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Resistance to targeted therapies in breast cancer

dc.contributor.authorBraga, Sofia
dc.date.accessioned2017-04-07T15:57:27Z
dc.date.available2017-04-07T15:57:27Z
dc.date.issued2016
dc.description.abstractSeventy five percent of all breast cancer (BC) patients express estrogen receptor (ER) but a quarter to half of patients with ER positive BC relapse on ET (endocrine therapy), tamoxifen, aromatase inhibitors (AIs), surgical castration, amongst other treatment strategies. ER positive BC at relapse loses ER expression in 20 % of cases and reduces quantitative ER expression most of the time. ER is not the only survival pathway driving ER positive BC and escape pathways intrinsic or acquired are activated during ET. This overview gives an account of ligand-independent ER activation, namely by receptor networks cross talk, and by the various genomic factors and mechanisms leading to ET response failure. Also the mechanisms of Her1 and Her2 inhibition resistance are dealt within this overview, along with the therapeutic indications and limitations of tyrosine kinase inhibitors, PARP inhibitors, PI3K/AKT/mTOR inhibitors, RAS/RAF/MEK/ERK/MAPK inhibitors, and antiangiogenic drugs. In spite of the many advances in controlling the division of BC cells and the progression of BC tumors these still remain the main cause of death among women in age range of 20-50 years requiring even more efforts in new therapeutic approaches besides the drugs within the scope of the overview.
dc.identifier.doi10.1007/978-1-4939-3347-1_8
dc.identifier.urihttp://hdl.handle.net/10400.1/9717
dc.language.isoeng
dc.peerreviewedyes
dc.relation.isbasedonMEDLINE:26910072
dc.titleResistance to targeted therapies in breast cancer
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage136
oaire.citation.startPage105
oaire.citation.titleMethods in molecular biology
oaire.citation.volume1395
person.familyNameAzambuja Duarte Santos Braga
person.givenNameSofia
person.identifier.ciencia-id3F1C-792B-93F2
rcaap.rightsrestrictedAccess
rcaap.typearticle
relation.isAuthorOfPublication12a87242-e3c0-4165-b9de-8c318b8e2e14
relation.isAuthorOfPublication.latestForDiscovery12a87242-e3c0-4165-b9de-8c318b8e2e14

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