Primary brain tumors constitute a substantial public health problem with 66,290 
cases diagnosed in the US in 2012, and 13,700 deaths recorded. With discovery of 
genetic factors associated with specific brain tumor subtypes, the goal of 
therapy is changing from treating a class of tumors to developing individualized 
therapies catering to the molecular composition of the actual tumor. For 
oligodendrogliomas, the loss of 1p/19q due to an unbalanced translocation 
improves both survival and the response to therapy, and is thus both a 
prognostic and a predictive marker. Several additional genetic alterations such 
as EGFR amplification, MGMT methylation, PDGFR activation, and 9p and 10q loss, 
have improved our understanding of the characteristics of these tumors and may 
help guide therapy in the future. For astrocytic tumors, MGMT is associated with 
a better prognosis and an improved response to temozolomide, and for all glial 
tumors, mutations in the IDH1 gene are possibly the most potent of good 
prognostic markers. Three of these markers - 1p/19q deletions, MGMT methylation 
status, and mutations in the IDH1 gene - are so potent that a new brain tumor 
subtype, the "triple negative" glioma (1p/19q intact, MGMT unmethylated, IDH1 
non-mutated) has entered common parlance. Newer markers, such as CD 133, require 
additional investigation to determine their prognostic and predictive utility. 
In medulloblastomas, markers of WNT activation, MYCC/MCYN amplification, and 
TrkC expression levels are reliable prognostic indicators, but do not yet drive 
specific treatment selection. Many other proposed markers, such as 17q gain, 
TP53 mutations, and hMOF protein expression show promise, but are not yet ready 
for prime time. In this chapter, we focus on the markers that have shown 
convincing prognostic, predictive, and diagnostic value, and discuss potential 
markers that are being currently being intensively investigated. We also discuss 
serum profiling of tumors in an effort to discover additional potential markers.