Joshua D. Rabinowitz

TL;DR: It is shown that cancer-associated IDH1 mutations result in a new ability of the enzyme to catalyse the NADPH-dependent reduction of α-ketoglutarate to R(-)-2-hydroxyglutarate (2HG), and that the excess 2HG which accumulates in vivo contributes to the formation and malignant progression of gliomas.

TL;DR: It is reported that tumor 2HG is elevated in a high percentage of patients with cytogenetically normal acute myeloid leukemia (AML), and AML patients with IDH mutations display a significantly reduced number of other well characterized AML-associated mutations and/or associated chromosomal abnormalities, potentially implicating IDH mutation in a distinct mechanism of AML pathogenesis.

TL;DR: A powerful promoter of metabolic homeostasis at both the cellular and whole-animal level, autophagy prevents degenerative diseases and does have a downside, however—cancer cells exploit it to survive in nutrient-poor tumors.

TL;DR: The data and analyses presented here highlight the ability to identify organizing metabolic principles from systems-level absolute metabolite concentration data, and facilitate efficient flux reversibility given thermodynamic and osmotic constraints.

TL;DR: In this paper, it was shown that Ras-transformed cells use macropinocytosis to transport extracellular protein into the cell, yielding amino acids including glutamine that can enter central carbon metabolism.