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Albert Koong

Academic Appointments

Key Documents

Contact Information

  • Clinical Offices
    Radiation Therapy 875 Blake Wilbur Dr Clinic D Stanford, CA 94305-5847
    Tel Work (650) 723-6171 Fax (650) 725-8231
  • Academic Offices
    Personal Information
    Email
    Not for medical emergencies or patient use

Professional Overview

Clinical Focus

  • Cancer> Radiation Oncology
  • Cancer> Radiation Oncology> Radiation Therapy
  • Pancreatic Cancer
  • Pancreatic Cancer - Radiation Oncology
  • Rectal Cancer - Radiation Oncology
View all 10clinical focus of Albert Koong

Professional Education

Residency: SUMC - Graduate Medical Education CA (2001)
Internship: Kaiser Permanente Medical Center CA (1997)
Medical Education: Northwestern University Medical School IL (1996)
Doctorate Degree: Stanford University School of Medicine CA (1994)

Postdoctoral Advisees

Dadi JiangJing Zhang

Graduate & Fellowship Program Affiliations

Industry Relationships

Stanford is committed to ethical and transparent interactions with our industrial and other commercial partners. It is our policy to disclose payments (exclusive of travel support) from, and/or equity in, companies or other commercial entities to Stanford faculty of $5,000 or more in total value, as well as any equity in a privately held company, when the faculty member also has institutional responsibilities related to his or her interactions with the company. View Full Information

Scientific Focus

Current Research Interests

Hypoxia induces endoplasmic reticulum (ER) stress in solid tumors. Previous studies have indicated that hypoxia is a major determinant of local, regional, and distant recurrence after anticancer therapy. The response of tumor cells to hypoxia depends on the severity and duration of oxygen deprivation. For example, hypoxia induced factor (HIF-1) is activated at physiological levels of oxygen change, whereas the unfolded protein response (UPR) is induced by severe oxygen deprivation. The UPR is an evolutionarily conserved pathway that functions to reduce protein accumulation in the ER resulting in increased capacity to tolerate ER stress. We hypothesize that since the UPR is also activated during hypoxia, it may be a critical regulator of cell survival during hypoxia and is necessary for tumor growth. The focus of my laboratory is to understand the relationship between hypoxia and ER stress, particularly as it relates to tumorigenesis.

Publications

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Publication Topics

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