| Predicate |
Object |
| assignee |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_43a72884e25aaecffebe0942132d704f
http://rdf.ncbi.nlm.nih.gov/pubchem/patentassignee/MD5_b603ecd95b3b1497ae9f30752a676c0e |
| classificationCPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-4439
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-427
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61P35-00
http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-5355 |
| classificationIPCInventive |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61P35-00
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-5377
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-553
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-427
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-443
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-437
http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-713 |
| filingDate |
2020-07-01-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| inventor |
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_61cb92d4956a1dcd8d5f3e857d291426
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_e71ad7e08d482ebf5dd738424e30d06d
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_01ed52c7cd92bc820b17efd30216f245
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_b44d048787f8d1df5cd9ae9c9d03876e |
| publicationDate |
2021-01-07-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| publicationNumber |
WO-2021001431-A1 |
| titleOfInvention |
Use of pi3ka-selective inhibitors for treating metastatic disease in patients suffering from pancreatic cancer |
| abstract |
Pancreatic ductal adenocarcinoma is a paradigmatic model of undetected micrometastatic disease. This clinical situation being poorly investigated, we devised a nove preclinical protocol using circulating cell-free DNA (cDNA) as a micrometastatic disease biomarker. Amongst actionable markers of disease progression, a novel PI3Kα activation signature specifically correlated with poor prognosis independently of patient tumour staging as confirmed in patient-derived early metastatic cultures. Tumour-restricted genetic or pharmacological PI3Kα inhibition reduced micro-metastatic disease by acting on both tumoural cell migratory behaviour independently of genetic alterations and on the protumoural CD206- positive stroma. PI3Kα therefore drives pro-inflammatory metastatic features that could be pharmacologically targeted to delay macro-metastatic dissemination. Thus the results herein disclosed justify that patients with high cDNA levels should be treated with PI3Kα-selective inhibitors. |
| priorityDate |
2019-07-02-04:00^^<http://www.w3.org/2001/XMLSchema#date> |
| type |
http://data.epo.org/linked-data/def/patent/Publication |