Bioscience, Oncology, IMED Biotech Unit, AstraZeneca, Cambridge, UK.
Biological Sciences Platform, Sunnybrook Research Institute, Toronto, Canada.
Nat Rev Clin Oncol. 2019 Aug;16(8):469-493. doi: 10.1038/s41571-019-0181-9.
All solid tumours require a vascular supply in order to progress. Although the ability to induce angiogenesis (new blood vessel growth) has long been regarded as essential to this purpose, thus far, anti-angiogenic therapies have shown only modest efficacy in patients. Importantly, overshadowed by the literature on tumour angiogenesis is a long-standing, but continually emerging, body of research indicating that tumours can grow instead by hijacking pre-existing blood vessels of the surrounding nonmalignant tissue. This process, termed vessel co-option, is a frequently overlooked mechanism of tumour vascularization that can influence disease progression, metastasis and response to treatment. In this Review, we describe the evidence that tumours located at numerous anatomical sites can exploit vessel co-option. We also discuss the proposed molecular mechanisms involved and the multifaceted implications of vessel co-option for patient outcomes.
所有实体肿瘤的生长都需要血管供应。虽然长期以来人们一直认为诱导血管生成（新血管生长）对于这一目的至关重要，但迄今为止，抗血管生成疗法在患者中的疗效仅为适度。重要的是，与肿瘤血管生成的文献相比，长期以来一直存在但不断涌现的大量研究表明，肿瘤可以通过劫持周围非恶性组织中预先存在的血管来生长。这个过程被称为血管选择，是肿瘤血管生成中经常被忽视的机制，它可以影响疾病的进展、转移和对治疗的反应。在这篇综述中，我们描述了许多解剖部位的肿瘤可以利用血管选择的证据。我们还讨论了所涉及的拟议分子机制以及血管选择对患者结局的多方面影响。
