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 94305-5847 Tel Work (650) 723-6171 Fax (650) 725-8231Practices at Stanford Hospital and Clinics and Lucile Packard Children's Hospital
- Academic Offices
Personal Information EmailNot 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
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
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
- Capecitabine, Gemcitabine, and Radiation Therapy in Treating Patients With Cholangiocarcinoma of the Gallbladder or Bile Duct Recruiting
- Novel Serum Markers for Monitoring Response to Anti-Cancer Therapy Recruiting
- Phase II Gemcitabine + Fractionated Stereotactic Radiotherapy for Unresectable Pancreatic Adenocarcinoma Recruiting
- PII Combination SBRT with TACE for Unresectable Hepatocellular Carcinoma Recruiting
- PII of SBRT & Chemo for Unresectable Cholangiocarcinoma Followed by Liver Transplantation Recruiting
Publications
- Antiangiogenic and radiation therapy: early effects on in vivo computed tomography perfusion parameters in human colon cancer xenografts in mice. Invest Radiol. 2012; (1): 25-32
- BRAF-mutated, Microsatellite-stable Adenocarcinoma of the Proximal Colon: An Aggressive Adenocarcinoma With Poor Survival, Mucinous Differentiation, and Adverse Morphologic Features. Am J Surg Pathol. 2012
- Modern radiation therapy techniques for pancreatic cancer. Gastroenterol Clin North Am. 2012; (1): 223-35
- Normal Tissue Complication Probability Modeling of Acute Hematologic Toxicity in Patients Treated with Intensity-Modulated Radiation Therapy for Squamous Cell Carcinoma of the Anal Canal. Int J Radiat Oncol Biol Phys. 2012
- Postchemoradiotherapy Positron Emission Tomography Predicts Pathologic Response and Survival in Patients with Esophageal Cancer. Int J Radiat Oncol Biol Phys. 2012
