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Neuro-Oncology

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: 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; first published online in THE ONCOLOGIST Express on November 19, 2008.

Disclosure: Employment/leadership position: None; Intellectual property rights/inventor/patent holder: None; Consultant/advisory role: Jeffrey Wefel, Genentech; Christina Meyers, Genentech, MGI Pharma, Regeneron; Honoraria: None; Research funding/contracted research: Jeffrey Wefel, AstraZeneca, Schering-Plough; Christina Meyers, Angiochem; Ownership interest: None; Expert testimony: None; Other: None. The content of this article has been reviewed by independent peer reviewers to ensure that it is balanced, objective, and free from commercial bias. No financial relationships relevant to the content of this article have been disclosed by the authors, planners, independent peer reviewers, or staff managers.

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.