). Multivariate Cox regression showed there was no difference in EFS (p = 0.81) or OS (p = 0.52) between obese, overweight, and normal/underweight breast cancer patients with a median follow-up time of 3.8 years.
We found no difference in pCR rates by BMI with actual body weight based neoadjuvant chemotherapy in this biologically high-risk breast cancer population in the I-SPY2 trial.
体重指数(BMI)升高与乳腺癌女性患者预后不良相关。我们在I-SPY 2试验中评估了BMI与病理完全缓解(pCR)之间的关联。
分析纳入了2010年3月至2016年11月在I-SPY 2试验中入组且在治疗前有记录的基线BMI的978例患者。肿瘤亚型由激素受体和HER2状态定义。治疗前BMI分为肥胖(BMI≥30kg/m²)、超重(25≤BMI<30kg/m²)和正常/体重过轻(<25kg/m²)。pCR定义为手术时乳腺和淋巴结中可检测到的浸润性癌消除(ypT0/Tis和ypN0)。采用逻辑回归分析确定BMI与pCR之间的关联。使用Cox比例风险回归检查不同BMI类别之间的无事件生存期(EFS)和总生存期(OS)。
研究人群的中位年龄为49岁。正常/体重过轻患者的pCR率为32.8%,超重患者为31.4%,肥胖患者为32.5%。在单变量分析中,pCR与BMI无显著差异。在对种族/民族、年龄、绝经状态、乳腺癌亚型和临床分期进行调整的多变量分析中,与正常/体重过轻患者相比,肥胖患者新辅助化疗后的pCR无显著差异(OR=1.1,95%CI:0.68-1.63,p=0.83),超重患者与正常/体重过轻患者相比也无显著差异(OR=1,95%CI:0.64-1.47,p=0.88)。我们测试了BMI与乳腺癌亚型之间的潜在相互作用;然而,在多变量模型中这种相互作用不显著(p=0.09)。多变量Cox回归显示,中位随访时间为3.8年的肥胖、超重和正常/体重过轻的乳腺癌患者在EFS(p=0.81)或OS(p=0.52)方面没有差异。
在I-SPY2试验中,我们发现在这个生物学高风险乳腺癌人群中,基于实际体重的新辅助化疗的pCR率在BMI方面没有差异。