Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-7-31
pubmed:abstractText
Cloned T9-C2 glioma cells transfected with membrane macrophage colony-stimulating factor (mM-CSF) never formed subcutaneous tumors when implanted into Fischer rats, whereas control T9 cells did. The T9-C2 cells were completely killed within 1 day through a mechanism that resembled paraptosis. Vacuolization of the T9-C2 cell's mitochondria and endoplasmic reticulum started within 4 hours after implantation. By 24 hours, the dead tumor cells were swollen and terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL)-positive. Bcl2-transduced T9-C2 cells failed to form tumors in rats. Both T9 and T9-C2 cells produced cytokine-induced neutrophil chemoattractant that recruited the granulocytes into the tumor injection sites, where they interacted with the tumor cells. Freshly isolated macrophages killed the T9-C2 cells in vitro by a mechanism independent of phagocytosis. Nude athymic rats treated with antiasialo GM1 antibody formed T9-C2 tumors, whereas rats treated with a natural killer cell (NK)-specific antibody failed to form tumors. When treated with antipolymorphonuclear leukocyte (anti-PMN) and antimacrophage antibodies, 80% of nude rats formed tumors, whereas only 40% of the rats developed a tumor when a single antibody was used. This suggests that both PMNs and macrophages are involved in the killing of T9-C2 tumor cells. Immunocompetent rats that rejected the living T9-C2 cells were immune to the intracranial rechallenge with T9 cells. No vaccinating effect occurred if the T9-C2 cells were freeze-thawed, x-irradiated, or treated with mitomycin-C prior to injection. Optimal tumor immunization using mM-CSF-transduced T9 cells requires viable tumor cells. In this study optimal tumor immunization occurred when a strong inflammatory response at the injection of the tumor cells was induced.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
100
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1373-80
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:12149220-Animals, pubmed-meshheading:12149220-Antibodies, pubmed-meshheading:12149220-Brain Neoplasms, pubmed-meshheading:12149220-Cell Death, pubmed-meshheading:12149220-Chemokines, CXC, pubmed-meshheading:12149220-Chemotactic Factors, pubmed-meshheading:12149220-Female, pubmed-meshheading:12149220-Freezing, pubmed-meshheading:12149220-Gene Expression, pubmed-meshheading:12149220-Glioma, pubmed-meshheading:12149220-Growth Substances, pubmed-meshheading:12149220-Hot Temperature, pubmed-meshheading:12149220-Immunization, pubmed-meshheading:12149220-In Situ Nick-End Labeling, pubmed-meshheading:12149220-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:12149220-Killer Cells, Natural, pubmed-meshheading:12149220-Macrophage Colony-Stimulating Factor, pubmed-meshheading:12149220-Macrophages, pubmed-meshheading:12149220-Microscopy, Electron, pubmed-meshheading:12149220-Mitomycin, pubmed-meshheading:12149220-Neutrophils, pubmed-meshheading:12149220-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:12149220-Rats, pubmed-meshheading:12149220-Rats, Inbred F344, pubmed-meshheading:12149220-Transfection, pubmed-meshheading:12149220-Tumor Cells, Cultured, pubmed-meshheading:12149220-X-Rays
pubmed:year
2002
pubmed:articleTitle
Living T9 glioma cells expressing membrane macrophage colony-stimulating factor produce immediate tumor destruction by polymorphonuclear leukocytes and macrophages via a "paraptosis"-induced pathway that promotes systemic immunity against intracranial T9 gliomas.
pubmed:affiliation
Diagnostic and Molecular Health Care Group, Veterans Affairs Medical Center, Long Beach, CA 90822, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't