Drosophila Muller F elements maintain a distinct set of genomic properties over 40 million years of evolution

Autor: Leung, W, Shaffer, CD, Reed, LK, Smith, ST, Barshop, W, Dirkes, W, Dothager, M, Lee, P, Wong, J, Xiong, D, Yuan, H, Bedard, JEJ, Machone, JF, Patterson, SD, Price, AL, Turner, BA, Robic, S, Luippold, EK, McCartha, SR, Walji, TA, Walker, CA, Saville, K, Abrams, MK, Armstrong, AR, Armstrong, W, Bailey, RJ, Barberi, CR, Beck, LR, Blaker, AL, Blunden, CE, Brand, JP, Brock, EJ, Brooks, DW, Brown, M, Butzler, SC, Clark, EM, Clark, NB, Collins, AA, Cotteleer, RJ, Cullimore, PR, Dawson, SG, Docking, CT, Dorsett, SL, Dougherty, GA, Downey, KA, Drake, AP, Earl, EK, Floyd, TG, Forsyth, JD, Foust, JD, Franchi, SL, Geary, JF, Hanson, CK, Harding, TS, Harris, CB, Heckman, JM, Holderness, HL, Howey, NA, Jacobs, DA, Jewell, ES, Kaisler, M, Karaska, EA, Kehoe, JL, Koaches, HC, Koehler, J, Koenig, D, Kujawski, AJ, Kus, JE, Lammers, JA, Leads, RR, Leatherman, EC, Lippert, RN, Messenger, GS, Morrow, AT, NewcombVictoria, HJ, Plasman, Potocny, SJ, Powers, MK, Reem, RM, Rennhack, JP, Reynolds, KR, Reynolds, LA, Rhee, DK, Rivard, AB, Ronk, AJ, Rooney, MB, Rubin, LS, Salbert, LR, Saluja, RK, Schauder, T, Schneiter, AR, Schulz, RW, Smith, KE, Spencer, S, Swanson, BR, Tache, MA, Tewilliager, AA, Tilot, AK, VanEck, E

Publikováno v: Leung, W; Shaffer, CD; Reed, LK; Smith, ST; Barshop, W; Dirkes, W; et al.(2015). Drosophila Muller F elements maintain a distinct set of genomic properties over 40 million years of evolution. G3: Genes, Genomes, Genetics, 5(5), 719-740. doi: 10.1534/g3.114.015966. UC San Diego: Retrieved from: http://www.escholarship.org/uc/item/33p4w55r

© 2015 Leung et al. The Muller F element (4.2 Mb, ~80 protein-coding genes) is an unusual autosome of Drosophila melanogaster; it is mostly heterochromatic with a low recombination rate. To investigate how these properties impact the evolution of re

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=od_______325::cc031dfedfe53dfa7ab21233df319320
http://www.escholarship.org/uc/item/33p4w55r

Aberrant cell state plasticity mediated by developmental reprogramming precedes colorectal cancer initiation.

Autor: Bala P; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.; Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA., Rennhack JP; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.; Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA., Aitymbayev D; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.; Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA., Morris C; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA., Moyer SM; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.; Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA., Duronio GN; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA., Doan P; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA., Li Z; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.; Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA., Liang X; Department of Gastroenterology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China., Hornick JL; Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA., Yurgelun MB; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.; Division of Gastrointestinal Oncology, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA., Hahn WC; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.; Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA., Sethi NS; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.; Broad Institute of Massachusetts Institute of Technology and Harvard University, Cambridge, MA, USA.; Division of Gastrointestinal Oncology, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.

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CREB5 reprograms FOXA1 nuclear interactions to promote resistance to androgen receptor-targeting therapies.

Autor: Hwang JH; Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, United States.; Department of Medicine, University of Minnesota, Minneapolis, United States., Arafeh R; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States.; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Harvard Medical School, Boston, United States., Seo JH; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States.; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Harvard Medical School, Boston, United States., Baca SC; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States.; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Harvard Medical School, Boston, United States., Ludwig M; Department of Pharmacology, University of Minnesota-Twin Cities, Minneapolis, United States., Arnoff TE; Warren Alpert Medical School of Brown University, Providence, United States., Sawyer L; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States., Richter C; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States.; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Harvard Medical School, Boston, United States., Tape S; Department of Medicine, University of Minnesota, Minneapolis, United States., Bergom HE; Department of Medicine, University of Minnesota, Minneapolis, United States., McSweeney S; Department of Medicine, University of Minnesota, Minneapolis, United States., Rennhack JP; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States.; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Harvard Medical School, Boston, United States., Klingenberg SA; Department of Medicine, University of Minnesota, Minneapolis, United States., Cheung ATM; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Grossman School of Medicine, New York University, New York, United States., Kwon J; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States.; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Harvard Medical School, Boston, United States., So J; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States.; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Harvard Medical School, Boston, United States., Kregel S; Department of Cancer Biology, Loyola University Chicago, Maywood, United States., Van Allen EM; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States.; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Harvard Medical School, Boston, United States., Drake JM; Masonic Cancer Center, University of Minnesota-Twin Cities, Minneapolis, United States.; Department of Pharmacology and Urology, University of Minnesota, Minneapolis, United States., Freedman ML; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States.; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Harvard Medical School, Boston, United States., Hahn WC; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, United States.; Broad Institute of MIT and Harvard, Cambridge, Cambridge, United States.; Harvard Medical School, Boston, United States.

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SMAD4 represses FOSL1 expression and pancreatic cancer metastatic colonization.

Autor: Dai C; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Rennhack JP; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Arnoff TE; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Thaker M; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Younger ST; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Doench JG; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Huang AY; Division of Genetics and Genomics, Boston Children's Hospital, Boston, MA 02115, USA., Yang A; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Aguirre AJ; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Wang B; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Mun E; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Northeastern University, Boston, MA 02115, USA., O'Connell JT; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Huang Y; Molecular Pathology Core Lab, Department of Oncologic Pathology, Dana-Farber Cancer Institute, Boston, MA 02115, USA., Labella K; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Talamas JA; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Li J; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Ilic N; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Hwang J; Masonic Cancer Center and Department of Medicine, University of Minnesota-Twin Cities, Minneapolis, MN 55455, USA., Hong AL; Department of Pediatrics, Emory University, Atlanta, GA 30322, USA., Giacomelli AO; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Princess Margaret Cancer Centre, University Health Network, Toronto, ON M5G 2M9, Canada., Gjoerup O; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Root DE; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA., Hahn WC; Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA; Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: william_hahn@dfci.harvard.edu.

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Low E2F2 activity is associated with high genomic instability and PARPi resistance.

Autor: Rennhack JP; Department of Physiology, Michigan State University, East Lansing, MI, USA., Andrechek ER; Department of Physiology, Michigan State University, East Lansing, MI, USA. Andrech1@msu.edu.; Department of Physiology, Michigan State University, 2194 BPS Building, 567 Wilson Road, East Lansing, MI, 48824, USA. Andrech1@msu.edu.

Publikováno v: Scientific reports [Sci Rep] 2020 Oct 21; Vol. 10 (1), pp. 17948. Date of Electronic Publication: 2020 Oct 21.