JEFFREY E SETTLEMAN

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi request reprint Inhibition of mutant EGF receptors by gefitinib: targeting an Achilles' heel of lung cancer
    Jeffrey Settleman
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Department of Medicine, Harvard Medical School, Charlestown, USA
    Cell Cycle 3:1496-7. 2004
  2. ncbi request reprint A memory GAP
    Jeffrey Settleman
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Trends Neurosci 26:285-7. 2003
  3. pmc Discovering tumor suppressor genes through genome-wide copy number analysis
    S Michael Rothenberg
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149, 13th Street, Charlestown, MA 02129, USA
    Curr Genomics 11:297-310. 2010
  4. pmc Haploinsufficiency for p190B RhoGAP inhibits MMTV-Neu tumor progression
    Brandy M Heckman-Stoddard
    Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
    Breast Cancer Res 11:R61. 2009
  5. pmc Integrating complex genomic datasets and tumour cell sensitivity profiles to address a 'simple' question: which patients should get this drug?
    Cyril Benes
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    BMC Med 7:78. 2009
  6. pmc Rho-kinase regulates tissue morphogenesis via non-muscle myosin and LIM-kinase during Drosophila development
    Valerie Verdier
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    BMC Dev Biol 6:38. 2006
  7. ncbi request reprint Rac 'n Rho: the music that shapes a developing embryo
    J Settleman
    Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Dev Cell 1:321-31. 2001
  8. doi request reprint Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK)
    Jeff Settleman
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Charlestown, MA, USA
    Semin Oncol 36:S36-41. 2009
  9. ncbi request reprint Intercalating Arabidopsis leaf cells: a jigsaw puzzle of lobes, necks, ROPs, and RICs
    Jeffrey Settleman
    MGH Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Cell 120:570-2. 2005
  10. doi request reprint A therapeutic opportunity in melanoma: ErbB4 makes a mark on skin
    Jeff Settleman
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Cancer Cell 16:278-9. 2009

Research Grants

  1. Gefitinib-sensitive EGF receptor mutants in lung cancer
    Jeffrey Settleman; Fiscal Year: 2009
  2. RHO GTPASE SIGNALING IN EMBRYO MORPHOGENESIS
    Jeffrey Settleman; Fiscal Year: 2003
  3. FASEB Summer Research Conference on Small G-Proteins
    Jeffrey Settleman; Fiscal Year: 2004
  4. Regulation and Functin of the p190 RhoGAPs
    Jeffrey Settleman; Fiscal Year: 2006
  5. Specific Biochemical Inactivation of Oncogenic Ras
    Jeffrey Settleman; Fiscal Year: 2008

