PMID- 11123429
OWN - NLM
STAT- MEDLINE
DCOM- 20010301
LR  - 20190513
IS  - 0910-5050 (Print)
IS  - 1876-4673 (Electronic)
IS  - 0910-5050 (Linking)
VI  - 91
IP  - 12
DP  - 2000 Dec
TI  - Synergistic suppressive effect of double transfection of tumor necrosis 
      factor-alpha and interleukin 12 genes on tumorigenicity of Meth-A cells.
PG  - 1296-302
AB  - Tumor necrosis factor-alpha (TNF-alpha) and interleukin 12 (IL-12), both potent 
      antitumor cytokines, are known to be involved in the host's antitumor immune 
      surveillance in tumor bearers, via different mechanisms. The former enhances the 
      activities of dendritic cells, natural killer / lymphocyte-activated killer (NK / 
      LAK) and cytotoxic T lymphocyte (CTL), while the latter induces Th1-type cellular 
      immunity and enhances the activities of natural killer T (NKT), NK / LAK and CTL. 
      In the present study, in the expectation of synergistic actions of these 
      cytokines in stimulating the host's immune responses, we investigated the 
      feasibility of a cancer vaccine involving double transfection with both genes in 
      a murine model. The expression of major histocompatibility complex (MHC) class I, 
      class II and B7.1 on the surface of the double transfectants was enhanced as 
      revealed by FACS analysis. A significant decrease in tumorigenicity was observed 
      in mice inoculated with the double transfectants. Cytotoxicity assay revealed 
      that the activities of NK / LAK and CTL from spleens of mice bearing the double 
      transfectants were enhanced. The induction of tumor-specific immunity was 
      confirmed by rechallenge with parental Meth-A cells in mice that had rejected the 
      double transfectants. Thus, double transfection of TNF-alpha and IL-12 genes was 
      considered to bring about synergistic suppressive effects on the tumorigenicity 
      of transfectants through the activation of killer cells by produced cytokines and 
      the enhancement of expression of MHC class I, II and B7.1 molecules.
FAU - Fujiwara, H
AU  - Fujiwara H
AD  - Department of Internal Medicine (Section 4), Sapporo Medical University School of 
      Medicine, Chuo-ku, Sapporo 060-0061, Japan. niitsu@sapmed.ac.jp
FAU - Yamauchi, N
AU  - Yamauchi N
FAU - Sato, Y
AU  - Sato Y
FAU - Sasaki, K
AU  - Sasaki K
FAU - Takahashi, M
AU  - Takahashi M
FAU - Okamoto, T
AU  - Okamoto T
FAU - Sato, T
AU  - Sato T
FAU - Iyama, S
AU  - Iyama S
FAU - Koshita, Y
AU  - Koshita Y
FAU - Hirayama, M
AU  - Hirayama M
FAU - Yamagishi, H
AU  - Yamagishi H
FAU - Niitsu, Y
AU  - Niitsu Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Japan
TA  - Jpn J Cancer Res
JT  - Japanese journal of cancer research : Gann
JID - 8509412
RN  - 0 (B7-1 Antigen)
RN  - 0 (Histocompatibility Antigens Class I)
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Adenocarcinoma/*immunology/pathology
MH  - Animals
MH  - B7-1 Antigen/analysis
MH  - Colonic Neoplasms/*immunology/pathology
MH  - *Cytotoxicity, Immunologic
MH  - Fibrosarcoma/*immunology/*pathology
MH  - Histocompatibility Antigens Class I/analysis
MH  - Histocompatibility Antigens Class II/analysis
MH  - Interleukin-12/genetics/*physiology
MH  - Killer Cells, Lymphokine-Activated/immunology
MH  - Killer Cells, Natural/immunology
MH  - Lymphoma/immunology/pathology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Recombinant Proteins/metabolism
MH  - T-Lymphocytes, Cytotoxic/immunology
MH  - Transfection/methods
MH  - Tumor Necrosis Factor-alpha/genetics/*physiology
PMC - PMC5926296
EDAT- 2000/12/21 11:00
MHDA- 2001/03/07 10:01
PMCR- 2000/12/01
CRDT- 2000/12/21 11:00
PHST- 2000/12/21 11:00 [pubmed]
PHST- 2001/03/07 10:01 [medline]
PHST- 2000/12/21 11:00 [entrez]
PHST- 2000/12/01 00:00 [pmc-release]
AID - CAE1296 [pii]
AID - 10.1111/j.1349-7006.2000.tb00917.x [doi]
PST - ppublish
SO  - Jpn J Cancer Res. 2000 Dec;91(12):1296-302. doi: 
      10.1111/j.1349-7006.2000.tb00917.x.