Alice C Fan

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. pmc Treatment of higher risk myelodysplastic syndrome patients unresponsive to hypomethylating agents with ON 01910.Na
    Mahesh Seetharam
    Department of Medicine Hematology, Stanford University Cancer Center, Stanford, CA, USA
    Leuk Res 36:98-103. 2012
  2. ncbi request reprint Real-time nanoscale proteomic analysis of the novel multi-kinase pathway inhibitor rigosertib to measure the response to treatment of cancer
    Alice C Fan
    Stanford University School of Medicine, Division of Oncology, Departments of Medicine and Pathology, Stanford, CA, USA
    Expert Opin Investig Drugs 22:1495-509. 2013
  3. pmc A quantitative PCR method to detect blood microRNAs associated with tumorigenesis in transgenic mice
    Alice C Fan
    Stanford University, School of Medicine, Division of Oncology, Department of Medicine, Stanford, CA 94305 5151, USA
    Mol Cancer 7:74. 2008
  4. pmc CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation
    Kavya Rakhra
    Division of Oncology, Departments of Medicine, Pathology and Molecular Imaging, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cancer Cell 18:485-98. 2010
  5. ncbi request reprint Nanofluidic proteomic assay for serial analysis of oncoprotein activation in clinical specimens
    Alice C Fan
    Stanford University, Departments of Medicine and Pathology, California, USA
    Nat Med 15:566-71. 2009
  6. pmc Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas
    Phuoc T Tran
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 3:e2125. 2008
  7. pmc Inhibition of HMGcoA reductase by atorvastatin prevents and reverses MYC-induced lymphomagenesis
    Catherine M Shachaf
    Division of Medical Oncology, Department of Medicine, Stanford University, Stanford, CA 94305 5151, USA
    Blood 110:2674-84. 2007
  8. pmc Cellular senescence is an important mechanism of tumor regression upon c-Myc inactivation
    Chi Hwa Wu
    Department of Medicine, Division of Oncology, Stanford University School of Medicine, CA 94305, USA
    Proc Natl Acad Sci U S A 104:13028-33. 2007
  9. pmc Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switch
    Sylvie Giuriato
    Departments of Medicine and Pathology, Division of Oncology, Stanford University School of Medicine, CCSR Building, Room 1120, 269 Campus Drive, Stanford, CA 94305 5151, USA
    Proc Natl Acad Sci U S A 103:16266-71. 2006
  10. pmc "Picolog," a synthetically-available bryostatin analog, inhibits growth of MYC-induced lymphoma in vivo
    Brian A DeChristopher
    Departments of Chemistry and Chemical and Systems Biology, Stanford University, Stanford, CA 94305 5080
    Oncotarget 3:58-66. 2012

