In contrast to normal differentiated cells, which rely primarily on mitochondrial oxidative
phosphorylation to generate the energy needed for cellular processes, most cancer cells instead …

Cell proliferation requires nutrients, energy, and biosynthetic activity to duplicate all
macromolecular components during each passage through the cell cycle. It is therefore not …

Tumorigenesis is dependent on the reprogramming of cellular metabolism as both direct and
indirect consequence of oncogenic mutations. A common feature of cancer cell metabolism …

Cancer-associated IDH mutations are characterized by neomorphic enzyme activity and
resultant 2-hydroxyglutarate (2HG) production. Mutational and epigenetic profiling of a large …

Mutations in the enzyme cytosolic isocitrate dehydrogenase 1 (IDH1) are a common feature
of a major subset of primary human brain cancers. These mutations occur at a single amino …

Recurrent mutations in isocitrate dehydrogenase 1 (IDH1) and IDH2 have been identified in
gliomas, acute myeloid leukaemias (AML) and chondrosarcomas, and share a novel …

Both genome-wide genetic and epigenetic alterations are fundamentally important for the
development of cancers, but the interdependence of these aberrations is poorly understood. …

In multicellular organisms, homeostasis is maintained through a balance between cell
proliferation and cell death. Although much is known about the control of cell proliferation, less is …

Proteins in the Bcl-2 family are central regulators of programmed cell death 1 , and members
that inhibit apoptosis, such as Bcl-X L and Bcl-2, are overexpressed in many cancers and …

Multiple death signals influence mitochondria during apoptosis, yet the critical initiating event
for mitochondrial dysfunction in vivo has been unclear. tBID, the caspase-activated form of …