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Clinical Patterns and Biological Correlates of Cognitive Dysfunction Associated with Cancer Therapy

^aDepartment of Neurology, Division of Neuro-Oncology, Stephen E. and Catherine Pappas Center for Neuro-Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA; ^bDepartments of Neurology and Developmental Biology, Stanford Institutes of Medicine, Stanford University, Palo Alto, California, USA; ^cDepartment of Neuro-Oncology, University of Texas MD Anderson Cancer Center, Houston, Texas, USA

Key Words. Neurotoxicity • Cognitive dysfunction • Chemotherapy • Radiation therapy • Progenitor cells • Neural stem cells

Correspondence: Correspondence: Jörg Dietrich, M.D., Ph.D., Department of Neurology, Division of Neuro-Oncology, Stephen E. and Catherine Pappas Center for Neuro-Oncology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USA. Telephone: 617-726-3650; Fax: 617-643-2591; e-mail: jdietrich1{at}partners.org

Received June 10, 2008; accepted for publication October 26, 2008.

ABSTRACT

Standard oncological therapies, such as chemotherapy and cranial radiotherapy, frequently result in a spectrum of neurocognitive deficits that includes impaired learning, memory, attention, and speed of information processing. In addition to classical mechanisms of neurotoxicity associated with chemo- and radiotherapy, such as radiation necrosis and leukoencephalopathy, damage to dynamic progenitor cell populations in the brain is emerging as an important etiologic factor. Radiation- and chemotherapy-induced damage to progenitor populations responsible for maintenance of white matter integrity and adult hippocampal neurogenesis is now believed to play a major role in the neurocognitive impairment many cancer survivors experience.