PMID- 17154174
OWN - NLM
STAT- MEDLINE
DCOM- 20070424
LR  - 20160303
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 120
IP  - 6
DP  - 2007 Mar 15
TI  - MCP-3 (CCL7) delivered by parvovirus MVMp reduces tumorigenicity of mouse 
      melanoma cells through activation of T lymphocytes and NK cells.
PG  - 1364-71
AB  - Monocyte chemotactic protein 3 (MCP-3/CCL7), a CC chemokine able to attract and 
      activate a large panel of leukocytes including natural killer cells and T 
      lymphocytes, could be beneficial in antitumor therapy. Vectors were constructed 
      based on the autonomous parvovirus minute virus of mice (MVMp), carrying the 
      human (MCP-3) cDNA. These vectors were subsequently evaluated in the poorly 
      immunogenic mouse melanoma model B78/H1. The infection of the tumor cells with 
      MCP3-transducing vector at low virus input multiplicities, but not with wild-type 
      virus, strongly inhibited tumor growth after implantation in euthymic mice. In a 
      therapeutic B78/H1 model, repeated intratumoral injections of MCP3-tranducing 
      virus prevented further tumor expansion as long as the treatment was pursued. The 
      antitumor effects of the MCP-3-transducing vector were not restricted to this 
      tumor model since they could also be observed in the K1735 melanoma. The 
      depletion of CD4, CD8, NK cells and of interferon gamma (IFNgamma) in mice 
      implanted with MVMp/MCP3-infected B78/H1 cells abolished the antitumor activity 
      of the vector. The latter data, together with tumor growth in nude mice and 
      reverse-transcriptase (RT)-PCR analyses of MVMp/MCP3-treated tumors, clearly 
      showed that activated CD4, CD8 and NK cells were indispensable for the 
      antineoplastic effect in the B78/H1 tumor. Altogether, our results show that 
      MCP3-transducing parvovirus vectors may be quite potent against poorly or 
      nonimmunogenic tumors, even in conditions where only a fraction of the tumor cell 
      population is efficiently infected with recombinant parvoviruses.
CI  - (c) 2006 Wiley-Liss, Inc.
FAU - Wetzel, Kristiane
AU  - Wetzel K
AD  - Infection and Cancer Program, Abteilung F010, and Institut National de la Sante 
      et de la Recherche Medicale U701, Deutsches Krebsforschungszentrum, Im 
      Neuenheimer Feld 242, D-69120 Heidelberg, Germany.
FAU - Struyf, Sofie
AU  - Struyf S
FAU - Van Damme, Jo
AU  - Van Damme J
FAU - Kayser, Tim
AU  - Kayser T
FAU - Vecchi, Annunciata
AU  - Vecchi A
FAU - Sozzani, Silvano
AU  - Sozzani S
FAU - Rommelaere, Jean
AU  - Rommelaere J
FAU - Cornelis, Jan J
AU  - Cornelis JJ
FAU - Dinsart, Christiane
AU  - Dinsart C
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 (CCL7 protein, human)
RN  - 0 (Ccl7 protein, mouse)
RN  - 0 (Chemokine CCL7)
RN  - 0 (Monocyte Chemoattractant Proteins)
RN  - 0 (Pore Forming Cytotoxic Proteins)
RN  - 0 (perforin, mouse)
RN  - 82115-62-6 (Interferon-gamma)
RN  - EC 3.4.21.- (Granzymes)
SB  - IM
MH  - Animals
MH  - Cell Proliferation
MH  - Chemokine CCL7
MH  - *Genetic Therapy
MH  - Genetic Vectors/genetics
MH  - Granzymes/genetics
MH  - Humans
MH  - Interferon-gamma/genetics
MH  - Killer Cells, Natural/*immunology
MH  - Lymphocyte Activation/genetics
MH  - Melanoma, Experimental/*therapy
MH  - Mice
MH  - Mice, Nude
MH  - Minute Virus of Mice/genetics
MH  - Monocyte Chemoattractant Proteins/*genetics
MH  - Pore Forming Cytotoxic Proteins/genetics
MH  - Skin Neoplasms/*therapy
MH  - T-Lymphocytes/*immunology
EDAT- 2006/12/13 09:00
MHDA- 2007/04/25 09:00
CRDT- 2006/12/13 09:00
PHST- 2006/12/13 09:00 [pubmed]
PHST- 2007/04/25 09:00 [medline]
PHST- 2006/12/13 09:00 [entrez]
AID - 10.1002/ijc.22421 [doi]
PST - ppublish
SO  - Int J Cancer. 2007 Mar 15;120(6):1364-71. doi: 10.1002/ijc.22421.