FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2528014738> ?p ?o ?g. }

• W2528014738 endingPage "74859" @default.
• W2528014738 startingPage "74846" @default.
• W2528014738 abstract "// Cristina L. Cotarelo 1 , Arno Schad 1 , Charles James Kirkpatrick 1 , Jonathan P. Sleeman 2, 3 , Erik Springer 1 , Marcus Schmidt 4 , Sonja Thaler 2 1 Institute of Pathology, University Medical Center, Johannes Gutenberg University, Mainz, Germany 2 Centre for Biomedicine and Medical Technology Mannheim (CBTM), Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany 3 KIT Campus Nord, Institute for Toxicology and Genetics, Karlsruhe, Germany 4 Department of Obstetrics and Gynecology, University Medical Center, Johannes Gutenberg University, Mainz, Germany Correspondence to: Sonja Thaler, email: Sonja.Thaler@medma.uni-heidelberg.de , Sonja.Thaler@gmx.de Keywords: cellular senescence, breast cancer subtypes, breast cancer pathology Received: December 23, 2015      Accepted: September 12, 2016      Published: October 04, 2016 ABSTRACT Oncogene-induced senescence is thought to act as a barrier to tumorigenesis by arresting cells at risk of malignant transformation. Nevertheless, numerous findings suggest that senescent cells may conversely promote tumor progression through the development of the senescence-associated secretome they produce. It is likely that the composition and the physiological consequences mediated by the senescence secretome are dependent on the oncogenes that trigger the senescence program. Breast cancer represents a heterogenous disease that can be divided into breast cancer subtypes due to different subsets of genetic and epigenetic abnormalities. As tumor initiation and progression of these breast cancer subtypes is triggered by diverse oncogenic stimuli, differences in the senescence secretomes within breast tumors might be responsible for tumor initiation, progression, metastasis and therapeutic response. Many studies have addressed the role of senescence as a barrier to tumor progression using murine xenograft models. However, few investigations have been performed to elucidate the degree to which senescent tumor cells are present within untreated human tumors, and if present, whether these senescent tumor cells may play a role in disease progression. In the present study we analysed the appearance of senescent cells within invasive breast cancers. Detection of cellular senescence by the use of SAβ-galactosidase (SAβ-gal) staining within invasive breast carcinoms from 129 untreated patients revealed differences in the amount of SAβ-gal+ tumor cells between breast cancer subtypes. The highest percentages of SAβ-gal+ tumor cells were found in HER2-positive and luminal A breast carcinomas whereas triple negative tumors showed either little or no positivity." @default.
• W2528014738 created "2016-10-14" @default.
• W2528014738 creator A5011248281 @default.
• W2528014738 creator A5025468397 @default.
• W2528014738 creator A5049117535 @default.
• W2528014738 creator A5054931625 @default.
• W2528014738 creator A5059885667 @default.
• W2528014738 creator A5064668347 @default.
• W2528014738 creator A5069801491 @default.
• W2528014738 date "2016-10-04" @default.
• W2528014738 modified "2023-10-10" @default.
• W2528014738 title "Detection of cellular senescence within human invasive breast carcinomas distinguishes different breast tumor subtypes" @default.
• W2528014738 cites W1979165906 @default.
• W2528014738 cites W1982395176 @default.
• W2528014738 cites W1990161819 @default.
• W2528014738 cites W2001733842 @default.
• W2528014738 cites W2004273407 @default.
• W2528014738 cites W2005248738 @default.
• W2528014738 cites W2010417927 @default.
• W2528014738 cites W2010871781 @default.
• W2528014738 cites W2015519364 @default.
• W2528014738 cites W2018330147 @default.
• W2528014738 cites W2034269086 @default.
• W2528014738 cites W2042140414 @default.
• W2528014738 cites W2044702943 @default.
• W2528014738 cites W2058871711 @default.
• W2528014738 cites W2059971436 @default.
