NIH Biosketch available OnlineMichael F. Clarke, M.D.
- Professor, Medicine - Oncology
- Member, Bio-X
- Member, Cancer Center
Contact Information
- Clinical Offices
Oncology 875 Blake Wilbur Dr MC 5826 Stanford, CA 94305 Telephone Work (650) 498-6000 Fax
- Academic Offices
Personal Information Email mfclarke@stanford.edu Tel (650) 498-5852, (650) 725-2495Administrative Contact Nini Gabra Administrative Assistant Email ngabra@stanford.edu Tel Work 650-736-9639Not for medical emergencies or patient use
Clinical Focus
- Colorectal Cancer
- Oncology
- Oncology (Cancer)
Department
- Cancer
Honors and Awards
- Rackham Award, University of Michigan (-)
- American Society of Clinical Investigation, - (-)
- American Association of Physicians, - (-)
Professional Education
- Indiana University School of Medicine (1980) IN
- University Of Missouri (1978) MO
- Indiana University School of Medicine (1977) IN
- M.D., Indiana University (1977)
- B.A., Indiana University (1973)
Postdoctoral Advisees
Industry Relationships
Stanford is committed to ethical and transparent interactions with our industry partners. It is our policy to disclose payments of $5,000 or more, equity valued at $5,000 or more in a publicly traded company, or any equity in a privately held company, to physicians and scientists employed by Stanford University from companies or other commercial entities with which they interact as part of their professional activities.
- Consulting: Oncomed Pharmaceuticals, Inc
- Equity: Oncomed Pharmaceuticals, Inc
Research Interests
Dr. Michael F. Clarke is the Associate Director of the Stanford Institute for Stem Cell and Regenerative Medicine. In addition to his clinical duties in the division of Oncology, Dr. Clarke maintains a laboratory focused on two areas of research: i) the control of self-renewal of normal stem cells and their malignant counterparts; and ii) the identification and characterization of cancer stem cells. A central issue in stem cell biology is to understand the mechanisms that regulate self-renewal of hematopoietic stem cells, which are required for hematopoiesis to persist for the lifetime of the animal. Until recently, the molecular mechanisms that regulate adult stem cell self-renewal were not known. His laboratory recently found that the proto-oncogene Bmi-1 regulates stem cell self-renewal via an epigenetic mechanism. By investigating the pathways upstream and downstream of Bmi1, the laboratory is actively investigating the molecular pathways that regulate self-renewal.
Cancers arise as a result of a series of genetic mutations. A better understanding of the consequences of these mutations on the underlying biology of the neoplastic cells will help to focus the development of more effective therapies. Solid tumors such as breast cancers contain heterogeneous populations of neoplastic cells. Dr. Clarke’s group has developed a technique that allows the isolation and characterization of tumorigenic and non-tumorigenic populations of cancer cells present in human breast, colon and head and neck cancer tumors. Only a small minority of cancer cells had the capacity to form new tumors in a xenograft model. This tumorigenic cell population could be identified prospectively and consistently had definable and identical phenotype. The tumorigenic cells displayed stem cell-like properties in that they were capable of generating new tumors containing additional stem cells as well as regenerating the phenotypically mixed populations of non-tumorigenic cells present in the original tumor. Effective treatment of cancer will require therapeutic strategies that are able to target and eliminate this tumorigenic subset of cells. The laboratory is pursuing the identification of cancer stem cells in other tumors so that they can be studied. Dr. Clarke’s laboratory will provide other members of the program with the expertise to identify and isolate cancer stem cells from solid tumors of epithelial origin. Finally, the laboratory is actively pursuing how cancer stem cells self-renew to maintain themselves and escape the genetic constraints on unlimited self-renewal that regulate normal stem cell numbers. Differences in self-renewal pathways between normal and malignant stem cells could be targeted by new therapeutic agents to eliminate cancer stem cells.
