Side effects
Common are:

infusion site reactions
low blood pressure
hair loss
pain and or burning at the IV site
constipation or diarrhea
metallic food taste
bone marrow suppression, leading to:
decreased white blood cell counts (leading to increased susceptibility to infections)
low red blood cell counts (anemia)
low platelet counts (leading to easy bruising and bleeding)Less common are:

nausea and vomiting
allergic-type reactions
rash
fever, often occurring shortly after IV administration and not due to infection
mouth sores
acute myeloid leukemia (which can be treated with etoposide itself)When given with warfarin, it may cause bleeding. Pharmacology
Mechanism of action
Etoposide forms a ternary complex with DNA and the topoisomerase II enzyme, which is an enzyme that aids in relaxing negative or positive supercoils in DNA. Topoisomerase II normally will form a double-stranded break in one DNA double-strand, allow another to pass through, and re-ligate the broken strands. Etoposides binding prevents topoisomerase II from re-ligating the broken DNA strands, which causes the DNA breaks made by topoisomerase II to stay broken, and also prevents the topoisomerase II molecule from leaving the site and relieving tension elsewhere. This results in a double-strand break in the DNA that can have various deleterious effects on the cell, and depletion of topoisomerase II available to relieve further tension. Cancer cells rely on this enzyme more than healthy cells, since they divide more rapidly. Therefore, this causes errors in DNA synthesis and promotes apoptosis of the cancer cell. Chemistry
Etoposide is a semisynthetic derivative of podophyllotoxin from the rhizome of the wild mandrake (Podophyllum peltatum). More specifically, it is a glycoside of podophyllotoxin with a D-glucose derivative.
Infantile neuronal ceroid lipofuscinoses (INCL) or Santavuori disease or Hagberg-Santavuori disease or Santavuori-Haltia disease or Infantile Finnish type neuronal ceroid lipofuscinosis or Balkan disease is a form of NCL and inherited as a recessive autosomal genetic trait. The disorder is progressive, degenerative and fatal, extremely rare worldwide – with approximately 60 official cases reported by 1982, perhaps 100 with the condition in total today – but relatively common in Finland due to the local founder effect. Presentation
The development of children born with INCL is normal for the first 8–18 months, but will then flounder and start to regress both physically and mentally. Motor skills and speech are lost, and optic atrophy causes blindness. A variety of neurological symptoms, such as epilepsy and myoclonic seizures, appear. The senses of hearing and touch remain unaffected. The average lifespan of an INCL child is 9–11 years. Causes
It has been associated with palmitoyl-protein thioesterase. Diagnosis
Treatment
Treatment is limited. Drugs can alleviate the symptoms, such as sleep difficulties and epilepsy. Physiotherapy helps affected children retain the ability to remain upright for as long as possible, and prevents some of the pain. Recent attempts to treat INCL with cystagon have been unsuccessful. See also
FAIDD (The Finnish Association on Intellectual and Developmental Disabilities)

References
External links

GeneReviews/NCBI/NIH/UW entry on Neuronal Ceroid-Lipofuscinosis
An overview (in Finnish)
The INCL organization of Finland (in Finnish)