N
Nicole M. Hermance
Researcher at Worcester Polytechnic Institute
Publications - 12
Citations - 298
Nicole M. Hermance is an academic researcher from Worcester Polytechnic Institute. The author has contributed to research in topics: Mitosis & Centrosome. The author has an hindex of 6, co-authored 11 publications receiving 111 citations.
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Journal ArticleDOI
Whole-genome doubling confers unique genetic vulnerabilities on tumour cells.
Ryan J. Quinton,Amanda DiDomizio,Marc A. Vittoria,Kristýna Kotýnková,Carlos J. Ticas,Sheena Patel,Yusuke Koga,Jasmine Vakhshoorzadeh,Nicole M. Hermance,Taruho S. Kuroda,Neha Parulekar,Alison M. Taylor,Amity L. Manning,Joshua D. Campbell,Joshua D. Campbell,Neil J. Ganem +15 more
TL;DR: This paper showed that WGD+ cells are more dependent than WGD-cells on signalling from the spindle-assembly checkpoint, DNA-replication factors and proteasome function and identified KIF18A, which encodes a mitotic kinesin protein, as being specifically required for the viability of whole-genome doubling (WGD+) cells.
Posted ContentDOI
Whole genome doubling confers unique genetic vulnerabilities on tumor cells
Ryan J. Quinton,Amanda DiDomizio,Marc A. Vittoria,Carlos J. Ticas,Sheena Patel,Yusuke Koga,Kristyna Kotynkova,Jasmine Vakhshoorzadeh,Nicole M. Hermance,Taruho S. Kuroda,Neha Parulekar,Alison M. Taylor,Amity L. Manning,Joshua D. Campbell,Neil J. Ganem +14 more
TL;DR: It is shown that WGD gives rise to common genetic traits that are accompanied by unique vulnerabilities, and KIF18A, which encodes for a mitotic kinesin, is identified as being specifically required for the viability of WGD+ cells.
Journal ArticleDOI
Identification of the kinase STK25 as an upstream activator of LATS signaling.
Sanghee Lim,Nicole M. Hermance,Tenny Mudianto,Tenny Mudianto,Hatim M. Mustaly,Ian Paolo Morelos Mauricio,Marc A. Vittoria,Ryan J. Quinton,Brian W. Howell,Hauke Cornils,Amity L. Manning,Neil J. Ganem +11 more
TL;DR: It is demonstrated that loss of STK25 promotes YAP/TAZ activation and enhanced cellular proliferation, even under normally growth-suppressive conditions both in vitro and in vivo, and is significantly focally deleted across a wide spectrum of human cancers.
Journal ArticleDOI
Phase I study of the aurora A kinase inhibitor alisertib with induction chemotherapy in patients with acute myeloid leukemia
Amir T. Fathi,Seth A. Wander,Traci M. Blonquist,Andrew M. Brunner,Philip C. Amrein,Jeffrey G. Supko,Nicole M. Hermance,Amity L. Manning,Hossein Sadrzadeh,Karen K. Ballen,Eyal C. Attar,Timothy A. Graubert,Gabriela S. Hobbs,Christelle Joseph,Ashley M. Perry,Meghan Burke,Regina Silver,Julia Foster,Meghan Bergeron,Aura Y. Ramos,Tina T. Som,Kaitlyn M. Fishman,Kristin McGregor,Christine Connolly,Donna Neuberg,Yi Bin Chen +25 more
TL;DR: Alisertib is well tolerated when combined with induction chemotherapy in acute myeloid leukemia, and this efficacy appears enhanced in combination with conventional chemotherapies.
Journal ArticleDOI
Aurora A inhibition limits centrosome clustering and promotes mitotic catastrophe in cells with supernumerary centrosomes
Bernat Navarro-Serer,Eva P. Childers,Nicole M. Hermance,Dayna L. Mercadante,Amity L. Manning +4 more
TL;DR: It is demonstrated that Aurora A kinase activity is required for spindle pole clustering in cells with extra centrosomes, suggesting that centrosome number and spindle polarity may serve as predictive biomarkers for response to therapeutic approaches that target Aurora A Kinase function.