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Daniel P. Rakiec
Researcher at Novartis
Publications - 20
Citations - 2338
Daniel P. Rakiec is an academic researcher from Novartis. The author has contributed to research in topics: MAPK/ERK pathway & Cancer. The author has an hindex of 14, co-authored 20 publications receiving 1854 citations. Previous affiliations of Daniel P. Rakiec include Harvard University & Howard Hughes Medical Institute.
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Journal ArticleDOI
An F876L Mutation in Androgen Receptor Confers Genetic and Phenotypic Resistance to MDV3100 (Enzalutamide)
Manav Korpal,Joshua M. Korn,Xueliang Gao,Daniel P. Rakiec,David A. Ruddy,Shivang Doshi,Jing Yuan,Steve Kovats,Sunkyu Kim,Vesselina G. Cooke,John Monahan,Frank Stegmeier,Thomas M. Roberts,William R. Sellers,Wenlai Zhou,Ping Zhu +15 more
TL;DR: It is suggested that emergence of F876L may serve as a novel biomarker for prediction of drug sensitivity, predict a "withdrawal" response to MDV3100, and be suitably targeted with other antiandrogens or CDK4/6 inhibitors.
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Studying clonal dynamics in response to cancer therapy using high-complexity barcoding
Hyo-eun C. Bhang,David A. Ruddy,Viveksagar Krishnamurthy Radhakrishna,Justina X. Caushi,Rui Zhao,Matthew M Hims,Angad P Singh,Iris Kao,Daniel P. Rakiec,Pamela Shaw,Marissa Balak,Alina Raza,Elizabeth Ackley,Nicholas Keen,Michael R. Schlabach,Michael Palmer,Rebecca Leary,Derek Y. Chiang,William R. Sellers,Franziska Michor,Vesselina G. Cooke,Joshua M. Korn,Frank Stegmeier +22 more
TL;DR: It is suggested that resistant clones are present before treatment, which would make up-front therapeutic combinations that target non-overlapping resistance a preferred approach and ClonTracer barcoding may be a valuable tool for optimizing therapeutic regimens with the goal of curative combination therapies for cancer.
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CRISPR screens provide a comprehensive assessment of cancer vulnerabilities but generate false-positive hits for highly amplified genomic regions
Diana M Munoz,Pamela J. Cassiani,Li Li,Eric Billy,Joshua M. Korn,Michael D. Jones,Javad Golji,David A. Ruddy,Kristine Yu,Gregory McAllister,Antoine deWeck,Dorothee Abramowski,Jessica Wan,Matthew D. Shirley,Sarah Y. Neshat,Daniel P. Rakiec,Rosalie de Beaumont,Odile Weber,Audrey Kauffmann,E. Robert McDonald,Nicholas Keen,Francesco Hofmann,William R. Sellers,Tobias Schmelzle,Frank Stegmeier,Michael R. Schlabach +25 more
TL;DR: It is shown that CRISPR-based screens have a significantly lower false-negative rate compared with RNAi- based screens, but have specific liabilities particularly in the interrogation of regions of genome amplification, therefore, this study provides critical insights for applying CRISpr-based screening toward the systematic identification of new cancer targets.
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Pharmacological and genomic profiling identifies NF-κB–targeted treatment strategies for mantle cell lymphoma
Rami Rahal,Mareike Frick,Rodrigo Romero,Joshua M. Korn,Robert Kridel,Fong Chun Chan,Barbara Meissner,Hyo-eun C. Bhang,Dave Ruddy,Audrey Kauffmann,Ali Farsidjani,Adnan Derti,Daniel P. Rakiec,Tara L. Naylor,Estelle Pfister,Steve Kovats,Sunkyu Kim,Kerstin Dietze,Bernd Dörken,Christian Steidl,Alexandar Tzankov,Michael Hummel,John Monahan,Michael Morrissey,Christine Fritsch,William R. Sellers,Vesselina G. Cooke,Randy D. Gascoyne,Georg Lenz,Frank Stegmeier +29 more
TL;DR: It is revealed that NIK is a new therapeutic target for MCL treatment, particularly for lymphomas that are refractory to BCR pathway inhibitors and provide critical insights into patient stratification strategies for NF-κB pathway–targeted agents.
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Tumor-derived IFN triggers chronic pathway agonism and sensitivity to ADAR loss.
Huayang Liu,Javad Golji,Lauren K. Brodeur,Franklin Chung,Julie T. Chen,Rosalie deBeaumont,Caroline Bullock,Michael D. Jones,Grainne Kerr,Li Li,Daniel P. Rakiec,Michael R. Schlabach,Sosathya Sovath,Joseph D. Growney,Raymond Pagliarini,David A. Ruddy,Kenzie MacIsaac,Joshua M. Korn,E. Robert McDonald +18 more
TL;DR: The output of IFN signaling, specifically IFN-stimulated gene (ISG) signatures, in primary tumors from The Cancer Genome Atlas is characterized and it is shown that ISG transcriptional state creates a novel genetic vulnerability.