Collaborators

Detail Information

Publications49

  1. ncbi request reprint Inhibition of mutant EGF receptors by gefitinib: targeting an Achilles' heel of lung cancer
    Jeffrey Settleman
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Department of Medicine, Harvard Medical School, Charlestown, USA
    Cell Cycle 3:1496-7. 2004
    ..In addition, the catalytic function of the mutant receptors exhibits increased sensitivity to Gefitinib, raising the possibility that two distinct consequences of Gefitinib action account for its clinical efficacy...
  2. ncbi request reprint A memory GAP
    Jeffrey Settleman
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Trends Neurosci 26:285-7. 2003
    ..A recent report has revealed that the Rho GTPase and its regulator p190 Rho-GTPase-activating protein (p190 RhoGAP) also play an important regulatory role in fear memory formation...
  3. pmc Discovering tumor suppressor genes through genome-wide copy number analysis
    S Michael Rothenberg
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149, 13th Street, Charlestown, MA 02129, USA
    Curr Genomics 11:297-310. 2010
    ..Here, we review the application of genome-wide copy number analysis to the specific problem of identifying tumor suppressor genes...
  4. pmc Haploinsufficiency for p190B RhoGAP inhibits MMTV-Neu tumor progression
    Brandy M Heckman-Stoddard
    Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA
    Breast Cancer Res 11:R61. 2009
    ..P190B is required for mammary gland morphogenesis, and overexpression of p190B in the mammary gland induces hyperplastic lesions. Hence, we hypothesized that p190B may play a pivotal role in mammary tumorigenesis...
  5. pmc Integrating complex genomic datasets and tumour cell sensitivity profiles to address a 'simple' question: which patients should get this drug?
    Cyril Benes
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    BMC Med 7:78. 2009
    ..See the associated research paper by Kuo et al: http://www.biomedcentral.com/1741-7015/7/77...
  6. pmc Rho-kinase regulates tissue morphogenesis via non-muscle myosin and LIM-kinase during Drosophila development
    Valerie Verdier
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    BMC Dev Biol 6:38. 2006
    ..Indeed, in Drosophila, a single ROCK ortholog, DRok, has been identified and has been found to be required for establishing planar cell polarity...
  7. ncbi request reprint Rac 'n Rho: the music that shapes a developing embryo
    J Settleman
    Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Dev Cell 1:321-31. 2001
    ..The Drosophila genetic system has proved particularly useful in establishing the in vivo functions of several of the Rho GTPases and their associated signaling pathway components during development...
  8. doi request reprint Cell culture modeling of genotype-directed sensitivity to selective kinase inhibitors: targeting the anaplastic lymphoma kinase (ALK)
    Jeff Settleman
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Charlestown, MA, USA
    Semin Oncol 36:S36-41. 2009
    ..Such findings suggest that genotype-based stratification of cancer patients for treatment with selective kinase inhibitors, even across multiple diseases of distinct tissue origin, may be essential for maximizing their clinical benefit...
  9. ncbi request reprint Intercalating Arabidopsis leaf cells: a jigsaw puzzle of lobes, necks, ROPs, and RICs
    Jeffrey Settleman
    MGH Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Cell 120:570-2. 2005
    ....
  10. doi request reprint A therapeutic opportunity in melanoma: ErbB4 makes a mark on skin
    Jeff Settleman
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Cancer Cell 16:278-9. 2009
    ..These tumor cells exhibit ErbB4 dependency, suggesting that ErbB4 kinase inhibition may constitute an effective therapeutic strategy in this setting...
  11. ncbi request reprint PAK-in' up cGMP for the move
    Jeffrey Settleman
    MGH Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Cell 128:237-8. 2007
    ....
  12. ncbi request reprint Thy-1 regulates fibroblast focal adhesions, cytoskeletal organization and migration through modulation of p190 RhoGAP and Rho GTPase activity
    Thomas H Barker
    Department of Medicine, The University of Alabama at Birmingham, Birmingham, AL 35294, USA
    Exp Cell Res 295:488-96. 2004
    ..We therefore conclude that Thy-1 surface expression regulates fibroblast focal adhesions, cytoskeletal organization and migration by modulating the activity of p190 RhoGAP and Rho GTPase...
  13. ncbi request reprint Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways
    Raffaella Sordella
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, Building 149, 13th Street, Charlestown, MA 02129, USA
    Science 305:1163-7. 2004
