https://scholars.lib.ntu.edu.tw/handle/123456789/477705
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Petrossian K. | en_US |
dc.contributor.author | Kanaya N. | en_US |
dc.contributor.author | Chiao Lo | en_US |
dc.contributor.author | Hsu P.-Y. | en_US |
dc.contributor.author | Nguyen D. | en_US |
dc.contributor.author | Yang L. | en_US |
dc.contributor.author | Yang L. | en_US |
dc.contributor.author | Warden C. | en_US |
dc.contributor.author | Wu X. | en_US |
dc.contributor.author | Pillai R. | en_US |
dc.contributor.author | Bernal L. | en_US |
dc.contributor.author | CHIUN-SHENG HUANG | en_US |
dc.contributor.author | Kruper L. | en_US |
dc.contributor.author | Yuan Y. | en_US |
dc.contributor.author | Somlo G. | en_US |
dc.contributor.author | Mortimer J. | en_US |
dc.contributor.author | Chen S. | en_US |
dc.creator | Petrossian K.;Kanaya N.;Lo C.;Hsu P.-Y.;Nguyen D.;Yang L.;Yang L.;Warden C.;Wu X.;Pillai R.;Bernal L.;Chiun-Sheng Huang;Kruper L.;Yuan Y.;Somlo G.;Mortimer J.;Chen S. | - |
dc.date.accessioned | 2020-03-23T07:18:55Z | - |
dc.date.available | 2020-03-23T07:18:55Z | - |
dc.date.issued | 2018 | - |
dc.identifier.issn | 1949-2553 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85048365983&doi=10.18632%2foncotarget.25552&partnerID=40&md5=fbebf942e2a0344f0e8d24a03289f658 | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/477705 | - |
dc.description.abstract | While ER has multiple biological effects, ER-cyclin D1-CDK4/6-RB is a critical pathway for the action of estrogen on the cell cycle, especially for breast cancers that rely on estrogen for growth. The latest and most efficient CDK4/6 inhibitors target the phosphorylation of retinoblastoma (RB) tumor suppressor gene; thus, altering levels of many cell cycle molecules. Estrogen receptor (ER)+/HER2- breast cancers have shown great progression free survival when CDK4/6 inhibitors are combined with endocrine therapies. Here we report the mechanism of antiestrogen (fulvestrant) combination with CDK4/6 inhibitors is due to synergism in the suppression of ERmediated cell cycle progression. Furthermore, we performed single cell analysis of cells from an estrogen dependent/hormone receptor-positive patient derived xenograft (PDX) tumor model treated with palbociclib. These single cells expressed various levels of ER and RB which are involved in cell cycle regulation; and the response to palbociclib treatment relies not only on the ER-cyclin D1-CDK4/6-RB pathway but it is also dependent on elevated levels of ER and/or RB. Our preclinical studies show that palbociclib response is dependent on cells with ER, which is directly involved in cell cycle progression in hormone receptor positive (HR+) breast cancer. ? Petrossian et al. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Impact Journals LLC | en_US |
dc.relation.ispartof | Oncotarget | en_US |
dc.subject | CDK4/6 inhibitors; DEPArray; Palbociclib; Patient-derived xenografts (PDX); Single cell analysis | en_US |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | cyclin D1; cyclin dependent kinase 4; cyclin dependent kinase 6; cyclin dependent kinase inhibitor; epidermal growth factor receptor 2; estrogen receptor alpha; fulvestrant; palbociclib; retinoblastoma protein; animal cell; animal experiment; animal model; antineoplastic activity; antiproliferative activity; Article; cancer combination chemotherapy; cancer inhibition; cell cycle progression; controlled study; drug mechanism; drug potentiation; estrogen receptor positive breast cancer; female; G2 phase cell cycle checkpoint; human; human tissue; mouse; nonhuman; progression free survival; protein expression | - |
dc.title | ERα-mediated cell cycle progression is an important requisite for CDK4/6 inhibitor response in HR+ breast cancer | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.18632/oncotarget.25552 | - |
dc.identifier.scopus | 2-s2.0-85048365983 | - |
dc.relation.pages | 27736-27751 | en_US |
dc.relation.journalvolume | 9 | en_US |
dc.relation.journalissue | 45 | en_US |
item.languageiso639-1 | en | - |
item.cerifentitytype | Publications | - |
item.fulltext | no fulltext | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.openairetype | journal article | - |
item.grantfulltext | none | - |
crisitem.author.dept | Surgery-NTUH | - |
crisitem.author.dept | Surgery-NTUH | - |
crisitem.author.dept | Surgery | - |
crisitem.author.orcid | 0000-0002-6557-211X | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
顯示於: | 醫學系 |
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