Roger S Lo

Summary

Affiliation: University of California
Country: USA

Publications

  1. pmc Melanoma whole-exome sequencing identifies (V600E)B-RAF amplification-mediated acquired B-RAF inhibitor resistance
    Hubing Shi
    Division of Dermatology, Department of Medicine, University of California, Los Angeles, 52 121 CHS, 10833 Le Conte Avenue, California 90095 1750, USA
    Nat Commun 3:724. 2012
  2. doi request reprint Melanoma prognostics and personalized therapeutics at a crossroad
    Roger S Lo
    Department of Medicine, Division of Dermatology, David Geffen School of Medicine, University of California, Jonsson Comprehensive Cancer Center, Los Angeles, California 90095, USA
    J Invest Dermatol 133:292-5. 2013
  3. pmc Future perspectives in melanoma research. Meeting report from the "Melanoma Bridge. Napoli, December 2nd-4th 2012"
    Paolo A Ascierto
    Istituto Nazionale Tumori, Fondazione G, Pascale, Naples, Italy
    J Transl Med 11:137. 2013
  4. doi request reprint Transforming growth factor-beta activation promotes genetic context-dependent invasion of immortalized melanocytes
    Roger S Lo
    Division of Dermatology Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California, USA
    Cancer Res 68:4248-57. 2008
  5. pmc Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation
    Ramin Nazarian
    Division of Dermatology Department of Medicine, UCLA s Jonsson Comprehensive Cancer Center, 52 121 CHS, Los Angeles, California 90095 1750, USA
    Nature 468:973-7. 2010
  6. pmc Preexisting MEK1 exon 3 mutations in V600E/KBRAF melanomas do not confer resistance to BRAF inhibitors
    Hubing Shi
    Division of Dermatology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095 1750, USA
    Cancer Discov 2:414-24. 2012
  7. pmc Reversing melanoma cross-resistance to BRAF and MEK inhibitors by co-targeting the AKT/mTOR pathway
    Mohammad Atefi
    Department of Medicine, Division of Hematology Oncology, University of California Los Angeles, Los Angeles, California, United States of America
    PLoS ONE 6:e28973. 2011
  8. pmc Combination therapy with vemurafenib (PLX4032/RG7204) and metformin in melanoma cell lines with distinct driver mutations
    Franziska Niehr
    Department of Medicine, Division of Hematology Oncology, University of California Los Angeles UCLA, USA
    J Transl Med 9:76. 2011
  9. pmc Combinatorial treatments that overcome PDGFRβ-driven resistance of melanoma cells to V600EB-RAF inhibition
    Hubing Shi
    Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA
    Cancer Res 71:5067-74. 2011
  10. pmc Acquired resistance and clonal evolution in melanoma during BRAF inhibitor therapy
    Hubing Shi
    1Division of Dermatology, Department of Medicine, 2Division of Surgical Oncology, Department of Surgery, 3Division of Hematology and Oncology, Department of Medicine 4Jonsson Comprehensive Cancer Center 5Department of Molecular and Medical Pharmacology 6David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California Departments of 7Medicine, 8Cancer Biology, and 9Surgery, 10Vanderbilt Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee 11Melanoma Institute of Australia, Westmead Millennium Institute, Westmead Hospital, University of Sydney, Sydney, New South Wales, Australia and 12Ludwig Institute for Cancer Research, Brussels Branch, Belgium
    Cancer Discov 4:80-93. 2014

