University of British Columbia, Vancouver, British Columbia, Canada.
Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada.
PLoS One. 2024 Nov 21;19(11):e0309471. doi: 10.1371/journal.pone.0309471. eCollection 2024.
The most common pediatric primary malignant bone tumor, osteosarcoma, is often described as genetically non-recurrent and heterogeneous. Neoadjuvant chemotherapy is typically followed by resection and assessment of treatment response, which helps inform prognosis. Identifying biomarkers that may impact chemotherapy response and survival could aid in upfront risk stratification and identify patients in highest need of innovative therapies for future clinical trials. Relative to conventional genetics, little is known about osteosarcoma epigenetics. We aimed to characterize the methylation and phosphorylation status in osteosarcoma using histone markers found in primary diagnostic biopsies and their paired metastases. We constructed two tissue microarray sets from 58 primary diagnostic samples and 54 temporally-separated but related metastatic or recurrent samples, with tissue blocks available from 2002-2022. Clinical charts were reviewed for post-therapy necrosis response, presence of metastatic disease or recurrence, and overall survival. We evaluated 6 histone H3 residues using immunohistochemistry, including H3K4me3, H3K9me3, H3K27me2, H3K27me3, H3S10T11phos, and H3S28phos. Tumors were scored with low (<25%) or high (≥25%) nuclear staining of tumor cells. Diagnostic biopsies with low H3K27me3 nuclear staining were associated with poor treatment response (≤90% necrosis) at the time of definitive excision (P<0.05). We observed loss of H3S10T11phos expression in metastatic and recurrent resections specimens compared to the primary tumor (P<0.05). Expression patterns for the remaining histone markers did not show significant associations with disease parameters or survival. Although larger cohort studies are needed, these results support the expanded evaluation of histone markers, particularly H3K27me3 and H3S10T11phos, in osteosarcoma biology and risk stratification.
最常见的儿科原发性恶性骨肿瘤骨肉瘤通常被描述为遗传上非重现和异质性的。新辅助化疗后通常会进行切除和治疗反应评估,这有助于提供预后信息。确定可能影响化疗反应和生存的生物标志物,可以帮助进行早期风险分层,并确定最需要创新疗法的患者,以便进行未来的临床试验。与传统遗传学相比,骨肉瘤的表观遗传学知之甚少。我们旨在使用原发性诊断活检及其配对转移灶中发现的组蛋白标记物来描述骨肉瘤的甲基化和磷酸化状态。我们从 58 个原发性诊断样本和 54 个时间上分离但相关的转移性或复发性样本中构建了两个组织微阵列集,从 2002 年至 2022 年有组织块可用。回顾了临床图表以了解治疗后坏死反应、转移性疾病或复发的存在以及总生存率。我们使用免疫组织化学评估了 6 个组蛋白 H3 残基,包括 H3K4me3、H3K9me3、H3K27me2、H3K27me3、H3S10T11phos 和 H3S28phos。肿瘤细胞的细胞核染色评分低(<25%)或高(≥25%)。在明确切除时,具有低 H3K27me3 核染色的诊断性活检与较差的治疗反应(≤90%坏死)相关(P<0.05)。与原发性肿瘤相比,我们观察到转移性和复发性切除标本中 H3S10T11phos 表达的丧失(P<0.05)。其余组蛋白标记物的表达模式与疾病参数或生存无显著关联。尽管需要更大的队列研究,但这些结果支持在骨肉瘤生物学和风险分层中扩大评估组蛋白标记物,特别是 H3K27me3 和 H3S10T11phos。