Albert Koong
Academic Appointments
- Associate Professor, Radiation Oncology - Radiation Therapy
- Member, Bio-X
- Member, Stanford Cancer Institute
Key Documents
Contact Information
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Clinical Offices
Radiation Therapy 875 Blake Wilbur Dr Clinic D Stanford, CA 94305 Tel Work (650) 723-6171 Fax (650) 725-8231Practices at Stanford Hospital and Clinics and Lucile Packard Children's Hospital
- Academic Offices
Not for medical emergencies or patient use
Professional Overview
Clinical Focus
- Cancer> GI Oncology
- Cancer> Radiation Oncology
- Pancreatic Cancer
- Pancreatic Cancer - Radiation Oncology
- Rectal Cancer - Radiation Oncology
- Liver Cancer - Radiation Oncology
Professional Education
| Residency: | Stanford University School of Medicine 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) |
Graduate & Fellowship Program Affiliations
Internet Links
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.
Clinical Trials
- Not Recruiting Combination SBRT (Stereotactic Body Radiotherapy) With TACE (Transarterial Chemoembolization) for Unresectable Hepatocellular Carcinoma
- Recruiting Perfusion CT as a Predictor of Treatment Response in Patients With Hepatic Malignancies
- Not Recruiting Prognostic Value of Baseline Computed Tomography (CT) Perfusion Parameters of Pancreatic Cancer for Patients Undergoing Stereotactic Body Radiotherapy or Surgical Resection
- Not Recruiting Transarterial Chemoembolization vs CyberKnife for Recurrent Hepatocellular Carcinoma
- Recruiting Perfusion CT as a Predictor of Treatment Response in Patients With Rectal Cancer
Publications
- Cost-effectiveness of modern radiotherapy techniques in locally advanced pancreatic cancer. Cancer. 2012; (4): 1119-29
- Identification of an Ire1alpha endonuclease specific inhibitor with cytotoxic activity against human multiple myeloma. Blood. 2011; (4): 1311-4
- Imaging the unfolded protein response in primary tumors reveals microenvironments with metabolic variations that predict tumor growth. Cancer Res. 2010; (1): 78-88
- Hypoxia-induced lysyl oxidase is a critical mediator of bone marrow cell recruitment to form the premetastatic niche. Cancer Cell. 2009; (1): 35-44
- Stereotactic radiotherapy for unresectable adenocarcinoma of the pancreas. Cancer. 2009; (3): 665-72
- The role of tumor cell-derived connective tissue growth factor (CTGF/CCN2) in pancreatic tumor growth. Cancer Res. 2009; (3): 775-84
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