Now showing items 1-8 of 8

    • Complementary Genomic Screens Identify SERCA as a Therapeutic Target in NOTCH1 Mutated Cancer 

      Roti, Giovanni; Carlton, Anne; Ross, Kenneth; Markstein, Michele; Pajcini, Kostandin; Su, Angela H.; Perrimon, Norbert; Pear, Warren S.; Kung, Andrew L.; Blacklow, Stephen; Aster, Jon; Stegmaier, Kimberly (Elsevier BV, 2013-03-18)
      Notch1 is a rational therapeutic target in several human cancers, but as a transcriptional regulator, it poses a drug discovery challenge. To identify Notch1 modulators, we performed two cell-based, high-throughput screens ...
    • Genetic and Proteomic Approaches to Identify Cancer Drug Targets 

      Roti, Giovanni; Stegmaier, Kimberly (Nature Publishing Group, 2012)
      While target-based small-molecule discovery has taken centre-stage in the pharmaceutical industry, there are many cancer-promoting proteins not easily addressed with a traditional target-based screening approach. In order ...
    • The Genomic Landscape of Juvenile Myelomonocytic Leukemia 

      Stieglitz, Elliot; Taylor-Weiner, Amaro N.; Chang, Tiffany Y.; Gelston, Laura C.; Wang, Yong-Dong; Mazor, Tali; Esquivel, Emilio; Yu, Ariel; Seepo, Sara; Olsen, Scott; Rosenberg, Mara; Archambeault, Sophie L.; Abusin, Ghada; Beckman, Kyle; Brown, Patrick A.; Briones, Michael; Carcamo, Benjamin; Cooper, Todd; Dahl, Gary V.; Emanuel, Peter D.; Fluchel, Mark N.; Goyal, Rakesh K.; Hayashi, Robert J.; Hitzler, Johann; Hugge, Christopher; Liu, Y. Lucy; Messinger, Yoav H.; Mahoney, Donald H.; Monteleone, Philip; Nemecek, Eneida R.; Roehrs, Philip A.; Schore, Reuven J.; Stine, Kimo C.; Takemoto, Clifford M.; Toretsky, Jeffrey A.; Costello, Joseph F.; Olshen, Adam B.; Stewart, Chip; Li, Yongjin; Ma, Jing; Gerbing, Robert B.; Alonzo, Todd A.; Getz, Gad; Gruber, Tanja; Golub, Todd; Stegmaier, Kimberly; Loh, Mignon L. (2015)
      Juvenile myelomonocytic leukemia (JMML) is a myeloproliferative neoplasm (MPN) of childhood with a poor prognosis. Mutations in NF1, NRAS, KRAS, PTPN11 and CBL occur in 85% of patients, yet there are currently no risk ...
    • High-throughput Gene Expression Profiling of Memory Differentiation in Primary Human T Cells 

      Haining, William Nicholas; Angelosanto, Jill; Brosnahan, Kathleen; Ross, Kenneth; Hahn, Cynthia; Russell, Kate; Drury, Linda; Norton, Stephanie; Nadler, Lee Marshall; Stegmaier, Kimberly (BioMed Central, 2008)
      Background: The differentiation of naive T and B cells into memory lymphocytes is essential for immunity to pathogens. Therapeutic manipulation of this cellular differentiation program could improve vaccine efficacy and ...
    • A Method for High-Throughput Gene Expression Signature Analysis 

      Peck, David; Crawford, Emily D; Ross, Kenneth N; Stegmaier, Kimberly; Golub, Todd R.; Lamb, Justin (BioMed Central, 2006)
      Genome-wide transcriptional profiling has shown that different biologic states (for instance, disease and response to pharmacologic manipulation) can be recognized by the expression pattern of relatively small numbers of ...
    • Signature-Based Small Molecule Screening Identifies Cytosine Arabinoside as an EWS/FLI Modulator in Ewing Sarcoma 

      Stegmaier, Kimberly; Wong, Jenny S; Ross, Kenneth N; Chow, Kwan T; Peck, David; Wright, Renee D; Lessnick, Stephen L; Kung, Andrew Li-Jen; Golub, Todd R. (Public Library of Science, 2007)
      Background: The presence of tumor-specific mutations in the cancer genome represents a potential opportunity for pharmacologic intervention to therapeutic benefit. Unfortunately, many classes of oncoproteins (e.g., ...
    • SYK Regulates mTOR Signaling in AML 

      Carnevale, Julia; Ross, Linda; Puissant, Alexandre; Banerji, Versha; Stone, Richard M.; DeAngelo, Daniel J.; Ross, Kenneth N.; Stegmaier, Kimberly (2014)
      Spleen Tyrosine Kinase (SYK) was recently identified as a new target in acute myeloid leukemia (AML); however, its mechanistic role in this disease is poorly understood. Based on the known interaction between SYK and mTOR ...
    • Triplication of a 21q22 region contributes to B cell transformation through HMGN1 overexpression and loss of histone H3 lysine 27 trimethylation 

      Lane, Andrew A.; Chapuy, Bjoern; Lin, Charles Y.; Tivey, Trevor; Li, Hubo; Townsend, Elizabeth C.; van Bodegom, Diederik; Day, Tovah A.; Wu, Shuo-Chieh; Liu, Huiyun; Yoda, Akinori; Alexe, Gabriela; Schinzel, Anna C.; Sullivan, Timothy J.; Malinge, Sébastien; Taylor, Jordan E.; Stegmaier, Kimberly; Jaffe, Jacob D.; Bustin, Michael; te Kronnie, Geertruy; Izraeli, Shai; Harris, Marian; Stevenson, Kristen E.; Neuberg, Donna; Silverman, Lewis B.; Sallan, Stephen E.; Bradner, James E.; Hahn, William C.; Crispino, John D.; Pellman, David; Weinstock, David M. (2014)
      Down syndrome confers a 20-fold increased risk of B cell acute lymphoblastic leukemia (B-ALL)1 and polysomy 21 is the most frequent somatic aneuploidy amongst all B-ALLs2. Yet, the mechanistic links between chr.21 triplication ...