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Brain Neoplasms and Coagulation—Lessons from Heterogeneity

机译:脑肿瘤和凝血—异质性的教训

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摘要

The coagulation system constitutes an important facet of the unique vascular microenvironment in which primary and metastatic brain tumors evolve and progress. While brain tumor cells express tissue factor (TF) and other effectors of the coagulation system (coagulome), their propensity to induce local and peripheral thrombosis is highly diverse, most dramatic in the case of glioblastoma multiforme (GBM), and less obvious in pediatric tumors. While the immediate medical needs often frame the discussion on current clinical challenges, the coagulation pathway may contribute to brain tumor progression through subtle, context-dependent, and non-coagulant effects, such as induction of inflammation, angiogenesis, or by responding to iatrogenic insults (e.g. surgery). In this regard, the emerging molecular diversity of brain tumor suptypes (e.g. in glioma and medulloblastoma) highlights the link between oncogenic pathways and the tumor repertoire of coagulation system regulators (coagulome). This relationship may influence the mechanisms of spontaneous and therapeutically provoked tumor cell interactions with the coagulation system as a whole. Indeed, oncogenes (EGFR, MET) and tumor suppressors (PTEN, TP53) may alter the expression, activity, and vesicular release of tissue factor (TF), and cause other changes. Conversely, the coagulant microenvironment may also influence the molecular evolution of brain tumor cells through selective and instructive cues. We suggest that effective targeting of the coagulation system in brain tumors should be explored through molecular stratification, stage-specific analysis, and more personalized approaches including thromboprophylaxis and adjuvant treatment aimed at improvement of patient survival.
机译:凝血系统构成了独特的血管微环境的重要方面,在该微环境中,原发性和转移性脑瘤得以发展。尽管脑肿瘤细胞表达组织因子(TF)和凝血系统的其他效应物(凝结组),但它们诱导局部和外周血栓形成的倾向却千差万别,在多形性胶质母细胞瘤(GBM)的情况下最为明显,而在儿科的则不太明显肿瘤。尽管眼前的医疗需求经常围绕当前的临床挑战展开讨论,但凝血途径可能通过微妙的,取决于上下文的非凝血作用(例如诱发炎症,血管生成或通过应对医源性侮辱)促进脑肿瘤的进展(例如手术)。在这方面,脑肿瘤亚型的新出现的分子多样性(例如在神经胶质瘤和髓母细胞瘤中)突显了致癌途径与凝血系统调节剂(凝结组)的肿瘤库之间的联系。这种关系可能会影响自发性和治疗性激发的肿瘤细胞与整个凝血系统的相互作用机制。实际上,癌基因(EGFR,MET)和肿瘤抑制因子(PTEN,TP53)可能会改变组织因子(TF)的表达,活性和囊泡释放,并引起其他变化。相反,凝血微环境也可能通过选择性和指导性线索影响脑肿瘤细胞的分子进化。我们建议应该通过分子分层,阶段特异性分析以及更多的个性化方法(包括血栓预防和辅助治疗,旨在提高患者生存率)来探索脑肿瘤中凝血系统的有效靶向。

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