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Steven Artandi

Academic Appointments

  • Professor of Medicine (Hematology) and of Biochemistry

Key Documents

Contact Information

  • Clinical Offices
    Hematology Clinic 300 Pasteur Dr A175 MC 5312 Stanford, CA 94305
    Tel Work (650) 498-6000 Fax (650) 725-8950
    Hematology Clinic 875 Blake Wilbur Dr Clinic C MC 5820 Stanford, CA 94305
    Tel Work (650) 498-6000 Fax (650) 498-5030
  • Academic Offices
    Personal Information
    Email Tel (650) 736-0975
    Not for medical emergencies or patient use

Professional Overview

Clinical Focus

  • Cancer> Hematology
  • Medical Oncology

Honors and Awards

  • Elected Member, American Society for Clinical Investigation (2008)
  • Fellow, American Association for the Advancement of Science (AAAS) (2008)

Boards, Advisory Committees, Professional Organizations

  • Editorial Board, Stem Cells (2006 - present)
  • Editorial Board, Molecular Cancer Research (2013 - present)

Professional Education

Medical Education: Columbia University NY (1995)
Residency: Massachusetts General Hospital MA (1997)
Fellowship: Dana-Farber Cancer Institute MA (2000)
Ph.D.: Columbia University, Microbiology (1995)
M.D.: Columbia University (1995)
A.B.: Princeton University, Chemistry (1986)



Prior Year Coursescourses of Steven Artandi

Graduate and Fellowship Program Affiliations

Scientific Focus

Current Research and Scholarly Interests

Telomeres, the nucleotide repeats that cap the ends of eukaryotic chromosomes, serve critical roles in promoting cell viability and in maintaining chromosomal stability. In humans, telomeres shorten progressively with cell division and aging because DNA polymerase cannot fully replicate the extreme ends of chromosomes. Critical telomere shortening and loss of the protective telomere capping function in cell culture initiates senescence and crisis responses that profoundly alter chromosome stability, cell cycle progression and survival. Expression of telomerase, the reverse transcriptase that synthesizes telomere repeats, is sufficient to lengthen and stabilize telomeres, thus enabling cells to proliferate in an unlimited fashion. Telomerase is expressed in stem cells and progenitor cells in self-renewing tissues, is downregulated with differentiation and upregulated in the vast majority of human cancers. In the Artandi lab, we are interested in unraveling the molecular and cellular mechanisms according to which telomeres and telomerase modulate stem cell function and carcinogenesis.


Telomerase is comprised of two subunits: TERT, the telomerase reverse transcriptase, and TERC, the telomerase RNA component. In stem cell and progenitor cell compartments, TERT serves a critical role in maintaining telomere length and function to support tissue homeostasis. However, TERT serves an additional function in stem cells, distinct from its role in telomere lengthening and we are actively studying this new role. We have devised new means of identifying telomerase-expressing cells in vivo and we are investigating the location and function of these cells in diverse tissues.


Aging in humans and other mammals is associated with impaired proliferative responses in settings of stress, suggesting that altered stem cell function may underlie certain aspects of aging. We are interested in understanding how stem cells self-renew and differentiate and how TERT modulates stem cell function. One major limitation to this understanding is the inability to identify telomerase-positive cells in vivo. We have developed new approaches to solve this problem and are investigating telomerase-positive cells in vivo.


Telomerase is a large RNP with complex regulation in human cells. Using IP-MS approaches, we identified a critical new component of the telomerase holoenzyme, TCAB1. TCAB1 is essential for guiding the trafficking of telomerase to Cajal bodies within the nucleus and also to chromosome ends. We seek to understand in molecular detail how telomerase interacts with telomeres and adds telomere repeats in human cells.


Germline mutations in telomerase components underlie several seemingly unrelated disease states, including the bone marrow failure syndrome dyskeratosis congenita, idiopathic pulmonary fibrosis, aplasic anemia and cirrhosis. We are using iPS cell-based approaches to study the mechanisms at play in these diseases with the goal of reversing the life-threatening phenotypes in these patients.


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