Urologic Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD.
Basic Science Program, Frederick National Laboratory for Cancer Research, Frederick, MD.
J Clin Oncol. 2020 Apr 10;38(11):1146-1153. doi: 10.1200/JCO.19.02263. Epub 2020 Feb 21.
Published series of growth rates of renal tumors on active surveillance largely consist of tumors without pathologic or genetic data. Growth kinetics of genetically defined renal tumors are not well known. Here, we evaluate the growth of genetically defined renal tumors and their association with patient clinical and genetic characteristics.
We evaluated patients with an inherited kidney cancer susceptibility syndrome as a result of a pathologic germline alteration of or with at least 1 solid renal mass managed with active surveillance at our institution. Tumor growth rates (GR) were calculated and patients were stratified by genetic alteration and other clinical and genetic factors to analyze differences in growth rates using linear regression and comparative statistics.
A total of 292 patients with 435 genetically defined tumors were identified, including 286 -deficient, 91 -deficient, 52 -activated, and 6 -deficient tumors. There were significant differences in GRs when stratified by genetic alteration. -deficient tumors had the fastest median GR (0.6 cm/y; interquartile range [IQR], 0.57-0.68 cm/y), followed by -deficient tumors (GR, 0.37 cm/y; IQR, 0.25-0.57 cm/y), -deficient tumors (GR, 0.10 cm/y; IQR, 0.04-0.24 cm/y), and tumors with activation (GR, 0.15 cm/y; IQR, 0.053-0.32 cm/y; < .001). Tumors from the same patient had similar GRs. Younger age was independently associated with higher GR ( = .005).
In a cohort of genetically defined tumors, tumor growth rates varied in a clinically and statistically different manner according to genetic subtype. Rapid growth of -deficient tumors indicates that these patients should be managed with caution. The faster growth of tumors in younger patients may support more frequent imaging, whereas the slower growth of other tumors may support extended surveillance beyond annual imaging in some instances.
发表的主动监测中肾肿瘤生长速度的系列研究主要包括缺乏病理或遗传数据的肿瘤。遗传定义的肾肿瘤的生长动力学尚不清楚。在此,我们评估遗传定义的肾肿瘤的生长情况及其与患者临床和遗传特征的关系。
我们评估了在我们机构接受主动监测的遗传性肾癌易感综合征患者,这些患者的病理种系改变为 或 ,至少有 1 个实体肾肿块。计算肿瘤生长率(GR),并按遗传改变和其他临床和遗传因素对患者进行分层,使用线性回归和比较统计学分析生长率的差异。
共确定了 292 例有 435 个遗传定义肿瘤的患者,其中 286 例为 -缺陷,91 例为 -缺陷,52 例为 -激活,6 例为 -缺陷肿瘤。按遗传改变分层时,GR 存在显著差异。-缺陷肿瘤的中位 GR 最快(0.6cm/y;四分位距[IQR],0.57-0.68cm/y),其次是 -缺陷肿瘤(GR,0.37cm/y;IQR,0.25-0.57cm/y), -缺陷肿瘤(GR,0.10cm/y;IQR,0.04-0.24cm/y)和 -激活肿瘤(GR,0.15cm/y;IQR,0.053-0.32cm/y;<.001)。同一患者的肿瘤具有相似的 GR。年龄较小与较高的 GR 独立相关(=0.005)。
在一组遗传定义的肿瘤中,肿瘤生长率根据遗传亚型以临床和统计学上不同的方式变化。-缺陷肿瘤的快速生长表明这些患者应谨慎处理。年轻患者的肿瘤生长较快可能支持更频繁的影像学检查,而其他肿瘤生长较慢可能在某些情况下支持延长每年影像学检查以外的监测。