Sarah Pegno
Icahn School of Medicine at Mount Sinai
3 Papers
Sarah Pegno is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Biology & Phosphorylation. The author has an hindex of 3, co-authored 3 publications. Previous affiliations of Sarah Pegno include Columbia University.
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Papers
A secreted PTEN phosphatase that enters cells to alter signaling and survival.
Benjamin D. Hopkins,Barry Fine,Nicole Steinbach,Nicole Steinbach,Meaghan Dendy,Zachary Rapp,Jacquelyn Shaw,Jacquelyn Shaw,Kyrie Pappas,Kyrie Pappas,Jennifer S. Yu,Cindy Hodakoski,Sarah M. Mense,Joshua U. Klein,Joshua U. Klein,Sarah Pegno,Maria Luisa Sulis,Maria Luisa Sulis,Hannah E. Goldstein,Hannah E. Goldstein,Benjamin Amendolara,Benjamin Amendolara,Liang Lei,Liang Lei,Matthew Maurer,Matthew Maurer,Jeffrey N. Bruce,Peter Canoll,Peter Canoll,Hanina Hibshoosh,Hanina Hibshoosh,Ramon Parsons +31 more
TL;DR: A 576–amino acid translational variant of PTEN, termed PTEN-Long, that arises from an alternative translation start site 519 base pairs upstream of the ATG initiation sequence, adding 173 N-terminal amino acids to the normal PTEN open reading frame may have therapeutic uses.
PTEN Regulates Glutamine Flux to Pyrimidine Synthesis and Sensitivity to Dihydroorotate Dehydrogenase Inhibition.
Deepti Mathur,Deepti Mathur,Elias E. Stratikopoulos,Sait Ozturk,Nicole Steinbach,Nicole Steinbach,Sarah Pegno,Sarah M. Schoenfeld,Raymund Yong,Vundavalli V. Murty,John M. Asara,Lewis C. Cantley,Ramon Parsons +12 more
TL;DR: This work has found a prospective targeted therapy for PTEN-deficient tumors, with efficacy in vitro and in vivo in tumors derived from different tissues, based upon the changes in glutamine metabolism, DNA replication, and DNA damage response which are consequences of inactivation of PTENCancer Discov.
Mouse ER+/PIK3CAH1047R breast cancers caused by exogenous estrogen are heterogeneously dependent on estrogen and undergo BIM-dependent apoptosis with BH3 and PI3K agents.
Elias E. Stratikopoulos,Nicole Kiess,Matthias Szabolcs,Sarah Pegno,Cheung Kakit,Xuewei Wu,Poulikos I. Poulikakos,Pamela Cheung,Hank Schmidt,Ramon Parsons +9 more
TL;DR: It is proposed that addition of BH3 mimetics offers a therapeutic strategy to markedly improve the cytotoxic activity of PI3Ki in hormonal therapy-resistant and ER−independent PIK3CA-mutant breast cancer.