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Christopher W. Schultz
Researcher at Thomas Jefferson University
Publications - 27
Citations - 429
Christopher W. Schultz is an academic researcher from Thomas Jefferson University. The author has contributed to research in topics: Medicine & Cancer. The author has an hindex of 6, co-authored 16 publications receiving 117 citations. Previous affiliations of Christopher W. Schultz include National Institutes of Health & Thomas Jefferson University Hospital.
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Journal ArticleDOI
Understanding and targeting the disease‐related RNA binding protein human antigen R (HuR)
TL;DR: The role HuR plays in the pathophysiology of different diseases and ongoing therapeutic strategies to target HuR will be reviewed, with a strong belief that targeting HuR could be a powerful therapeutic target to treat different diseases, particularly cancer, in the near future.
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Therapeutic targeting of ATR yields durable regressions in small cell lung cancers with high replication stress
Anish Thomas,Nobuyuki Takahashi,Vinodh N. Rajapakse,Xiaohu Zhang,Yilun Sun,Michele Ceribelli,Kelli M. Wilson,Yang Zhang,Erin S Beck,Linda Sciuto,Samantha Nichols,Brian Elenbaas,Janusz Puc,Janusz Puc,Heike Dahmen,Astrid Zimmermann,Jillian Varonin,Christopher W. Schultz,Sehyun Kim,Hirity Shimellis,Parth Rakesh Desai,Carleen Klumpp-Thomas,Lu Chen,Jameson Travers,Crystal McKnight,Sam Michael,Zina Itkin,Sunmin Lee,Akira Yuno,Min-Jung Lee,Christophe E. Redon,Jessica Kindrick,Cody J. Peer,Jun S. Wei,Mirit I. Aladjem,William D. Figg,Seth M. Steinberg,Jane B. Trepel,Frank Zenke,Yves Pommier,Javed Khan,Craig J. Thomas +41 more
TL;DR: In this paper, the authors used chemical genetic screens to identify inhibition of ataxia telangiectasia and rad3 related (ATR), the primary activator of the replication stress response, and topoisomerase I (TOP1), nuclear enzyme that suppresses genomic instability, as synergistically cytotoxic in small cell lung cancer.
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ATM Dysfunction in Pancreatic Adenocarcinoma and Associated Therapeutic Implications.
Samantha A. Armstrong,Christopher W. Schultz,Ariana Azimi-Sadjadi,Jonathan R. Brody,Michael J. Pishvaian +4 more
TL;DR: The function of ATM is detailed, the current data on ATM deficiency in PDAC is reviewed, the therapeutic implications of ATM alterations are examined, and the current clinical trials surrounding the ATM pathway are explored.
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Novel and Highly Potent ATR Inhibitor M4344 Kills Cancer Cells With Replication Stress, and Enhances the Chemotherapeutic Activity of Widely Used DNA Damaging Agents
Ukhyun Jo,Ilya S. Senatorov,Astrid Zimmermann,Liton Kumar Saha,Yasuhisa Murai,Se Hyun Kim,Vinodh N. Rajapakse,Fathi Elloumi,Nobuyuki Takahashi,Christopher W. Schultz,Anish Thomas,Frank Zenke,Yves Pommier +12 more
TL;DR: In this article, a new ATR-based chemotherapy drug, M4344, was proposed and compared with the clinically developed ATR inhibitors BAY1895344, berzosertib, and ceralasertib using in vitro and in vivo models.
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Abemaciclib is effective against pancreatic cancer cells and synergizes with HuR and YAP1 inhibition
Teena Dhir,Christopher W. Schultz,Aditi Jain,Samantha Z. Brown,Alex Haber,Austin Goetz,Chun-Hua Xi,Gloria H. Su,Liang Xu,James Posey,Wei Jiang,Charles J. Yeo,Talia Golan,Talia Golan,Michael J. Pishvaian,Jonathan R. Brody +15 more
TL;DR: The data suggest that abemaciclib may be therapeutically relevant for the treatment in PDAC, especially as part of a combination regimen inhibiting YAP1 or HuR and siRNA oligonucleotides targeted against HuR, Yap1, and their common target cyclin D1, validated the synergy studies.