Introduction

Leukemia is the most common form of pediatric cancer, accounting for 25% of all cancers occurring before 20 years of age [1]. Acute lymphoblastic leukemia (ALL) accounts for roughly 75% of all leukemia diagnoses, with roughly 3000 new cases diagnosed annually [1]. Lymphomas are the third most common form of childhood cancer, occurring in roughly 1700 new cases annually [1]. Improvements in the treatment of leukemia and lymphoma have led to a remarkable increase in the survival rate, which currently exceeds 80% [2]. At these incidence and survival rates, it is estimated that 1 out of every 640 young adults will be a pediatric cancer survivor [3]. As many as two-thirds of all pediatric cancer survivors experience one or more permanent side effects of their treatment, often referred to as “late effects” (i.e. persisting or developing 5 or more years following cancer diagnosis) [4]. The late effects that commonly occur in patients with leukemia include neurocognitive impairment, obesity, short stature, osteoporosis, osteonecrosis, and cardiac dysfunction [5]. Neurocognitive late effects are often associated with treatment for leukemia, given that central nervous system (CNS) prophylaxis is a standard of care. As pediatric cancer survivors constitute a significant proportion of young adults, and as neurocognitive late effects appear relatively common, the public health consequences are substantial. This chapter will provide a review of the basic pathophysiology of acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), Hodgkin lymphoma (HL), and non-Hodgkin lymphoma (NHL) as well as a review of treatment factors, mediators and moderators that may influence neurocognitive and psychosocial outcomes, and evaluation, management, and prevention of these outcomes.