• W2528014738 cites W2061619522 @default.
• W2528014738 cites W2062107951 @default.
• W2528014738 cites W2063864717 @default.
• W2528014738 cites W2066503677 @default.
• W2528014738 cites W2067117191 @default.
• W2528014738 cites W2077450385 @default.
• W2528014738 cites W2080769506 @default.
• W2528014738 cites W2087404852 @default.
• W2528014738 cites W2087999409 @default.
• W2528014738 cites W2096283457 @default.
• W2528014738 cites W2097265055 @default.
• W2528014738 cites W2101063496 @default.
• W2528014738 cites W2101657563 @default.
• W2528014738 cites W2104222537 @default.
• W2528014738 cites W2104908670 @default.
• W2528014738 cites W2105571100 @default.
• W2528014738 cites W2108929503 @default.
• W2528014738 cites W2115852450 @default.
• W2528014738 cites W2121022075 @default.
• W2528014738 cites W2122804955 @default.
• W2528014738 cites W2124742058 @default.
• W2528014738 cites W2135564059 @default.
• W2528014738 cites W2135829603 @default.
• W2528014738 cites W2141223216 @default.
• W2528014738 cites W2150740687 @default.
• W2528014738 cites W2154799239 @default.
• W2528014738 cites W2236415406 @default.
• W2528014738 cites W2288763477 @default.
• W2528014738 cites W2470774921 @default.
• W2528014738 cites W2560367415 @default.
• W2528014738 doi "https://doi.org/10.18632/oncotarget.12432" @default.
• W2528014738 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5342706" @default.
• W2528014738 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27713152" @default.
• W2528014738 hasPublicationYear "2016" @default.
• W2528014738 type Work @default.
• W2528014738 sameAs 2528014738 @default.
• W2528014738 citedByCount "15" @default.
• W2528014738 countsByYear W25280147382019 @default.
• W2528014738 countsByYear W25280147382020 @default.
• W2528014738 countsByYear W25280147382021 @default.
• W2528014738 countsByYear W25280147382022 @default.
• W2528014738 countsByYear W25280147382023 @default.
• W2528014738 crossrefType "journal-article" @default.
• W2528014738 hasAuthorship W2528014738A5011248281 @default.
• W2528014738 hasAuthorship W2528014738A5025468397 @default.
• W2528014738 hasAuthorship W2528014738A5049117535 @default.
• W2528014738 hasAuthorship W2528014738A5054931625 @default.
• W2528014738 hasAuthorship W2528014738A5059885667 @default.
• W2528014738 hasAuthorship W2528014738A5064668347 @default.
• W2528014738 hasAuthorship W2528014738A5069801491 @default.
• W2528014738 hasBestOaLocation W25280147381 @default.
• W2528014738 hasConcept C104317684 @default.
• W2528014738 hasConcept C121608353 @default.
• W2528014738 hasConcept C126322002 @default.
• W2528014738 hasConcept C143998085 @default.
• W2528014738 hasConcept C2779256057 @default.
• W2528014738 hasConcept C29537977 @default.
• W2528014738 hasConcept C41091548 @default.
• W2528014738 hasConcept C502942594 @default.
• W2528014738 hasConcept C522857546 @default.
• W2528014738 hasConcept C530470458 @default.
• W2528014738 hasConcept C54355233 @default.
• W2528014738 hasConcept C555283112 @default.
• W2528014738 hasConcept C67082663 @default.
• W2528014738 hasConcept C71924100 @default.
• W2528014738 hasConcept C86803240 @default.
• W2528014738 hasConceptScore W2528014738C104317684 @default.
• W2528014738 hasConceptScore W2528014738C121608353 @default.
• W2528014738 hasConceptScore W2528014738C126322002 @default.
• W2528014738 hasConceptScore W2528014738C143998085 @default.
• W2528014738 hasConceptScore W2528014738C2779256057 @default.

• next