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.

For years, the KRAS oncogene was considered a key cancer driver but impossible to target with drugs. Through resilient investigation, scientists recently developed effective therapies against it, proving that even long-held beliefs about 'undruggable' targets can be overturned with persistence.

Step Pharma's synthetic lethality approach targets two redundant enzymes in the same pathway. Deleting one makes cancer cells entirely dependent on the other. This direct dependency is harder for biology to circumvent compared to approaches targeting different, interconnected pathways, creating a "cleaner" kill mechanism.

The IDH1 inhibitor olutasidenib demonstrates a much longer duration of response than ivosidenib. One hypothesis is that olutasidenib's weaker affinity for wild-type IDH1 makes it a more selective inhibitor of the mutant protein, leading to more durable disease control.

Chondrosarcomas arise from chondrocytes, cells adapted to low-oxygen, low-nutrient joint environments. This cellular resilience makes them inherently resistant to traditional chemotherapies, which are most effective against cells with high metabolic and division rates.

Pathways like integrins have long been of interest but lacked effective therapeutic approaches. The advent of new technologies, such as antibody-drug conjugates and checkpoint inhibitors, has created opportunities to re-explore these older targets with potent, modern drugs, breathing new life into decades-old research.

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.

Traditional targeted cancer therapies inhibit or 'cool down' overactive pathways, like pumping brakes on a runaway car. Delpha Therapeutics employs a counterintuitive 'activation lethality' approach, further over-activating pathways to 'overheat the engine' and cause catastrophic failure in cancer cells—a fundamentally opposite but highly effective strategy.