http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2011060120-A1
Outgoing Links
| Predicate | Object |
|---|---|
| assignee | http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_436833b972882eeb555022d92878dc46 |
| classificationCPCAdditional | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K2039-5152 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N2800-52 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N2800-245 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N2800-26 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N2500-10 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N2510-00 |
| classificationCPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/G01N33-564 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K38-1709 http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K38-45 |
| classificationIPCInventive | http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/C07K2-00 |
| filingDate | 2010-09-14-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor | http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_9eebecbeeab4ef7cef621b573d83c542 |
| publicationDate | 2011-03-10-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber | US-2011060120-A1 |
| titleOfInvention | Immunogenic treatment of cancer by peptides inducing the plasma membrane exposure of erp57 |
| abstract | We have recently identified (a) ectocalreticulin as the main source of immunogenicity of cancer cell death induced by chemotherapy or radiotherapy, (b) ectoERP57 as critical protein for inducing cell surface exposure of calreticulin, and (c) that ectoERP57 and ectocalreticulin are cotranslocated together to the tumor cell surface by the mediator of the inhibition of PP1/GADD34 complex. Here, I show the design of a peptide that inhibits the interaction between PP1 and GADD34 complex. These inhibitor peptide (a) induce ectocalreticulin and ectoERP57 in a variety of tumor cell lines by the mediator of the inhibition of the interaction between PP1 and GADD34, (b) increase the phagocytosis of anticancer targeted proapoptotic peptide and chemotherapy-treated tumor cells by dendritic cells, and (c) improve highly the anticancer activity of proapoptotic peptides and chemotherapy by suppressing or reducing the tumor growth in several isogenic mouse models of colon, mammary, and fibrosarcoma tumors and by increasing the lifespan of transgenic adenocarcinoma mouse prostate mice. These results suggest that these targeted peptides combination approach could serve as a new powerful autonomous anticancer therapy. |
| isCitedBy | http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2017198054-A1 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-10793633-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-11278543-B2 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-2017128433-A1 http://rdf.ncbi.nlm.nih.gov/pubchem/patent/US-10745483-B2 |
| priorityDate | 2006-09-08-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type | http://data.epo.org/linked-data/def/patent/Publication |
Incoming Links
Total number of triples: 168.