Clinical Trials
Publications
- Cell. 2009; (3): 592-603
- Nature. 2009; (7239): 780-3
- Nature. 2008; (7192): 228-32
- N Engl J Med. 2007; (3): 217-26
- Cell. 2006; (6): 1111-5
- Proc Natl Acad Sci U S A. 2003; (7): 3983-8
- Nature. 2003; (6937): 302-5
- Lab Chip. 2009; (10): 1365-70
- Semin Radiat Oncol. 2009; (2): 78-86
- Proc Natl Acad Sci U S A. 2009; (9): 3396-401
- Adv Exp Med Biol. 2008; 17-22
- Curr Opin Genet Dev. 2008; (1): 48-53
- Annu Rev Cell Dev Biol. 2007; 675-99
- Proc Natl Acad Sci U S A. 2007; (24): 10158-63
- Annu Rev Med. 2007; 267-84
- Cell Stem Cell. 2007; (3): 241-2
- Stem Cells. 2007; (7): 1635-44
- Pathol Biol (Paris). 2006; (2): 109-11
- Curr Opin Genet Dev. 2006; (5): 496-501
- Sci Am. 2006; (1): 52-9
- Cancer Res. 2006; (19): 9339-44
- Ann N Y Acad Sci. 2005; 90-3
- Cancer Chemother Pharmacol. 2005; 64-8
- Biol Blood Marrow Transplant. 2005; (2 Suppl 2): 14-6
- J Clin Invest. 2004; (2): 175-9
- N Engl J Med. 2004; (7): 634-6
- Curr Opin Genet Dev. 2004; (1): 43-7
- Nature. 2004; (7015): 281-2
- Oncogene. 2004; (43): 7274-82
- Genes Dev. 2003; (10): 1253-70
- Cell Prolif. 2003; 59-72
- Nature. 2003; (6961): 962-7
- Nat Rev Cancer. 2003; (12): 895-902
- Cancer Cell. 2002; (4): 249-51
- Hum Gene Ther. 2002; (14): 1737-50
- Blood. 2002; (2): 488-98
- J Immunol. 2002; (2): 635-42
- Nature. 2001; (6859): 105-11
- Cancer Gene Ther. 2001; (4): 298-307
- Eur J Biochem. 2001; (10): 2779-83
- J Biol Chem. 2001; (2): 915-23
- Hum Gene Ther. 2000; (14): 2009-24
- Mol Ecol. 2000; (9): 1339-47
- Oncogene. 1999; (12): 2163-6
- J Biol Chem. 1999; (46): 32699-703
- Radiology. 1999; (1): 249-56
- Mol Genet Metab. 1998; (2): 155-64
- J Biol Chem. 1998; (31): 19817-21
- BMJ. 1998; (7152): 205-6
- Hum Gene Ther. 1998; (8): 1209-16
- Springer Semin Immunopathol. 1998; (3): 279-88
- Mol Pharmacol. 1997; (4): 600-5
- Mol Ecol. 1997; (11): 1103-5
- Br J Haematol. 1997; (4): 846-9
- Cancer Res. 1996; (9): 1965-9
- Hum Gene Ther. 1996; (13): 1527-34
- Cancer Res. 1996; (24): 5734-40
- Oncogene. 1995; (7): 1389-94
- Blood. 1995; (10): 3754-62
- Proc Natl Acad Sci U S A. 1995; (24): 11024-8
- Carcinogenesis. 1995; (8): 1761-7
- Cancer Treat Res. 1995; 215-23
- Cancer Res. 1995; (12): 2507-10
- Trends Cell Biol. 1994; (11): 399-403
- Proc Natl Acad Sci U S A. 1994; (13): 5878-82
- Leuk Res. 1994; (8): 617-21
- Mol Cell Biol. 1993; (1): 711-9
- Oncogene. 1992; (5): 901-7
- Exp Hematol. 1992; (1): 87-91
- Mol Carcinog. 1992; (4): 311-9
- Cytotechnology. 1992; (3): 217-24
- Bioconjug Chem. 1991 Nov-Dec; (6): 466-74
- Biotechnol Prog. 1991 Jan-Feb; (1): 1-8
- Blood. 1991; (12): 3155-61
- J Cell Biochem. 1991; (3): 268-72
- Science. 1990; (4974): 1291-3
- Oncogene. 1990; (8): 1117-24
- Leukemia. 1989; (4): 314-5
- Mol Cell Biol. 1988; (2): 884-92
- J Biol Chem. 1986; (10): 4615-9
- J Biol Chem. 1985; (23): 12394-7
- Nature. 1984 Mar 29-Apr 4; (5958): 464-7
- Virology. 1984; (1): 97-104
- Science. 1984; (4662): 636-9
- Mol Cell Biol. 1984; (5): 890-7
- Leuk Res. 1984; (6): 965-73
- Nature. 1983 Sep 1-7; (5929): 60-2
- Clin Exp Immunol. 1983; (3): 505-11
- Haematol Blood Transfus. 1983; 459-61
- Lancet. 1982; (8297): 564
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- Rheumatol Int. 1982; (4): 175-8
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- Anal Biochem. 1969; (1): 81-90
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