Collaborators

Detail Information

Publications16

  1. pmc Melanoma whole-exome sequencing identifies (V600E)B-RAF amplification-mediated acquired B-RAF inhibitor resistance
    Hubing Shi
    Division of Dermatology, Department of Medicine, University of California, Los Angeles, 52 121 CHS, 10833 Le Conte Avenue, California 90095 1750, USA
    Nat Commun 3:724. 2012
    ..Thus, alternative clinical strategies may potentially overcome distinct modes of extracellular signal-regulated kinase reactivation underlying acquired B-RAF inhibitor resistance in melanoma...
  2. doi request reprint Melanoma prognostics and personalized therapeutics at a crossroad
    Roger S Lo
    Department of Medicine, Division of Dermatology, David Geffen School of Medicine, University of California, Jonsson Comprehensive Cancer Center, Los Angeles, California 90095, USA
    J Invest Dermatol 133:292-5. 2013
    ..Emerging evidence points to these predictive biomarkers doubling as prognostic biomarkers for high-risk stage III patients, promising to help stratify these patients for the application of novel adjuvant therapies...
  3. pmc Future perspectives in melanoma research. Meeting report from the "Melanoma Bridge. Napoli, December 2nd-4th 2012"
    Paolo A Ascierto
    Istituto Nazionale Tumori, Fondazione G, Pascale, Naples, Italy
    J Transl Med 11:137. 2013
    ....
  4. doi request reprint Transforming growth factor-beta activation promotes genetic context-dependent invasion of immortalized melanocytes
    Roger S Lo
    Division of Dermatology Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California, USA
    Cancer Res 68:4248-57. 2008
    ..Evidence of genetic interactions among PTEN deficiency, Braf activation, and cell autonomous TGF-beta activation shows that distinct stages of human melanoma are genetically tractable in the proper tissue architecture...
  5. pmc Melanomas acquire resistance to B-RAF(V600E) inhibition by RTK or N-RAS upregulation
    Ramin Nazarian
    Division of Dermatology Department of Medicine, UCLA s Jonsson Comprehensive Cancer Center, 52 121 CHS, Los Angeles, California 90095 1750, USA
    Nature 468:973-7. 2010
    ....
  6. pmc Preexisting MEK1 exon 3 mutations in V600E/KBRAF melanomas do not confer resistance to BRAF inhibitors
    Hubing Shi
    Division of Dermatology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California 90095 1750, USA
    Cancer Discov 2:414-24. 2012
    ..Thus, activating MEK1 exon 3 mutations identified herein and concurrent with V600E/KBRAF do not cause BRAFi resistance in melanoma...
  7. pmc Reversing melanoma cross-resistance to BRAF and MEK inhibitors by co-targeting the AKT/mTOR pathway
    Mohammad Atefi
    Department of Medicine, Division of Hematology Oncology, University of California Los Angeles, Los Angeles, California, United States of America
    PLoS ONE 6:e28973. 2011
    ..Clinical trials are in progress using MEK inhibitors following disease progression in patients receiving BRAF inhibitors. However, the PI3K/AKT pathway can also induce resistance to the inhibitors of MAPK pathway...
  8. pmc Combination therapy with vemurafenib (PLX4032/RG7204) and metformin in melanoma cell lines with distinct driver mutations
    Franziska Niehr
    Department of Medicine, Division of Hematology Oncology, University of California Los Angeles UCLA, USA
    J Transl Med 9:76. 2011
    ..A molecular linkage between the MAPK and the LKB1-AMPK energy sensor pathways suggests that combined MAPK oncogene inhibition and metabolic modulation of AMPK would be more effective than either manipulation alone in melanoma cell lines...
  9. pmc Combinatorial treatments that overcome PDGFRβ-driven resistance of melanoma cells to V600EB-RAF inhibition
    Hubing Shi
    Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA, USA
    Cancer Res 71:5067-74. 2011
    ..Together, our findings offer a rational strategy to guide clinical testing in preidentified subsets of patients who relapse during treatment with (V600E)B-RAF inhibitors...
  10. pmc Acquired resistance and clonal evolution in melanoma during BRAF inhibitor therapy
    Hubing Shi
