Alice C Fan
Affiliation: Stanford University
- Treatment of higher risk myelodysplastic syndrome patients unresponsive to hypomethylating agents with ON 01910.NaMahesh 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...
- Real-time nanoscale proteomic analysis of the novel multi-kinase pathway inhibitor rigosertib to measure the response to treatment of cancerAlice 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...
- A quantitative PCR method to detect blood microRNAs associated with tumorigenesis in transgenic miceAlice 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...
- CD4(+) T cells contribute to the remodeling of the microenvironment required for sustained tumor regression upon oncogene inactivationKavya 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...
- Nanofluidic proteomic assay for serial analysis of oncoprotein activation in clinical specimensAlice 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...
- Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomasPhuoc 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...
- Inhibition of HMGcoA reductase by atorvastatin prevents and reverses MYC-induced lymphomagenesisCatherine 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...
- Cellular senescence is an important mechanism of tumor regression upon c-Myc inactivationChi 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...
- Alteration of the lipid profile in lymphomas induced by MYC overexpressionLivia S Eberlin
Department of Chemistry, Stanford University, Stanford, CA 94305 5080
Proc Natl Acad Sci U S A 111:10450-5. 2014..Our results suggest a relationship between the appearance of specific lipid species and the overexpression of MYC in lymphomas. ..
- Sustained regression of tumors upon MYC inactivation requires p53 or thrombospondin-1 to reverse the angiogenic switchSylvie 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...
- "Picolog," a synthetically-available bryostatin analog, inhibits growth of MYC-induced lymphoma in vivoBrian 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...
- Definition of an enhanced immune cell therapy in mice that can target stem-like lymphoma cellsChristopher 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...
- Apoptosis-stimulating protein of p53 (ASPP2) heterozygous mice are tumor-prone and have attenuated cellular damage-response thresholdsKerstin 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....
- Conditional animal models: a strategy to define when oncogenes will be effective targets to treat cancerSylvie 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...