BMI 增加与前列腺癌发病率和死亡率增加有关。基线肿瘤基因表达谱（GEP）可以提供与治疗反应和疾病进展相关的生物过程的全面图景。我们根据前列腺腺癌患者的 BMI 询问并验证肿瘤 GEP 的潜在差异。纳入标准包括组织学证实的前列腺腺癌以及从未经治疗的原发性前列腺组织获得的 RNA 测序数据的可用性。 RNA 测序由临床实验室改进修正案认证的实验室（Tempus 或 Caris Life Sciences）进行。 Tempus 队列用于询问，Caris 队列用于验证。根据前列腺癌诊断时的 BMI 对患者进行分层：BMI 高（BMIH；BMI ≥30）和 BMI 低（BMIL；BMI <30）。使用 DEseq2 管道进行两个队列之间的差异基因表达分析。使用 Gene Set Enrichment 软件进一步分析所得的 GEP，以确定每个队列中表现出富集的途径。总体而言，102 名患者符合资格，其中 Tempus 队列中有 60 名患者（BMIL = 38，BMIH = 22），Caris 中有 42 名患者队列（BMIL = 24，BMIH = 18）。从BMIL组患者获得的肿瘤组织表现出与炎症途径相关的基因的较高表达。 BMIH 显示参与血红素代谢和雄激素反应等途径的基因表达增加。我们的研究表明，与患有前列腺癌的 BMIH 患者相比，BMIL 中不同基因组途径的上调。这些假设生成数据可以解释两组不同的生存结果，并指导前列腺癌男性的个性化治疗。

An increased BMI is linked to increased prostate adenocarcinoma incidence and mortality. Baseline tumor gene expression profiling (GEP) can provide a comprehensive picture of the biological processes related to treatment response and disease progression. We interrogate and validate the underlying differences in tumor GEP on the basis of BMI in patients with prostate adenocarcinoma.The inclusion criteria consisted of histologically confirmed prostate adenocarcinoma and the availability of RNA sequencing data obtained from treatment-naïve primary prostate tissue. RNA sequencing was performed by a Clinical Laboratory Improvement Amendments-certified laboratory (Tempus or Caris Life Sciences). The Tempus cohort was used for interrogation and the Caris cohort for validation. Patients were stratified on the basis of BMI at the time of prostate cancer diagnosis: BMI-high (BMIH; BMI ≥30) and BMI-low (BMIL; BMI <30). Differential gene expression analysis between the two cohorts was conducted using the DEseq2 pipeline. The resulting GEPs were further analyzed using Gene Set Enrichment software to identify pathways that exhibited enrichment in each cohort.Overall, 102 patients were eligible, with 60 patients in the Tempus cohort (BMIL = 38, BMIH = 22) and 42 patients in the Caris cohort (BMIL = 24, BMIH = 18). Tumor tissues obtained from patients in the BMIL group exhibited higher expression of genes associated with inflammation pathways. BMIH displayed increased expression of genes involved in pathways such as heme metabolism and androgen response.Our study shows the upregulation of distinct genomic pathways in BMIL compared with BMIH patients with prostate cancer. These hypothesis-generating data could explain different survival outcomes in both groups and guide personalized therapy for men with prostate cancer.