Skip to Main Content

Paper Details

MYC drives aggressive prostate cancer by disrupting transcriptional pause release at androgen receptor targets.
Nat Commun
53
2022
AR, AR protein, AR-, AR-dependent genes, MYC, Pol II, RNA polymerase II, androgen, androgen receptor, c, c-MYC, castration-resistant disease, genes, prostate cancer, prostate tumor, regulated genes
Author NameAffiliation
Nadia BoufaiedResearch Institute of the McGill University Health Centre
Connor BellDana-Farber Cancer Institute, Harvard Medical School
Edward O'ConnorDana-Farber Cancer Institute, Harvard Medical School
Yang Liu
Edward M SchaefferNorthwestern University
R Jeffrey KarnesMayo Clinic
Sheila WeinmannCenter for Health Research, Kaiser Permanente Northwest
Elai Davicioni
Colm MorrisseyUniversity of Washington
Leigh EllisCedars-Sinai Medical Center
Leigh EllisCedars-Sinai Samuel Oschin Comprehensive Cancer Institute
Leigh EllisCenter for Bioinformatics and Functional Genomics, Cedars-Sinai Medical Center
Massimo Loda
Mark M PomerantzDana-Farber Cancer Institute, Harvard Medical School
Mark M PomerantzDana-Farber Cancer Institute, Harvard Medical School
Daniel E SprattUniversity Hospitals Seidman Cancer Center, Case Western Reserve University School of Medicine
Eva CoreyUniversity of Washington
Matthew L FreedmanCenter for Functional Cancer Epigenetics, Dana-Farber Cancer Institute
Matthew L FreedmanDana-Farber Cancer Institute, Harvard Medical School
Matthew L FreedmanThe Eli and Edythe L. Broad Institute
Matthew L FreedmanCenter for Functional Cancer Epigenetics, Dana-Farber Cancer Institute
Matthew L FreedmanDana-Farber Cancer Institute, Harvard Medical School
Matthew L FreedmanThe Eli and Edythe L. Broad Institute
Myles BrownCenter for Functional Cancer Epigenetics, Dana-Farber Cancer Institute
Myles BrownDana-Farber Cancer Institute, Harvard Medical School
  • 1 - 25

Datasets