Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
1997-8-14
|
| pubmed:abstractText |
In this analysis, we examined whether peptides derived from a wild-type murine proto-oncogene, c-erbB-2, function as tumor rejection Ags. Expression of murine c-erbB-2 examined by means of reverse transcription-PCR was observed in several normal adult tissues, such as intestine, kidney, and testis. We then transduced human and murine c-erbB-2 cDNA into two mutually noncross-reactive fibrosarcoma lines of BALB/c origin, CMS7 and CMS17. In BALB/c mice immunized with CMS17HE (CMS17 transduced with human c-erbB-2 cDNA), the growth of subsequently challenged CMS7HE (CMS7 transduced with human c-erbB-2 cDNA) was significantly suppressed. CTL against human c-erbB-2-expressing cells were generated from BALB/c spleen cells in vivo and in vitro sensitized by CMS17HE. The CTL activity was also directed against murine c-erbB-2-expressing cells, CMS7ME and CMS17ME, and was blocked by anti-CD8 or anti-Kd mAbs. A series of peptides of human or murine c-erbB-2 compatible with the Kd binding motif was synthesized. The CTL were reactive with P1.HTR (H-2d) pulsed with three of these peptides, p63-71 (human c-erbB-2 derived), p63-71(A) (murine c-erbB-2 derived), and p780-788 (common for human and murine c-erbB-2). Spleen cells immunized in vivo and in vitro with syngeneic spleen cells pulsed with these peptides became cytotoxic for CMS17HE and/or CMS17ME, but not CMS17neo (CMS17 transduced with control vector). The growth of CMS7ME was suppressed in mice immunized with the murine c-erbB-2-derived peptide, p63-71(A) or p780-788. There was no apparent pathologic change in mice that rejected CMS7ME after vaccination with these peptides.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Immunosuppressive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Methylcholanthrene,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, erbB-2
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
159
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1336-43
|
| pubmed:dateRevised |
2009-11-19
|
| pubmed:meshHeading |
pubmed-meshheading:9233630-3T3 Cells,
pubmed-meshheading:9233630-Amino Acid Sequence,
pubmed-meshheading:9233630-Animals,
pubmed-meshheading:9233630-Antineoplastic Agents,
pubmed-meshheading:9233630-Cloning, Molecular,
pubmed-meshheading:9233630-Cytotoxicity, Immunologic,
pubmed-meshheading:9233630-Female,
pubmed-meshheading:9233630-Fibrosarcoma,
pubmed-meshheading:9233630-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:9233630-Growth Inhibitors,
pubmed-meshheading:9233630-H-2 Antigens,
pubmed-meshheading:9233630-Humans,
pubmed-meshheading:9233630-Immunosuppressive Agents,
pubmed-meshheading:9233630-Immunotherapy, Active,
pubmed-meshheading:9233630-Lymphocyte Activation,
pubmed-meshheading:9233630-Mast-Cell Sarcoma,
pubmed-meshheading:9233630-Methylcholanthrene,
pubmed-meshheading:9233630-Mice,
pubmed-meshheading:9233630-Mice, Inbred BALB C,
pubmed-meshheading:9233630-Mice, Inbred C3H,
pubmed-meshheading:9233630-Mice, Inbred DBA,
pubmed-meshheading:9233630-Molecular Sequence Data,
pubmed-meshheading:9233630-Peptide Fragments,
pubmed-meshheading:9233630-Receptor, erbB-2,
pubmed-meshheading:9233630-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:9233630-Transfection,
pubmed-meshheading:9233630-Tumor Cells, Cultured
|
| pubmed:year |
1997
|
| pubmed:articleTitle |
Peptides derived from a wild-type murine proto-oncogene c-erbB-2/HER2/neu can induce CTL and tumor suppression in syngeneic hosts.
|
| pubmed:affiliation |
Second Department of Surgery, Nagasaki University School of Medicine, Japan.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|