Now showing items 1-8 of 8

    • CBL Is Frequently Altered in Lung Cancers: Its Relationship to Mutations in MET and EGFR Tyrosine Kinases 

      Tan, Yi-Hung Carol; Krishnaswamy, Soundararajan; Nandi, Suvobroto; Kanteti, Rajani; Vora, Sapana; Onel, Kenan; Hasina, Rifat; Lo, Fang-Yi; El-Hashani, Essam; Cervantes, Gustavo; Lipkowitz, Stanley; Karrison, Theodore; Vokes, Everett E.; Wang, Yi-Ching; Salgia, Ravi; Najbauer, Joseph; Robinson, Matthew; Kales, Stephen C.; Sattler, Martin (Public Library of Science, 2010)
      Background: Non-small cell lung cancer (NSCLC) is a heterogeneous group of disorders with a number of genetic and proteomic alterations. c-CBL is an E3 ubiquitin ligase and adaptor molecule important in normal homeostasis ...
    • Kinase domain mutations confer resistance to novel inhibitors targeting JAK2V617F in myeloproliferative neoplasms 

      Deshpande, Anagha; Reddy, Mamatha M.; Schade, Georg O.M.; Ray, Arghya; Chowdary, Tirumala K.; Griffin, James D.; Sattler, Martin (2011)
      The transforming JAK2V617F kinase is frequently associated with myeloproliferative neoplasms (MPNs) and thought to be instrumental for the overproduction of myeloid lineage cells. Several small molecule drugs targeting ...
    • Mutant Cbl Proteins as Oncogenic Drivers in Myeloproliferative Disorders 

      Naramura, Mayumi; Nadeau, Scott; Mohapatra, Bhopal; Ahmad, Gulzar; Mukhopadhyay, Chandrani; Raja, Srikumar M; Natarajan, Amarnath; Band, Vimla; Band, Hamid; Sattler, Martin (Impact Journals LLC, 2011)
      Casitas B-lineage lymphoma (Cbl) family proteins are evolutionarily-conserved attenuators of protein tyrosine kinase (PTK) signaling. Biochemical analyses over the past two decades have firmly established that the negative ...
    • NADPH oxidases regulate cell growth and migration in myeloid cells transformed by oncogenic tyrosine kinases 

      Reddy, Mamatha M.; Fernandes, Margret S.; Salgia, Ravi; Levine, Ross L.; Griffin, James D.; Sattler, Martin (2014)
      Transformation by tyrosine kinase oncogenes in myeloid malignancies, including BCR-ABL in chronic myeloid leukemia, FLT3ITD in acute myeloid leukemia (AML) or JAK2V617F in myeloproliferative neoplasms (MPN), is associated ...
    • Pathological glycogenesis through glycogen synthase 1 and suppression of excessive AMP kinase activity in myeloid leukemia cells 

      Bhanot, Haymanti; Reddy, Mamatha M.; Nonami, Atsushi; Weisberg, Ellen L.; Bonal, Dennis; Kirschmeier, Paul T.; Salgia, Sabrina; Podar, Klaus; Galinsky, Ilene; Chowdary, Tirumala K.; Neuberg, Donna; Tonon, Giovanni; Stone, Richard M.; Asara, John; Griffin, James D.; Sattler, Martin (2015)
      The rapid proliferation of myeloid leukemia cells is highly dependent on increased glucose metabolism. Through an unbiased metabolomics analysis of leukemia cells, we found that the glycogenic precursor UDP-D-glucose is ...
    • RESCUE OF HIPPO CO-ACTIVATOR YAP1 TRIGGERS DNA DAMAGE-INDUCED APOPTOSIS IN HEMATOLOGICAL CANCERS 

      Cottini, Francesca; Hideshima, Teru; Xu, Chunxiao; Sattler, Martin; Dori, Martina; Agnelli, Luca; Hacken, Elisa ten; Bertilaccio, Maria Teresa; Antonini, Elena; Neri, Antonino; Ponzoni, Maurilio; Marcatti, Magda; Richardson, Paul G.; Carrasco, Ruben; Kimmelman, Alec C.; Wong, Kwok-Kin; Caligaris-Cappio, Federico; Blandino, Giovanni; Kuehl, W. Michael; Anderson, Kenneth C.; Tonon, Giovanni (2014)
      Oncogene–induced DNA damage elicits genomic instability in epithelial cancer cells, but apoptosis is blocked through inactivation of the tumor suppressor p53. In hematological cancers, the relevance of ongoing DNA damage ...
    • Selective Akt Inhibitors Synergize with Tyrosine Kinase Inhibitors and Effectively Override Stroma-Associated Cytoprotection of Mutant FLT3-Positive AML Cells 

      Weisberg, Ellen; Liu, Qingsong; Zhang, Xin; Nelson, Erik; Sattler, Martin; Liu, Feiyang; Nicolais, Maria; Zhang, Jianming; Mitsiades, Constantine S; Smith, Robert Walsh; Stone, Richard; Galinsky, Ilene; Nonami, Atsushi; Griffin, James D.; Gray, Nathanael (Public Library of Science, 2013)
      Objectives: Tyrosine kinase inhibitor (TKI)-treated acute myeloid leukemia (AML) patients commonly show rapid and significant peripheral blood blast cell reduction, however a marginal decrease in bone marrow blasts. This ...
    • Structure of a pseudokinase domain switch that controls oncogenic activation of Jak kinases 

      Toms, Angela V.; Deshpande, Anagha; McNally, Randall; Jeong, Youngjee; Rogers, Julia M.; Kim, Chae Un; Gruner, Sol M.; Ficarro, Scott B.; Marto, Jarrod A.; Sattler, Martin; Griffin, James D.; Eck, Michael J. (2013)
      The V617F mutation in the Jak2 pseudokinase domain causes myeloproliferative neoplasms, and the equivalent mutation in Jak1 (V658F) is found in T-cell leukemias. Crystal structures of wild type and V658F mutant human Jak1 ...