    ..Thus, mutant EGFRs selectively transduce survival signals on which NSCLCs become dependent; inhibition of those signals by gefitinib may contribute to the drug's efficacy...
  14. pmc Drosophila Rho-kinase (DRok) is required for tissue morphogenesis in diverse compartments of the egg chamber during oogenesis
    Valerie Verdier
    Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA 02129, USA
    Dev Biol 297:417-32. 2006
    ....
  15. pmc Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib
    Eunice L Kwak
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 102:7665-70. 2005
    ..Our findings suggest that one of these, HKI-272, may prove highly effective in the treatment of EGFR-mutant NSCLCs, including tumors that have become resistant to gefitinib or erlotinib...
  16. ncbi request reprint Modulation of CREB activity by the Rho GTPase regulates cell and organism size during mouse embryonic development
    Raffaella Sordella
    MGH Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Dev Cell 2:553-65. 2002
    ..Together, these results suggest that activity of the Rho GTPase modulates a signal from insulin/IGFs to CREB that determines cell size and animal size during embryogenesis...
  17. doi request reprint The T790M "gatekeeper" mutation in EGFR mediates resistance to low concentrations of an irreversible EGFR inhibitor
    Nadia Godin-Heymann
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Mol Cancer Ther 7:874-9. 2008
    ..Our findings suggest that HKI-272 treatment at maximally tolerated dosing may lead to the emergence of T790M-mediated resistance, whereas treatment with a more potent irreversible inhibitor could yield a resistance mutation at EGFR C797...
  18. ncbi request reprint Epidermal growth factor receptor mutants from human lung cancers exhibit enhanced catalytic activity and increased sensitivity to gefitinib
    Roseann Mulloy
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Cancer Res 67:2325-30. 2007
    ....
  19. doi request reprint First-line gefitinib in patients with advanced non-small-cell lung cancer harboring somatic EGFR mutations
    Lecia V Sequist
    Massachusetts General Hospital Cancer Center, 32 Fruit St, Yawkey Suite 7B, Boston, MA 02114, USA
    J Clin Oncol 26:2442-9. 2008
    ..The multicenter iTARGET trial prospectively examined first-line gefitinib in advanced NSCLC patients harboring EGFR mutations and explored the significance of EGFR mutation subtypes and TKI resistance mechanisms...
  20. ncbi request reprint Modulation of Rho GTPase signaling regulates a switch between adipogenesis and myogenesis
    Raffaella Sordella
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Cell 113:147-58. 2003
    ..Together, these results identify the Rho GTPase as an essential modulator of IGF-1 signals that direct the adipogenesis-myogenesis cell fate decision...
  21. pmc Reduced Erlotinib sensitivity of epidermal growth factor receptor-mutant non-small cell lung cancer following cisplatin exposure: a cell culture model of second-line erlotinib treatment
    Tan Min Chin
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Clin Cancer Res 14:6867-76. 2008
    ..NSCLC-derived cell lines have provided a powerful system for modeling EGFR mutation-correlated sensitivity to EGFR inhibitors and for modeling mechanisms of acquired drug resistance that are observed clinically...
  22. ncbi request reprint GAPs in growth factor signalling
    Andre Bernards
    Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA
    Growth Factors 23:143-9. 2005
    ..Here, some of these mechanisms of GAP regulation in the context of signaling responses to growth factors are reviewed...
  23. ncbi request reprint Overcoming acquired resistance to Iressa/Tarceva with inhibitors of a different class
    Daniel A Haber
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Cell Cycle 4:1057-9. 2005
    ....
  24. ncbi request reprint An FF domain-dependent protein interaction mediates a signaling pathway for growth factor-induced gene expression
    Wei Jiang
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Mol Cell 17:23-35. 2005
    ..These findings reveal a pathway by which mitogens promote gene transcription and indicate a role for FF domains in phosphorylation-mediated signal transduction...
  25. doi request reprint High-throughput lung cancer cell line screening for genotype-correlated sensitivity to an EGFR kinase inhibitor
    Ultan McDermott
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts, USA
    Methods Enzymol 438:331-41. 2008
    ....
  26. pmc Modeling oncogene addiction using RNA interference
    S Michael Rothenberg
    Massachusetts General Hospital Cancer Center, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 105:12480-4. 2008
