Hideho Okada, MD, PhDProfessor of Neurological Surgery, Surgery and Immunology
Hideho Okada, MD, PhD, joined the faculty in the Department of Neurological Surgery in 1996 as a visiting research associate. Currently, Dr. Okada is a professor in the departments of Neurological Surgery, Surgery and Immunology as well as co-leader of the Brain Tumor Program at the University of Pittsburgh Cancer Institute.
From 1985 to 1991, Dr. Okada received his medical training at the Nagoya University School of Medicine and graduated in 1991 with a bachelor of medicine degree. In 1992, he completed his internship at Handa Municipal Hospital in Japan and then received neurosurgical residency training at Nagoya University School of Medicine. In 1996, Dr. Okada received his PhD from the Graduate School of Nagoya University School of Medicine in Japan. Dr. Okada received a certificate of board of neurological surgery in Japan in 2003, and a license as a medical physician and surgeon from Commonwealth of Pennsylvania in 2004.
In 2010, he was elected to be a member of the American Society for Clinical Investigations (ASCI), an honor society of physician-scientists, those who translate findings in the laboratory to the advancement of clinical practice.
Dr. Okada's publications can be reviewed through the National Library of Medicine's publication database.
Japanese Board of Neurological Surgery
Medical Physician and Surgeon, PA Department of State
University of Pittsburgh Cancer Institute
Professional Organization Membership
American Association for Cancer Research
The Society for Neuro-oncology
Society for Immunotherapy of Cancer
Adult Brain Tumor Consortium
Japan Society of Neurosurgery
American Society for Clinical Investigations (ASCI)
UPMC Doctor to Test Cancer Vaccine
April 8, 2010
KDKA-TV Evening News
Cancer vaccines may be on the verge of wider use
April 7, 2010
1) Phase I Vaccine Study in Patients with WHO Grade II Low-Grade Glioma (LGG).
Based on promising data from our phase I/II study in patients with recurrent high-grade gliomas, we conducted a phase I vaccine study with: newly diagnosed high-risk LGG without prior radiation therapy (RT) (Cohort 1); newly diagnosed high-risk LGG with prior RT (Cohort 2); or recurrent LGG (Cohort 3). Primary endpoints were safety and CD8+ T-cell responses against vaccine-targeted glioma-associated antigen (GAAs): IL-13Rα2, EphA2, WT1, and Survivin. Cohorts 1, 2, and 3 have enrolled 12, 1, and 10 patients, respectively. No regimen-limiting toxicity has been encountered except for one case with Grade 3 fever (Cohort 1). Based on ELISPOT assays for GAA-specific T-cell responses, Cohort 1 patients demonstrated significantly higher magnitude of IFN-γ responses than Cohort 3 patients for all 4 GAA epitopes, suggesting that newly diagnosed patients may have better vaccine-responsiveness than recurrent patients. Although longer follow-up is needed to evaluate any clinical efficacy, these data support safety and a potent immunological activity of the vaccine regimen; and larger studies with therapeutic endpoints as the primary endpoints are warranted.
2) Loss of Heterozygocity (LOH) in the Human Leukocyte Antigen (HLA) Class I region at 6p21 is Associated with Shorter Survival in Newly Diagnosed Adult Glioblastoma.
Glioblastoma (GBM) demonstrates down-regulated expression of HLA Class I to evade the recognition by CD8+ cytotoxic T cells. In this investigation, we found, for the first time, that LOH in the HLA Class I gene is associated with shorter overall survival in newly diagnosed GBM patients. This sheds new light onto the allelic status of these well-characterized genes and its importance in GBM immunosurveillance. These findings provide greater understanding of how GBM evade the immune system and allow further prognostication for GBM patients.
3) Premetastatic Soil and Prevention of Breast Cancer Brain Metastasis.
As therapies for systemic cancer improve and patients survive longer, the risk of brain metastases increases. We evaluated whether immune mechanisms are involved in development of brain metastasis. Our results in mouse breast cancer models suggest that the primary tumor induces accumulation of CD11b+Gr1+ myeloid cells in the brain to form “pre-metastatic soil” and inflammation mediators, such as S100A9, attract additional myeloid cells as well as metastatic tumor cells. Celecoxib and anti-Gr1 treatment may be useful for blockade of these processes, thereby preventing brain metastasis in patients with breast cancer.