L
Lauren S. Fink
Researcher at Fox Chase Cancer Center
Publications - 9
Citations - 328
Lauren S. Fink is an academic researcher from Fox Chase Cancer Center. The author has contributed to research in topics: DNA repair & Triple-negative breast cancer. The author has an hindex of 7, co-authored 9 publications receiving 278 citations. Previous affiliations of Lauren S. Fink include Drexel University.
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Journal ArticleDOI
Resistance to BET Bromodomain Inhibitors Is Mediated by Kinome Reprogramming in Ovarian Cancer
Alison Kurimchak,Claude Shelton,Kelly E. Duncan,Katherine J. Johnson,Jennifer Brown,Shane W. O'Brien,Rashid Gabbasov,Rashid Gabbasov,Lauren S. Fink,Yuesheng Li,Nicole Lounsbury,Magid Abou-Gharbia,Wayne E. Childers,Denise C. Connolly,Jonathan Chernoff,Jeffrey R. Peterson,James S. Duncan +16 more
TL;DR: It is demonstrated that BETi resistance is mediated by adaptive kinome reprogramming, where activation of compensatory pro-survival kinase networks overcomes BET protein inhibition.
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Identifying three-dimensional structures of autophosphorylation complexes in crystals of protein kinases.
Qifang Xu,Kimberly L. Malecka,Lauren S. Fink,E. Joseph Jordan,Erin M. Duffy,Samuel Kolander,Jeffrey R. Peterson,Roland L. Dunbrack +7 more
TL;DR: The identified autoph phosphorylation sites are conserved in many kinases, suggesting that, by homology, these complexes may provide insight into autophosphorylation complex interfaces of kinases that are relevant drug targets.
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Metabolite profiling reveals the glutathione biosynthetic pathway as a therapeutic target in triple negative breast cancer
Alexander Beatty,Lauren S. Fink,Tanu Singh,Alexander Strigun,Erik Peter,Christina M. Ferrer,Emmanuelle Nicolas,Kathy Q. Cai,Timothy P. Moran,Mauricio J. Reginato,Ulrike Rennefahrt,Jeffrey R. Peterson +11 more
TL;DR: Findings support the potential of targeting the glutathione biosynthetic pathway as a therapeutic strategy in TNBC and identify the non-basal-like subset as most likely to respond.
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53BP1 contributes to a robust genomic stability in human fibroblasts
Lauren S. Fink,Michaela Roell,Emanuela Caiazza,Chad A. Lerner,Thomas D. Stamato,Silvana Hrelia,Antonello Lorenzini,Christian Sell +7 more
TL;DR: A difference in the levels and recruitment of 53BP1 in mouse and human cells following DNA damage is demonstrated and evidence that unresolved DNA damage correlates with species lifespan is presented.
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Ku80 facilitates chromatin binding of the telomere binding protein, TRF2
TL;DR: The Ku70/80 heterodimer is central to non-homologous end joining repair of DNA double-strand breaks and the Ku80 gene appears to be essential for human but not rodent cell survival, and inhibitor studies indicate that this loss of TRF2 is mediated by the proteasome.