    ..Quantitative "oncogene rescue" analysis allows mechanistic dissection of oncogene addiction, and, when broadly applied, may provide functional validation for potential therapeutic targets identified through large-scale RNAi screens...
  27. doi request reprint ErbBs in lung cancer
    Sreenath V Sharma
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Exp Cell Res 315:557-71. 2009
    ....
  28. pmc Oncogenic activity of epidermal growth factor receptor kinase mutant alleles is enhanced by the T790M drug resistance mutation
    Nadia Godin-Heymann
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Cancer Res 67:7319-26. 2007
    ....
  29. ncbi request reprint Drugging the bad "AKT-TOR" to overcome TKI-resistant lung cancer
    Jeffrey Settleman
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Cancer Cell 12:6-8. 2007
    ..However, combining HKI-272 with rapamycin promoted rapid tumor regression, suggesting a therapeutic strategy to overcome drug resistance...
  30. ncbi request reprint Rho-LIM kinase signaling regulates ecdysone-induced gene expression and morphogenesis during Drosophila metamorphosis
    Guang Chao Chen
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Curr Biol 14:309-13. 2004
    ..Together, these findings indicate a link between Rho-LIMK signaling and steroid hormone-induced gene expression in the context of metamorphosis and thereby establish a novel role for the Rho GTPase in development...
  31. ncbi request reprint Tension precedes commitment-even for a stem cell
    Jeffrey Settleman
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Mol Cell 14:148-50. 2004
    ..An article in the April issue of Developmental Cell demonstrates that lineage commitment by mesenchymal stem cells is regulated by shape-induced changes in Rho GTPase activity and cytoskeletal tension...
  32. ncbi request reprint Epidermal growth factor receptor mutations in lung cancer
    Sreenath V Sharma
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA
    Nat Rev Cancer 7:169-81. 2007
    ....
  33. ncbi request reprint A nuclear MAL-function links Rho to SRF
    Jeffrey Settleman
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Mol Cell 11:1121-3. 2003
    ..2003)...
  34. pmc Regulation of Rho and Rac signaling to the actin cytoskeleton by paxillin during Drosophila development
    Guang Chao Chen
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Mol Cell Biol 25:979-87. 2005
    ..Taken together, these data indicate the importance of paxillin modulation of Rho family GTPases during development and identify the LIMK pathway as a critical target of paxillin-mediated Rho regulation...
  35. ncbi request reprint Specific biochemical inactivation of oncogenic Ras proteins by nucleoside diphosphate kinase
    Michael A Fischbach
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Cancer Res 63:4089-94. 2003
    ..Moreover, the results suggest that the loss of NM23 expression that is commonly observed during tumor progression could lead to increased potency of oncogenic Ras proteins...
  36. ncbi request reprint GAP control: regulating the regulators of small GTPases
    Andre Bernards
    MGH Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Trends Cell Biol 14:377-85. 2004
    ..So far, findings suggest that GAP activity is regulated by several mechanisms, including protein-protein interactions, phospholipid interactions, phosphorylation, subcellular translocation and proteolytic degradation...
  37. pmc Ligand-dependent platelet-derived growth factor receptor (PDGFR)-alpha activation sensitizes rare lung cancer and sarcoma cells to PDGFR kinase inhibitors
    Ultan McDermott
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Cancer Res 69:3937-46. 2009
    ..These findings suggest that, in addition to gastrointestinal stromal tumors, rare tumors that show PDGFC-mediated PDGFRA activation may also be clinically responsive to pharmacologic PDGFRA or PDGFC inhibition...
  38. ncbi request reprint The Drosophila ATM ortholog, dATM, mediates the response to ionizing radiation and to spontaneous DNA damage during development
    Young Han Song
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th St, Charlestown, MA 02129, USA
    Curr Biol 14:1354-9. 2004
    ....
  39. pmc Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer
    Eunice L Kwak
    Massachusetts General Hospital Cancer Center, Boston, MA 02114, USA
    N Engl J Med 363:1693-703. 2010
    ..We explored the therapeutic efficacy of inhibiting ALK in such tumors in an early-phase clinical trial of crizotinib (PF-02341066), an orally available small-molecule inhibitor of the ALK tyrosine kinase...
  40. pmc Elevated CRAF as a potential mechanism of acquired resistance to BRAF inhibition in melanoma
    Clara Montagut
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, Massachusetts, USA
    Cancer Res 68:4853-61. 2008
