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Blood and lymphatic vessel invasion (BLVI) has been long recognised as a category I prognostic factor in colorectal carcinomas (CRC) along with the pT and pN categories of the Tumour-Node-Metastasis system, preoperative carcinoembryonal antigen levels and the residual tumour (R) classification.1
Small vessel involvement includes the invasion of capillary-type vessels (figure 1A), where a reliable distinction between lymphatic and blood capillaries cannot be made on H&E-stained or general endothelial marker (eg, CD31, CD34) immunostained sections. Theoretically, the two types of capillary invasion lead to different consequences: lymphatic vessel invasion (LI) precedes and may be predictive of lymph node metastasis, whereas blood capillaries may be the source of systemic dissemination.2–4 The development of lymphatic endothelial markers like podoplanin (D2-40) or lymphatic endothelial hyaluronan receptor (LYVE-1) enables a distinction between lymphatic and blood capillaries: lymphatics can be defined as D2-40, LYVE-1, CD31 and CD34 positive capillaries, whereas blood capillaries are D2-40 and LYVE-1 negative but can be highlighted by CD31 or CD34 antibodies.4–7 Without such a distinction, small vessel invasion is best recorded as (lympho-)vascular invasion (LVI) or angiolymphatic invasion.1 The impact of LI or LVI is mainly seen in patients with conservative removal (eg, polypectomy) of invasive carcinomas without a resection allowing the histopathologic assessment of the lymph nodes.
By contrast, large vessel invasion includes venous invasion (VI) (figure 1B,C) which is associated with synchronous or metachronous distant, …
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