Различни епидемиологични, клинични и експериментални студии не само демонстрират връзка между хроничното възпаление и инициирането на неопластичния процес, но и показват, че медиаторите на възпалението имат значимо място в допринасянето за туморната прогресия. Доказано е, че ангиогенезата има решаваща роля в създаването на кръвоносна мрежа, позволяваща на тумора да расте и метастазира. Въпреки че се смята, че туморните клетки са основният двигател за туморна неоангигенеза, все повече доказателства се появяват в полза на теорията, че тумор-инфилтриращите миелоидни клетки като моноцити/макрофаги, неутрофили, еозинофили, мастоцити и дендритни клетки заемат централна роля в този процес. Това ревю се фокусира върху многостранните способности на всяка една от тези клетки да промотира туморна ангиогенеза и начина, по който тези про-туморни функции се активират и модулират от туморната микросреда. Възможната роля в туморната ангиогенеза на други клетки, произлизащи от костния мозък, като тромбоцити, прогениторни ендотелни клетки и хемопоетични стволови клетки, също трябва да бъде дискутирана.
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Various epidemiological, clinical and experimental studies have not only demonstrated a link between chronic inflammation and cancer onset but also shown that inflammatory mediators such as myeloid cells significantly contribute to tumour progression. Tumour angiogenesis is a crucial step in tumour development as tumours have to establish a blood supply in order to grow and metastasize. Although tumour cells were first thought to drive the cellular events underpinning tumour angiogenesis, considerable evidence has now emerged for the central role of tumour-infiltrating myeloid cells such as monocyte/macrophages, neutrophils, eosinophils, mast cells (MC) and dendritic cells (DC) in this phenomenon. This Review focuses on the multifaceted ability of each of these cell types to promote tumour angiogenesis and the way in which these pro-tumour functions are activated and modulated by the tumour microenvironment.
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