The Cancer Genome Atlas Network recently cataloged recurrent genomic abnormalities in
glioblastoma multiforme (GBM). We describe a robust gene expression-based molecular …

Phosphorylation at Ser-15 may be a critical event in the up-regulation and functional
activation of p53 during cellular stress. In this report we provide evidence that the ATM–Rad3-…

Caffeine exposure sensitizes tumor cells to ionizing radiation and other genotoxic agents.
The radiosensitizing effects of caffeine are associated with the disruption of multiple DNA …

Members of the phosphatidylinositol-3 kinase related kinase (PIKK) family function in both cell
cycle progression and DNA damage-induced cell cycle checkpoints. The fungal metabolite…

Poly(ADP-ribose) polymerase (PARP) inhibitors are strikingly toxic to cells with defects in
homologous recombination (HR). The mechanistic basis for these findings is incompletely …

The blood–brain barrier (BBB) excludes the vast majority of cancer therapeutics from
normal brain. However, the importance of the BBB in limiting drug delivery and efficacy is …

Like all cancers, brain tumors require a continuous source of energy and molecular resources
for new cell production. In normal brain, glucose is an essential neuronal fuel, but the …

Intrinsic or acquired chemoresistance to alkylating agents is a major cause of treatment
failure in patients with malignant brain tumors. Alkylating agents, the mainstay of treatment for …

Temozolomide (TMZ)-based therapy is the standard of care for patients with glioblastoma
multiforme (GBM), and resistance to this drug in GBM is modulated by the DNA repair protein …

Purpose : Proliferation of surviving tumor clonogens during a course of protracted radiation
therapy may be a cause of local failure in cervical carcinoma. The effect of total treatment …