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Paracrine angiogenic loop between head‐and‐neck squamous‐cell carcinomas and macrophages
Author(s) -
Liss Cory,
Fekete Mary Jo,
Hasina Rifat,
Lam Christy Diemthuy,
Lingen Mark W.
Publication year - 2001
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.1407
Subject(s) - angiogenesis , paracrine signalling , head and neck squamous cell carcinoma , stromal cell , cancer research , secretion , macrophage , tumor microenvironment , tumor necrosis factor alpha , medicine , biology , immunology , cancer , in vitro , receptor , tumor cells , head and neck cancer , biochemistry
Abstract Angiogenesis, an essential step in the development of neoplasia, is a complex process that involves the interaction of tumor cells with stromal cells. Tumor‐associated macrophages (TAMs) can participate in the induction of tumor angiogenesis and are thought to be of prognostic value in some neoplasms. We have investigated how macrophages contribute to angiogenesis in head‐and‐neck squamous‐cell carcinoma (HNSCC) and have found that tumor cells attract monocytes and activate them to secrete angiogenic factors. The attraction of macrophages was due to the secretion of monocyte chemotactic protein‐1 and TGF‐β1 by tumor cells, while tumor production of TGF‐β1 was responsible for activating macrophages. In addition, activated macrophages produced cytokines that acted in a paracrine fashion by secreting both TNF‐α and IL‐1, which in turn stimulated tumor cells to secrete increased levels of IL‐8 and VEGF. These data demonstrate that TAMs play an important role in the in vivo induction of angiogenesis in HNSCC and suggest that anti‐angiogenic therapies for HNSCC and perhaps other neoplasms must include strategies that will block the ability of tumor cells to recruit macrophages into the tumor micro‐environment. © 2001 Wiley‐Liss, Inc.