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创伤后伤口愈合可能导致肺癌转移:潜在机制综述。

Wound healing after trauma may predispose to lung cancer metastasis: review of potential mechanisms.

机构信息

Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Denver Anschutz Medical Campus, Denver, Colorado, USA.

出版信息

Am J Respir Cell Mol Biol. 2011 May;44(5):591-6. doi: 10.1165/rcmb.2010-0187RT. Epub 2010 Dec 22.

Abstract

Inflammatory oncotaxis, the phenomenon in which mechanically injured tissues are predisposed to cancer metastases, has been reported for a number of tumor types, but not previously for histologically proven lung cancer. We review clinical and experimental evidence and mechanisms that may underlie inflammatory oncotaxis, and provide illustrative examples of two patients with squamous cell carcinoma of the lung who developed distant, localized metastatic disease at sites of recent physical trauma. Trauma may predispose to metastasis through two distinct, but not mutually exclusive, mechanisms: (1) physical trauma induces tissue damage and local inflammation, creating a favorable environment that is permissive for seeding of metastatic cells from distant sites; and/or (2) micrometastatic foci are already present at the time of physical injury, and trauma initiates changes in the microenvironment that stimulate the proliferation of the metastatic cells. Further exploration of post-traumatic inflammatory oncotaxis may elucidate fundamental mechanisms of metastasis and could provide novel strategies to prevent cancer metastasis.

摘要

炎症趋化作用,即机械损伤组织易发生癌症转移的现象,已在多种肿瘤类型中得到报道,但尚未在组织学上证实的肺癌中得到报道。我们回顾了可能存在于炎症趋化作用下的临床和实验证据及机制,并提供了两个具有鳞癌的肺癌患者的实例,他们在最近的身体创伤部位发生了远处局限性转移疾病。创伤可能通过两种不同但不相互排斥的机制导致转移:(1)物理创伤引起组织损伤和局部炎症,创造了有利于来自远处的转移细胞播种的有利环境;和/或(2)在物理损伤时已经存在微转移病灶,创伤引发微环境变化,刺激转移细胞增殖。进一步研究创伤后的炎症趋化作用可能阐明转移的基本机制,并为预防癌症转移提供新的策略。

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