Mitochondrial calcium: a crucial hub for cancer cell metabolism?

According to the current concept, a typical tumor contains “driver gene” mutations that establish a growth advantage to the tumor cell (1). It was proposed that one of the first mutations must have either a mutation that introduces a selective growth advantage to a normal cell (1) or one of the first mutations results in genomic instability, thus, increasing the chance for the accumulation of further mutations (2). Recent data indicate that metabolic reprogramming by (somatic) mutations of key metabolic genes promotes cancer growth (3). In this context metabolic adaptations upon aging need to be considered as hallmark of cancer (4).