PMID- 20008545
OWN - NLM
STAT- MEDLINE
DCOM- 20100518
LR  - 20211020
IS  - 1530-6860 (Electronic)
IS  - 0892-6638 (Print)
IS  - 0892-6638 (Linking)
VI  - 24
IP  - 5
DP  - 2010 May
TI  - Tumor growth and angiogenesis are dependent on the presence of immature dendritic 
      cells.
PG  - 1411-8
LID - 10.1096/fj.09-147025 [doi]
AB  - Dendritic cells (DCs)--immunomodulatory cells that initiate adaptive immune 
      responses--have recently been shown to exert proangiogenic effects when 
      infiltrating the tumor microenvironment. As tumors that escape immune 
      surveillance inhibit DC maturation, we explored whether maturation status 
      determines their ability to promote angiogenesis and whether angiogenesis depends 
      on the presence of DCs. Using mouse xenograft models of human tumors, we show 
      that fast-growing "angiogenic" tumors are infiltrated by a more immature DC 
      population than respective dormant avascular tumors. Accordingly, supplementation 
      of immature DCs, but not mature DCs, enhanced tumor growth. When DCs were mixed 
      with Matrigel and injected subcutaneously into mice, only immature DCs promoted 
      the ingrowth of patent blood vessels. Notably, depletion of DCs in a transgenic 
      mouse model that allows for their conditional ablation completely abrogated basic 
      fibroblast growth factor-induced angiogenesis in Matrigel plugs, and 
      significantly inhibited tumor growth in these mice. Because immature DCs actively 
      promote angiogenesis and tumor growth, whereas DC maturation or ablation 
      suppresses this response, we conclude that angiogenesis is dependent on the 
      presence of immature DCs. Thus, cancer immunotherapies that promote DC maturation 
      may act by both augmenting the host immune response to the tumor and by 
      suppressing tumor angiogenesis.
FAU - Fainaru, Ofer
AU  - Fainaru O
AD  - Vascular Biology Program and Department of Surgery, Childrens' Hospital Boston, 
      Harvard Medical School, Boston, Massachusetts 02115, USA.
FAU - Almog, Nava
AU  - Almog N
FAU - Yung, Chong Wing
AU  - Yung CW
FAU - Nakai, Kei
AU  - Nakai K
FAU - Montoya-Zavala, Martin
AU  - Montoya-Zavala M
FAU - Abdollahi, Amir
AU  - Abdollahi A
FAU - D'Amato, Robert
AU  - D'Amato R
FAU - Ingber, Donald E
AU  - Ingber DE
LA  - eng
GR  - P01 CA045548/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20091214
PL  - United States
TA  - FASEB J
JT  - FASEB journal : official publication of the Federation of American Societies for 
      Experimental Biology
JID - 8804484
SB  - IM
MH  - Animals
MH  - Cell Line, Tumor
MH  - Cell Movement
MH  - Dendritic Cells/*immunology
MH  - Endothelium, Vascular/immunology/pathology
MH  - Humans
MH  - *Immunomodulation
MH  - Mice
MH  - Mice, Transgenic
MH  - Neoplasms/*blood supply/immunology/*pathology
MH  - Neovascularization, Pathologic/*immunology
MH  - Xenograft Model Antitumor Assays
PMC - PMC2879945
EDAT- 2009/12/17 06:00
MHDA- 2010/05/19 06:00
PMCR- 2011/05/01
CRDT- 2009/12/17 06:00
PHST- 2009/12/17 06:00 [entrez]
PHST- 2009/12/17 06:00 [pubmed]
PHST- 2010/05/19 06:00 [medline]
PHST- 2011/05/01 00:00 [pmc-release]
AID - fj.09-147025 [pii]
AID - 09-147025 [pii]
AID - 10.1096/fj.09-147025 [doi]
PST - ppublish
SO  - FASEB J. 2010 May;24(5):1411-8. doi: 10.1096/fj.09-147025. Epub 2009 Dec 14.