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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Molecular Mechanisms Underlying Lymphovascular Invasion in Invasive Breast Cancer
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Molecular Mechanisms Underlying Lymphovascular Invasion in Invasive Breast Cancer

机译：浸润性乳腺癌中淋巴血管浸润的分子机制

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摘要

Lymphovascular invasion (LVI), the presence of malignant cells within lymphovascular channels, is a crucial step in the invasion-metastasis cascade. LVI, when identified morphologically in the peritumoural area, is regarded as an indicator of metastatic potential and is strongly associated with a poor prognosis in many solid tumours, including breast cancer (BC). Although molecular mechanisms associated with the development of LVI have been extensively studied, details of driver genes, and molecular pathways and mechanisms involved in its development in BC, remain poorly defined. Although invasive BC cells have the ability to invade surrounding stroma, only those that can interact with endothelial cells, penetrate the vascular wall and withstand the intravascular stress will develop LVI and complete metastatic dissemination. Identification of additional molecular events associated with LVI in the primary tumour and characterisation of the contribution of the tumour micro-environment to modulating biological processes leading to LVI in BC remain a challenging task. This stems not only from the complexity of the molecular alterations in the primary tumour and the interactions with different components of its micro-environment but also from the subjective nature of LVI assessment in human BC. In this review, we discuss the clinicopathological features and the current knowledge of the molecular mechanisms underlying LVI in BC. (C) 2015 S. Karger AG, Basel
机译：淋巴管通道内恶性细胞的存在是淋巴管浸润（LVI），是侵袭-转移级联中的关键步骤。当在肿瘤周围区域进行形态学鉴定时，LVI被认为是转移潜能的指标，并且与包括乳腺癌（BC）在内的许多实体瘤的不良预后密切相关。尽管已广泛研究了与LVI发生有关的分子机制，但对于驱动基因的详细信息，以及与BC发生有关的分子途径和机制仍不清楚。尽管浸润性BC细胞具有侵袭周围基质的能力，但是只有那些能够与内皮细胞相互作用，穿透血管壁并承受血管内压力的细胞才会形成LVI和完整的转移性扩散。鉴定与原发肿瘤中LVI相关的其他分子事件以及表征肿瘤微环境对调节导致BC中LVI的生物学过程的贡献仍然是一项艰巨的任务。这不仅源于原发肿瘤中分子改变的复杂性及其与微环境不同组成部分的相互作用，还源于人类BC中LVI评估的主观性质。在这篇综述中，我们讨论了临床病理特征和卑诗省LVI分子机制的最新知识。 （C）2015 S.Karger AG，巴塞尔

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