    ..Geldanamycin effectively promotes the degradation of CRAF, thereby revealing a potential therapeutic strategy to overcome resistance to RAF inhibition in a subset of BRAF mutant tumors...
  41. ncbi request reprint GEFs in growth factor signaling
    Andre Bernards
    Harvard Medical School and Massachusetts General Hospital, Center for Cancer Research, Charlestown, MA 02129, USA
    Growth Factors 25:355-61. 2007
    ..In this companion review, we highlight recent findings relating to the regulation of another major class of Ras superfamily regulatory proteins, the guanine nucleotide exchange factors...
  42. doi request reprint Acquired resistance to tyrosine kinase inhibitors during cancer therapy
    Jeffrey A Engelman
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, MA 02129, USA
    Curr Opin Genet Dev 18:73-9. 2008
    ....
  43. pmc A rho-binding protein kinase C-like activity is required for the function of protein kinase N in Drosophila development
    Martha Betson
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    Genetics 176:2201-12. 2007
    ..Interestingly, we also identified a requirement for Pkn in wing morphogenesis, thereby revealing the first postembryonic function for Pkn...
  44. doi request reprint Genomic alterations of anaplastic lymphoma kinase may sensitize tumors to anaplastic lymphoma kinase inhibitors
    Ultan McDermott
    Center for Molecular Therapeutics, Massachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, MA 02129, USA
    Cancer Res 68:3389-95. 2008
    ..These findings suggest that a subset of lung cancers, lymphomas, and neuroblastomas that harbor genomic ALK alterations may be clinically responsive to pharmacologic ALK inhibition...
  45. pmc A common signaling cascade may underlie "addiction" to the Src, BCR-ABL, and EGF receptor oncogenes
    Sreenath V Sharma
    Massachusetts General Hospital Cancer Center and Harvard Medical School, 149 13th Street, Charlestown, Massachusetts 02129, USA
    Cancer Cell 10:425-35. 2006
    ..Moreover, these observations implicate a common profile of signal attenuation for multiple oncogenes and suggest that "addiction" associated with apoptosis reflects an active rather than a passive process...
  46. pmc p190A RhoGAP is a glycogen synthase kinase-3-beta substrate required for polarized cell migration
    Wei Jiang
    Massachusetts General Hospital Cancer Center and Harvard Medical School, Charlestown, MA 02129, USA
    J Biol Chem 283:20978-88. 2008
    ..These studies identify p190A as a novel GSK-3beta substrate and reveal a mechanism by which GSK-3beta contributes to cellular polarization in directionally migrating cells via effects on Rho GTPase activity...
  47. pmc Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752
    Gromoslaw A Smolen
    Cancer Center and Department of Pathology, Molecular Pathology Research Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA
    Proc Natl Acad Sci U S A 103:2316-21. 2006
    ..MET amplification may thus identify a subset of epithelial cancers that are uniquely sensitive to disruption of this pathway and define a patient group that is appropriate for clinical trials of targeted therapy using MET inhibitors...
  48. pmc Detection of mutations in EGFR in circulating lung-cancer cells
    Shyamala Maheswaran
    Massachusetts General Hospital Cancer Center, Boston 02129, USA
    N Engl J Med 359:366-77. 2008
    ..Molecular characterization of circulating tumor cells may provide a strategy for noninvasive serial monitoring of tumor genotypes during treatment...
  49. doi request reprint Case records of the Massachusetts General Hospital. Case 23-2008. A 26-year-old man with back pain and a mass in the lung
    Lecia V Sequist
    Cancer Center, Massachusetts General Hospital, USA
    N Engl J Med 359:405-14. 2008

Research Grants5

  1. Gefitinib-sensitive EGF receptor mutants in lung cancer
    Jeffrey Settleman; Fiscal Year: 2009
    ....
  2. RHO GTPASE SIGNALING IN EMBRYO MORPHOGENESIS
    Jeffrey Settleman; Fiscal Year: 2003
    ..abstract_text> ..
  3. FASEB Summer Research Conference on Small G-Proteins
    Jeffrey Settleman; Fiscal Year: 2004
    ..The conference will cover the biochemical, structural, and functional aspects of the various small GTPases and their regulators and targets. ..
  4. Regulation and Functin of the p190 RhoGAPs
    Jeffrey Settleman; Fiscal Year: 2006
    ..This is an important step toward establishing an accurate picture of the regulatory mechanisms for small GTPases in vivo, and the nature of their dysregulation in human cancers. ..
  5. Specific Biochemical Inactivation of Oncogenic Ras
    Jeffrey Settleman; Fiscal Year: 2008
    ..Together, the proposed studies are expected to lead to the eventual development of a novel therapeutic approach for achieving specific targeting of human tumors that harbor oncogenic mutant forms of Ras. ..