Linda Boxer
Academic Appointments
- Professor, Medicine - Hematology
- Member, Bio-X
- Member, Stanford Cancer Institute
Key Documents
Contact Information
-
Clinical Offices
Hematology Clinic 875 Blake Wilbur Dr Clinic C MC 5820 Stanford, CA 94305 Tel Work (650) 498-6000 Fax (650) 723-1269Hematology Clinic 875 Blake Wilbur Dr Clinic C MC 5820 Stanford, CA 94305 Tel Work (650) 498-6000 Fax (650) 723-1269
- Academic Offices
Personal Information Email Tel (650) 723-5057Alternate Contact Pornprang Plangsrisakul Executive Assistant Email Tel Work 650-721-1166Not for medical emergencies or patient use
Professional Overview
Clinical Focus
- Cancer> Hematology
- Hematology
- Multiple Myeloma
- Multiple Myeloma - Medical Oncology
- Plasmacytoma
- Plasmacytoma - Hematology
Administrative Appointments
- Chief, Division of Hematology, Stanford University School of Medicine (2004 - present)
Professional Education
| Fellowship: | Stanford University School of Medicine CA (1990) |
| Fellowship: | Stanford University School of Medicine CA (1989) |
| Residency: | Stanford University School of Medicine CA (1984) |
| Internship: | Stanford University School of Medicine CA (1982) |
| Board Certification: | Medical Oncology, American Board of Internal Medicine (1987) |
| Board Certification: | Internal Medicine, American Board of Internal Medicine (1984) |
Graduate & Fellowship Program Affiliations
Internet Links
Scientific Focus
Current Research Interests
We are studying the transcriptional deregulation of several oncogenes in human hematologic malignancies.
Activation of c-myc in Burkitt's lymphoma: We are examining the transcriptional deregulation of the translocated c-myc gene and the silencing of the normal c-myc gene in Burkitt's lymphoma. We are looking at the c-myc promoter and regions of the immunoglobulin locus that are responsible for the deregulation of the translocated c-myc gene. Several model systems have been designed.
Activation of bcl-2 in hematologic malignancies: In lymphomas with the t(14;18) translocation, the bcl-2 gene is translocated to the immunoglobulin locus and expressed at high levels. We are studying the mechanism of activation at a molecular level in human lymphoma tissue. We have also developed a model system to determine which region of the immunoglobulin locus is responsible for the activation of the translocated bcl-2 gene.
Expression profiling in ALL: We are examining gene expression profiles in acute lymphoblastic leukemia in response to chemotherapeutic agents.
Publications
- The immunoglobulin heavy chain gene 3' enhancers induce Bcl2 deregulation and lymphomagenesis in murine B cells. Leukemia. 2011; (9): 1484-93
- Functional long-range interactions of the IgH 3' enhancers with the bcl-2 promoter region in t(14;18) lymphoma cells. Oncogene. 2008; (53): 6720-8
- Activation of the c-myc p1 promoter in Burkitt's lymphoma by the hs3 immunoglobulin heavy-chain gene enhancer. Leukemia. 2007; (4): 747-53
- Protein/DNA arrays identify nitric oxide-regulated cis-element and trans-factor activities some of which govern neuroblastoma cell viability. Nucleic Acids Res. 2007; (16): 5439-51
- The immunoglobulin heavy-chain gene 3' enhancers deregulate bcl-2 promoter usage in t(14;18) lymphoma cells. Oncogene. 2007; (18): 2635-41
- Oct transcription factors mediate t(14;18) lymphoma cell survival by directly regulating bcl-2 expression. Oncogene. 2006; (6): 888-98
Help