PMID- 10417778
OWN - NLM
STAT- MEDLINE
DCOM- 19990813
LR  - 20190708
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 82
IP  - 5
DP  - 1999 Aug 27
TI  - Induction of inflammatory angiogenesis by monocyte chemoattractant protein-1.
PG  - 765-70
AB  - Almost any growth of tumors is to some extent associated with an inflammatory 
      reaction which may be anti-tumorigenic by acting directly on tumor cells or 
      protumorigenic cells presumably by inducing tumor-associated angiogenesis. In 
      this study, we have analyzed the angiogenesis-inducing capacity of monocyte 
      chemoattractant protein-1 (MCP-1), a key regulatory molecule of monocyte 
      trafficking to sites of inflammation. MCP-1 was found to be potently angiogenic 
      when implanted into rabbit cornea, exerting potency similar to the specific 
      angiogenic vascular endothelial growth factor (VEGF)-A(121). MCP-1-induced 
      angiogenesis in the cornea is associated with prominent recruitment of 
      macrophages, whereas VEGF-A(121)-induced corneal angiogenesis is devoid of 
      inflammatory cell recruitment. Based on these findings, we studied MCP-1 
      expression and macrophage recruitment in human invasive ductal mammary carcinomas 
      in comparison with the physiological angiogenic processes in bovine ovarian 
      corpus luteum. Macrophage recruitment was always associated with MCP-1 
      expression. High macrophage counts in mammary tumors corresponded with poor 
      prognosis. In contrast, physiological ovarian angiogenesis was associated with 
      only minimal inflammatory recruitment of macrophages. Our data show that MCP-1 is 
      an indirect inflammation-associated inducer of angiogenesis and demonstrate 
      distinct qualitative differences between tumor angiogenesis in human mammary 
      tumors and physiological angiogenesis in the ovary.
CI  - Copyright 1999 Wiley-Liss, Inc.
FAU - Goede, V
AU  - Goede V
AD  - Cell Biology Laboratory, Department of Gynecology and Obstetrics, University of 
      Gottingen Medical School, Gottingen, Germany.
FAU - Brogelli, L
AU  - Brogelli L
FAU - Ziche, M
AU  - Ziche M
FAU - Augustin, H G
AU  - Augustin HG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (Chemokine CCL2)
RN  - 0 (Endothelial Growth Factors)
RN  - 0 (Lymphokines)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (Vascular Endothelial Growth Factors)
SB  - IM
MH  - Animals
MH  - Breast Neoplasms/blood supply/pathology
MH  - Carcinoma, Ductal, Breast/blood supply/pathology
MH  - Cattle
MH  - Chemokine CCL2/*physiology
MH  - Cornea/blood supply
MH  - Corpus Luteum/blood supply/pathology
MH  - Endothelial Growth Factors/physiology
MH  - Female
MH  - Humans
MH  - Lymphokines/physiology
MH  - Macrophages/physiology
MH  - Neovascularization, Pathologic/*physiopathology
MH  - Ovary/blood supply/pathology
MH  - Rabbits
MH  - Vascular Endothelial Growth Factor A
MH  - Vascular Endothelial Growth Factors
EDAT- 1999/07/27 00:00
MHDA- 1999/07/27 00:01
CRDT- 1999/07/27 00:00
PHST- 1999/07/27 00:00 [pubmed]
PHST- 1999/07/27 00:01 [medline]
PHST- 1999/07/27 00:00 [entrez]
AID - 10.1002/(SICI)1097-0215(19990827)82:5<765::AID-IJC23>3.0.CO;2-F [pii]
AID - 10.1002/(sici)1097-0215(19990827)82:5<765::aid-ijc23>3.0.co;2-f [doi]
PST - ppublish
SO  - Int J Cancer. 1999 Aug 27;82(5):765-70. doi: 
      10.1002/(sici)1097-0215(19990827)82:5<765::aid-ijc23>3.0.co;2-f.