Experiments show that transferring a cancer cell's dysfunctional mitochondria—but not its nucleus—into a healthy cell is what induces cancer. This disruptive finding supports the view of cancer as a metabolic disease that can be targeted by starving its mitochondria of fuels like glucose.

The drug exhibits a multimodal mechanism. It not only reverses chemoresistance and halts tumor growth but also 'turns cold tumors hot' by forcing cancer cells to display markers that make them visible to the immune system. This dual action of direct attack and immune activation creates a powerful synergistic effect.

Traditional 2D cell cultures can be misleading. Advanced 3D models, by reconstituting the tumor microenvironment with stromal cells, can uncover mechanisms of drug resistance (e.g., to ADCs) that are completely invisible in simpler systems, providing more clinically relevant data.

Zelenorstat inhibits NMT, an enzyme that attaches a "GPS tag" to proteins, guiding them within the cell. By blocking this process, it renders key cancer-driving proteins useless, effectively confusing the cancer's operating system rather than using brute-force poison like chemotherapy.

The IDH1 enzyme, part of the Krebs cycle, is mutated in up to 60% of chondrosarcomas, driving cancer growth. Drugs like Ivosidenib block this mutated enzyme, showing how basic metabolic pathways from textbooks are now at the forefront of targeted cancer therapy.

The efficacy of some established drugs, like the chemotherapy oxaliplatin, may be due to an unknown mechanism: they partition into and disrupt cellular condensates. This reframes our understanding of drug action and could explain why certain drugs are more effective in some cancers than others.

Cancer should be viewed not just as rogue cells, but as a complex system with its own supply chains and communication infrastructure. This perspective shift justifies novel therapies like Zelenorstat, which aim to dismantle this entire operating system by cutting its power source.

Despite its name, the mesenchymal subtype of chondrosarcoma has a unique gene fusion that makes its biology distinct. Consequently, treatment follows protocols for Ewing sarcoma, including neoadjuvant chemotherapy, rather than the surgery-first approach used for conventional chondrosarcomas.

Researchers are exploring combination therapies for chondrosarcoma's heterogeneity. One strategy is to combine IDH1 inhibitors, which may work better on lower-grade tumors, with DR5 agonists, potentially more effective on higher-grade tumors, to attack different components of the cancer simultaneously.