Reply to "Contextualizing racial associations in prostate cancer to expose structural causes".
Reply to "Contextualizing racial associations in prostate cancer to expose structural causes".
复制标题
回复“前列腺癌中的种族关联以揭示结构性原因”。
DOI：
10.1002/cncr.35167
复制
发表时间：
2024
期刊：
影响因子：
6.2
通讯作者：
Chinnaiyan,ArulM
中科院分区：
文献类型：
--
作者：
Karan,Dev;Wick,Jo;Dubey,Seema;Kumar-Sinha,Chandan;Siddiqui,Javed;Kunju,LakshmiP;Iczkowski,KennethA;Chinnaiyan,ArulM
我们感谢Rollin等人对我们的研究感兴趣，并强调在描述种族间隐含的遗传差异时需要更多的细微差别，这些差异可以说主要是一种社会结构。然而，我们的研究注意到，在非裔美国人（AA）样本与白人样本中，CXCL2、CXCL5和CCL23的趋化因子特征存在显著差异——与这些差异的潜在驱动因素没有直接或隐含的联系。正如我们在文章中提到的，AA患者前列腺癌与白人前列腺癌患者趋化因子谱的遗传和/或环境关联已经在之前的文章中描述过。由于我们的一些值得注意的观察结果与以前的报告一致，我们也按照这些思路表达了我们的推论。我们同意，在前列腺癌（和其他癌症）方面，已经描述的黑人和白人之间的许多种族差异可能受到社会经济因素和环境暴露的高度影响，其方式类似于适应负荷与其他几个健康和疾病指标的关联。然而，一个值得注意的同行评议文献，包括前列腺癌的研究，2-4也指出，自我认同的种族群体之间的基因差异是某些健康和疾病易感性的基础。然而，我们的研究结果本质上是描述性的，我们没有提供关于这些差异是否由于遗传、种族或社会经济方面的机制数据。
We thank Rollin et al. for their interest in our study 1 and for highlighting the need for more nuance in describing implied genetic differences along racial lines that are arguably primarily a social construct. We also agree on using the term White instead of Caucasian as advocated by Rollin et al.However, our study noted significant differences in the chemokine profile of CXCL2, CXCL5, and CCL23 across African American (AA) samples versus White samples—with no direct or implied association with underlying drivers of these differences. As noted in our article, the genetic and/or environmental associations of chemokine profiles in AA patients with prostate cancer versus White patients with prostate cancer have been described previously. As some of our notable observations track with previous reports, we have expressed our inferences along these lines as well. We agree that numerous racial differences that have been described between AAs and Whites with respect to prostate cancer (and other cancers) may be highly influenced by socioeconomic factors and environmental exposures in a way similar to the association of allostatic load with several other metrics of health and disease. However, a notable body of peer‐reviewed literature, including studies specifically in prostate cancer, 2–4 also points to genetically based differences between self‐identified racial groups underlying certain health and disease predispositions. Our findings, however, are descriptive in nature, and we do not provide mechanistic data concerning whether these differences are due to genetic, racial, or socioeconomic aspects.