    1Division of Dermatology, Department of Medicine, 2Division of Surgical Oncology, Department of Surgery, 3Division of Hematology and Oncology, Department of Medicine 4Jonsson Comprehensive Cancer Center 5Department of Molecular and Medical Pharmacology 6David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California Departments of 7Medicine, 8Cancer Biology, and 9Surgery, 10Vanderbilt Ingram Cancer Center, Vanderbilt University Medical Center, Nashville, Tennessee 11Melanoma Institute of Australia, Westmead Millennium Institute, Westmead Hospital, University of Sydney, Sydney, New South Wales, Australia and 12Ludwig Institute for Cancer Research, Brussels Branch, Belgium
    Cancer Discov 4:80-93. 2014
    ..Thus, melanoma genomic heterogeneity contributes significantly to BRAF inhibitor treatment failure, implying upfront, cotargeting of two core pathways as an essential strategy for durable responses. ..
  11. ncbi request reprint Detecting mechanisms of acquired BRAF inhibitor resistance in melanoma
    Roger S Lo
    Department of Medicine, Jonsson Comprehensive Cancer Center, David Geffen School of Medicine, University of California, Los Angeles, CA, USA
    Methods Mol Biol 1102:163-74. 2014
    ..In this chapter, we review the major acquired BRAFi resistance mechanisms, highlight their therapeutic implications, and provide the diagnostic methods from clinical samples...
  12. pmc A novel AKT1 mutant amplifies an adaptive melanoma response to BRAF inhibition
    Hubing Shi
    1The Division of Dermatology, Department of Medicine, 2Division of Surgical Oncology, Department of Surgery, 3Division of Hematology and Oncology, Department of Medicine, 4Jonsson Comprehensive Cancer Center, 5Department of Molecular and Medical Pharmacology, 6David Geffen School of Medicine, University of California, Los Angeles, California 7Melanoma Institute of Australia, 8Royal Prince Alfred Hospital, 9Westmead Millennium Institute, and 10Westmead Hospital, University of Sydney, New South Wales, Australia
    Cancer Discov 4:69-79. 2014
    ..In addition, mitogen-activated protein kinase pathway inhibition enhanced clonogenic growth dependency on PI3K or AKT. Thus, adaptive or genetic upregulation of AKT critically participates in melanoma survival during BRAFi therapy. ..
  13. pmc Differential sensitivity of melanoma cell lines with BRAFV600E mutation to the specific Raf inhibitor PLX4032
    Jonas N Søndergaard
    Department of Medicine, Division of Hematology Oncology, University of California Los Angeles, Los Angeles, CA, USA
    J Transl Med 8:39. 2010
    ..In conclusion, BRAFV600E mutant melanoma cell lines displayed a range of sensitivities to PLX4032 and metabolic imaging using PET probes can be used to assess sensitivity...
  14. pmc COX-2 inhibition prevents the appearance of cutaneous squamous cell carcinomas accelerated by BRAF inhibitors
    Helena Escuin-Ordinas
    Department of Medicine Division of Hematology Oncology, David Geffen School of Medicine, University of California Los Angeles UCLA, Los Angeles, CA, USA
    Mol Oncol 8:250-60. 2014
    ....
  15. pmc Glucose deprivation activates a metabolic and signaling amplification loop leading to cell death
    Nicholas A Graham
    Crump Institute for Molecular Imaging, University of California, Los Angeles, CA, USA
    Mol Syst Biol 8:589. 2012
    ..Taken together, these findings illustrate the systems-level cross-talk between metabolism and signaling in the maintenance of cancer cell homeostasis...
  16. pmc Polymer nanofiber-embedded microchips for detection, isolation, and molecular analysis of single circulating melanoma cells
    Shuang Hou
    Department of Molecular and Medical Pharmacology, Crump Institute for Molecular Imaging CIMI, California NanoSystems Institute CNSI, University of California, Los Angeles, 570 Westwood Plaza, Building 114, Los Angeles, CA 90095 1770 USA http www tseng lab com
    Angew Chem Int Ed Engl 52:3379-83. 2013
    ..This method is able to separate CMCs from normal white blood cells (WBCs) and sequence individual cells for a specific mutation related to cancer progression, allowing for more personalized cancer therapy...