FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W1555082791> ?p ?o ?g. }

• W1555082791 endingPage "1602" @default.
• W1555082791 startingPage "1589" @default.
• W1555082791 abstract "Acquisition of resistance to aromatase inhibitors (AIs) remains a major drawback in the treatment of estrogen receptor alpha (ERα)‐positive breast cancers. The Res‐Ana cells, a new model of acquired resistance to anastrozole, were established by long‐term exposure of aromatase‐overexpressing MCF‐7 cells to this drug. These resistant cells developed ER‐independent mechanisms of resistance and decreased sensitivity to the AI letrozole or to ERα antagonists. They also displayed a constitutive activation of the PI3K/Akt/mTOR pathway and a deregulated expression of several ErbB receptors. An observed increase in the phospho‐Akt/Akt ratio between primary and matched recurrent breast tumors of patients who relapsed under anastrozole adjuvant therapy also argued for a pivotal role of the Akt pathway in acquired resistance to anastrozole. Ectopic overexpression of constitutively active Akt1 in control cells was sufficient to induce de novo resistance to anastrozole. Strikingly, combining anastrozole with the highly selective and allosteric Akt inhibitor MK‐2206 or with the mTOR inhibitor rapamycin increased sensitivity to this AI in the control cells and was sufficient to overcome resistance and restore sensitivity to endocrine therapy in the resistant cells. Our findings lead to us proposing a model of anastrozole‐acquired resistance based on the selection of cancer‐initiating‐like cells possessing self‐renewing properties, intrinsic resistance to anastrozole and sensitivity to MK‐2206. Altogether, our work demonstrated that the Akt/mTOR pathway plays a key role in resistance to anastrozole and that combining anastrozole with Akt/mTOR pathway inhibitors represents a promising strategy in the clinical management of hormone‐dependent breast cancer patients." @default.
• W1555082791 created "2016-06-24" @default.
• W1555082791 creator A5019064417 @default.
• W1555082791 creator A5033930917 @default.
• W1555082791 creator A5035131109 @default.
• W1555082791 creator A5041410352 @default.
• W1555082791 creator A5042280442 @default.
• W1555082791 creator A5051717406 @default.
• W1555082791 creator A5063289374 @default.
• W1555082791 creator A5066431987 @default.
• W1555082791 creator A5079971350 @default.
• W1555082791 creator A5088843766 @default.
• W1555082791 creator A5089319662 @default.
• W1555082791 date "2013-05-02" @default.
• W1555082791 modified "2023-10-18" @default.
• W1555082791 title "Molecular characterization of anastrozole resistance in breast cancer: Pivotal role of the Akt/mTOR pathway in the emergence of<i>de novo</i>or acquired resistance and importance of combining the allosteric Akt inhibitor MK-2206 with an aromatase inhibitor" @default.
• W1555082791 cites W1965124339 @default.
• W1555082791 cites W1967949926 @default.
• W1555082791 cites W1972320456 @default.
• W1555082791 cites W1977254575 @default.
• W1555082791 cites W1987523323 @default.
• W1555082791 cites W1996965514 @default.
• W1555082791 cites W1998458200 @default.
• W1555082791 cites W2010959069 @default.
• W1555082791 cites W2012672176 @default.
• W1555082791 cites W2016744320 @default.
• W1555082791 cites W2026151244 @default.
• W1555082791 cites W2026493214 @default.
• W1555082791 cites W2027953312 @default.
• W1555082791 cites W2028298924 @default.
• W1555082791 cites W2041799604 @default.
• W1555082791 cites W2043065181 @default.
• W1555082791 cites W2043753066 @default.
• W1555082791 cites W2046131175 @default.
• W1555082791 cites W2050300062 @default.
• W1555082791 cites W2055498399 @default.
• W1555082791 cites W2074437753 @default.
• W1555082791 cites W2096400548 @default.
• W1555082791 cites W2100090122 @default.
• W1555082791 cites W2101008725 @default.
• W1555082791 cites W2102085111 @default.
• W1555082791 cites W2102369206 @default.
• W1555082791 cites W2106286200 @default.
• W1555082791 cites W2108360575 @default.
• W1555082791 cites W2109528348 @default.
• W1555082791 cites W2113458582 @default.
• W1555082791 cites W2114694330 @default.
• W1555082791 cites W2117357260 @default.
• W1555082791 cites W2121971175 @default.
• W1555082791 cites W2125713798 @default.
• W1555082791 cites W2126783165 @default.
• W1555082791 cites W2127617517 @default.
• W1555082791 cites W2129665115 @default.
• W1555082791 cites W2132776799 @default.
• W1555082791 cites W2132950000 @default.
• W1555082791 cites W2146778486 @default.
• W1555082791 cites W2152637502 @default.
• W1555082791 cites W2153061474 @default.
• W1555082791 cites W2159640574 @default.
• W1555082791 cites W2159750196 @default.
• W1555082791 cites W2161861008 @default.
• W1555082791 cites W2166342810 @default.
• W1555082791 cites W2167188058 @default.
• W1555082791 cites W2169689529 @default.
• W1555082791 doi "https://doi.org/10.1002/ijc.28182" @default.
• W1555082791 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23553037" @default.
• W1555082791 hasPublicationYear "2013" @default.
• W1555082791 type Work @default.
• W1555082791 sameAs 1555082791 @default.
• W1555082791 citedByCount "43" @default.
• W1555082791 countsByYear W15550827912013 @default.
• W1555082791 countsByYear W15550827912014 @default.
• W1555082791 countsByYear W15550827912015 @default.
• W1555082791 countsByYear W15550827912016 @default.
• W1555082791 countsByYear W15550827912017 @default.
• W1555082791 countsByYear W15550827912018 @default.
• W1555082791 countsByYear W15550827912019 @default.
• W1555082791 countsByYear W15550827912020 @default.
• W1555082791 countsByYear W15550827912021 @default.
• W1555082791 countsByYear W15550827912023 @default.
• W1555082791 crossrefType "journal-article" @default.
• W1555082791 hasAuthorship W1555082791A5019064417 @default.
• W1555082791 hasAuthorship W1555082791A5033930917 @default.
• W1555082791 hasAuthorship W1555082791A5035131109 @default.
• W1555082791 hasAuthorship W1555082791A5041410352 @default.
• W1555082791 hasAuthorship W1555082791A5042280442 @default.
• W1555082791 hasAuthorship W1555082791A5051717406 @default.
• W1555082791 hasAuthorship W1555082791A5063289374 @default.
• W1555082791 hasAuthorship W1555082791A5066431987 @default.
• W1555082791 hasAuthorship W1555082791A5079971350 @default.
• W1555082791 hasAuthorship W1555082791A5088843766 @default.
• W1555082791 hasAuthorship W1555082791A5089319662 @default.
• W1555082791 hasConcept C121608353 @default.
• W1555082791 hasConcept C126322002 @default.
• W1555082791 hasConcept C2776166826 @default.
• W1555082791 hasConcept C2776215463 @default.
• W1555082791 hasConcept C2778504769 @default.
• W1555082791 hasConcept C502942594 @default.

• next