PO.TB10.13 · 肿瘤生物学
吸烟行为与前列腺癌中肿瘤相关神经发生的增加相关
Smoking behavior is associated with increased tumor-associated neurogenesis in prostate cancer
作者与单位 Authors & Affiliations
摘要 Abstract
中文摘要
肿瘤相关神经发生越来越被认为是癌症进展和治疗抵抗的一个促成因素。虽然已知烟草吸烟会影响炎症和微血管重塑,但其与肿瘤神经生物学的关系仍知之甚少。在本研究中,我们探究了吸烟行为是否与前列腺癌微环境内神经密度的改变相关。选取了有记录吸烟史的前列腺癌患者的前列腺切除标本(n=53),吸烟状态分类为从不吸烟(n=24)、既往吸烟(n=18)或当前吸烟(n=11)者。对肿瘤组织进行切片并针对S100B(施万细胞)和TUBB3(神经元轴突)进行免疫组织化学检测。神经密度通过测量五个随机视野中神经簇的数量进行量化,并为每个肿瘤计算平均值。使用Kruskal-Wallis非参数检验比较当前、既往和从不吸烟者之间神经密度的差异。当前吸烟者和既往吸烟者与从不吸烟者相比表现出显著更高(p<0.001)的肿瘤内神经密度。然而,当前吸烟者与既往吸烟者之间的差异不显著(p=0.268)。在按分级的比较中,在低/中级别(Gleason评分≤7)肿瘤中观察到从不吸烟者与当前/既往吸烟者之间的显著差异(p<0.001),但在高级别肿瘤(Gleason评分>7)中未观察到。有趣的是,肿瘤边缘的神经小束在当前吸烟者中也比在从不吸烟者或既往吸烟者中更频繁。总之,我们的数据表明吸烟行为与前列腺癌中增强的神经重塑相关,其特征为肿瘤边缘神经密度增加及施万细胞/轴突聚集。这些发现提示宿主暴露于烟草烟雾会促进一种嗜神经性的肿瘤微环境,这可能与前列腺癌的侵袭性及更高的复发风险相关联。
查看英文原文 English abstract
Tumor-associated neurogenesis is being increasingly recognized as a contributor to cancer progression and therapeutic resistance. While tobacco smoking is known to influence inflammation and microvascular remodeling, its relationship with tumor neurobiology remains poorly understood. In this study, we investigated whether smoking behavior is associated with alterations in nerve density within the prostate cancer microenvironment. Prostatectomy specimens from prostate cancer patients with documented smoking history were selected (n=53), and smoking status was categorized as never (n=24), former (n=18), or current (n=11) smoker. The tumor tissues were sectioned and subjected to immunohistochemistry for S100B (Schwann cells) and TUBB3 (neuronal axons). Nerve density was quantified by measuring the number of neural clusters in five random fields, and an average value was calculated for each tumor. The difference in nerve density was compared between current, former, and never smokers using Kruskal-Wallis non-parametric test. Current smokers and former smokers exhibited significantly higher (p < 0.001) intratumoral nerve density compared to never-smokers. However, the difference was not significant (p=0.268) between current smokers and former smokers. In grade-wise comparisons, a significant difference (p < 0.001) between never smokers and current /former smokers was observed in low/medium (Gleason's score ≤7) grade tumors but not in high-grade tumors (Gleason's score >7). Interestingly, nerve mini-bundles at tumor edges were also more frequent in current smokers than in never smokers or former smokers. Altogether, our data demonstrate that the smoking behavior is associated with enhanced neural remodeling in prostate cancer, characterized by increased nerve density and Schwann cell/axon clustering at tumor margins. These findings suggest that host exposure to tobacco smoke promotes a neurotrophic tumor microenvironment, which may be linked to prostate cancer aggressiveness and a higher risk of recurrence.
利益披露 Disclosure
K. Vikramdeo, None..
S. Anand, None..
A. Sharma, None..
M. Tahir, None..
V. Manucha, None..
S. Singh, None..
A. Singh, None.