Collaborators

Detail Information

Publications13

  1. pmc Treatment of higher risk myelodysplastic syndrome patients unresponsive to hypomethylating agents with ON 01910.Na
    Mahesh Seetharam
    Department of Medicine Hematology, Stanford University Cancer Center, Stanford, CA, USA
    Leuk Res 36:98-103. 2012
    ..These data demonstrate encouraging efficacy and drug tolerance with ON 01910.Na treatment of higher risk MDS patients...
  2. ncbi request reprint Real-time nanoscale proteomic analysis of the novel multi-kinase pathway inhibitor rigosertib to measure the response to treatment of cancer
    Alice C Fan
    Stanford University School of Medicine, Division of Oncology, Departments of Medicine and Pathology, Stanford, CA, USA
    Expert Opin Investig Drugs 22:1495-509. 2013
    ..Moreover, rigosertib has potential clinical activity in a multitude of solid tumors...
  3. pmc A quantitative PCR method to detect blood microRNAs associated with tumorigenesis in transgenic mice
    Alice C Fan
    Stanford University, School of Medicine, Division of Oncology, Department of Medicine, Stanford, CA 94305 5151, USA
    Mol Cancer 7:74. 2008
    ..Our results suggest that specific changes in blood miRNA can be detected during tumorigenesis and tumor regression...
  4. pmc CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivation
    Kavya Rakhra
    Division of Oncology, Departments of Medicine, Pathology and Molecular Imaging, Stanford University School of Medicine, Stanford, CA 94305, USA
    Cancer Cell 18:485-98. 2010
    ..Hence, CD4(+) T cells are required for the remodeling of the tumor microenvironment through the expression of chemokines, such as thrombospondins, in order to elicit oncogene addiction...
  5. ncbi request reprint Nanofluidic proteomic assay for serial analysis of oncoprotein activation in clinical specimens
    Alice C Fan
    Stanford University, Departments of Medicine and Pathology, California, USA
    Nat Med 15:566-71. 2009
    ..Therefore, we have described a new and highly sensitive method for determining oncoprotein expression and phosphorylation in clinical specimens for the development of new therapeutics for cancer...
  6. pmc Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas
    Phuoc T Tran
    Department of Radiation Oncology, Stanford University School of Medicine, Stanford, California, United States of America
    PLoS ONE 3:e2125. 2008
    ..However, most cancers are caused by multiple genetic events making it difficult to determine which oncogenes or combination of oncogenes will be the most effective targets for their treatment...
  7. pmc Inhibition of HMGcoA reductase by atorvastatin prevents and reverses MYC-induced lymphomagenesis
    Catherine M Shachaf
    Division of Medical Oncology, Department of Medicine, Stanford University, Stanford, CA 94305 5151, USA
    Blood 110:2674-84. 2007
    ..Thus, atorvastatin, by inhibiting HMGcoA reductase, induces changes in phosphoprotein signaling that in turn prevent MYC-induced lymphomagenesis...
  8. pmc Cellular senescence is an important mechanism of tumor regression upon c-Myc inactivation
    Chi Hwa Wu
    Department of Medicine, Division of Oncology, Stanford University School of Medicine, CA 94305, USA
    Proc Natl Acad Sci U S A 104:13028-33. 2007
    ..Our results suggest that cellular senescence programs remain latently functional, even in established tumors, and can become reactivated, serving as a critical mechanism of oncogene addiction associated with MYC inactivation...
  9. pmc Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switch
    Sylvie Giuriato
    Departments of Medicine and Pathology, Division of Oncology, Stanford University School of Medicine, CCSR Building, Room 1120, 269 Campus Drive, Stanford, CA 94305 5151, USA
    Proc Natl Acad Sci U S A 103:16266-71. 2006
    ..Therefore, the combined inactivation of oncogenes and angiogenesis may be a more clinically effective treatment of cancer. We conclude that angiogenesis is an essential component of oncogene addiction...
  10. pmc "Picolog," a synthetically-available bryostatin analog, inhibits growth of MYC-induced lymphoma in vivo
    Brian A DeChristopher
    Departments of Chemistry and Chemical and Systems Biology, Stanford University, Stanford, CA 94305 5080
    Oncotarget 3:58-66. 2012
    ..We provide the first in vivo validation that the bryostatin analog, picolog, is a potential therapeutic agent for the treatment of cancer and other diseases...
  11. pmc Definition of an enhanced immune cell therapy in mice that can target stem-like lymphoma cells
    Christopher H Contag
    Department of Pediatrics, Stanford University, Stanford, California, USA
    Cancer Res 70:9837-45. 2010
    ..Our approach offers a potentially powerful new way to clear residual cancer cells, showing how restoring immune surveillance is critical for maintenance of a disease-free state...
  12. pmc Apoptosis-stimulating protein of p53 (ASPP2) heterozygous mice are tumor-prone and have attenuated cellular damage-response thresholds
    Kerstin M Kampa
    Department of Medicine, Division of Hematology and Medical Oncology, Oregon Health and Science University, Portland, OR 97239, USA
    Proc Natl Acad Sci U S A 106:4390-5. 2009
    ....
  13. ncbi request reprint Conditional animal models: a strategy to define when oncogenes will be effective targets to treat cancer
    Sylvie Giuriato
    Division of Oncology, Stanford University, CCSR 1105, 269 Campus Drive, Stanford, CA 94305 5151, USA
    Semin Cancer Biol 14:3-11. 2004
    ..Thus, these animal models will be useful to define the specific genes that will be therapeutically useful to target for the treatment of particular human cancers...