Albert Koong
Academic Appointments
- Associate Professor, Radiation Oncology - Radiation Therapy
- Member, Bio-X
- Member, Cancer Center
Contact Information
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Clinical Offices
Radiation Therapy 875 Blake Wilbur Dr Clinic D Stanford, CA 94305-5847 Tel Work (650) 723-6171Practices at Stanford Hospital and Clinics and Lucile Packard Children's Hospital
Professional Snapshot
Clinical Focus
- Cancer> Radiation Oncology
- Cancer> Radiation Oncology> Radiation Therapy
- Colorectal Cancer
- Colorectal Cancer - Radiation Oncology
- Esophageal Cancer
Professional Education
| Board Certification: | Radiation Oncology, American Board of Radiology (2001) |
| 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
Web Site Links
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
- Novel Serum Markers for Monitoring Response to Anti-Cancer Therapy Recruiting
- Ph I of FG-3019, Gemcitabine and Erlotinib for Locally Advanced or Metastatic Pancreatic Cancer Recruiting
- Phase II Gemcitabine + Fractionated Stereotactic Radiotherapy for Unresectable Pancreatic Adenocarci Recruiting
- Assessment of Health Related Quality of Life in Patients Treated for Rectal Cancer Recruiting
- PII Combination SBRT with TACE for Unresectable Hepatocellular Carcinoma Recruiting
Publications
- Activation of the unfolded protein response in wound healing. J Surg Res. 2010; (2): 209
- Imaging the unfolded protein response in primary tumors reveals microenvironments with metabolic variations that predict tumor growth. Cancer Res. 2010; (1): 78-88
- The role of tumor cell-derived connective tissue growth factor (CTGF/CCN2) in pancreatic tumor growth. Cancer Res. 2009; (3): 775-84
- Stereotactic radiotherapy for unresectable adenocarcinoma of the pancreas. Cancer. 2009; (3): 665-72
- Hypoxia-induced lysyl oxidase is a critical mediator of bone marrow cell recruitment to form the premetastatic niche. Cancer Cell. 2009; (1): 35-44
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