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.
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Many cancer cells rely heavily on glucose (the Warburg effect) and cannot efficiently use ketones. A strict ketogenic diet may starve these tumors while nourishing healthy cells. In one case, it led to a 70% reduction in cancer markers in six weeks, far exceeding chemotherapy's expected 30%.
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.
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.
Mitochondria in different organs are not identical. Despite sharing the same genes, they differentiate into specialized "mitotypes" with distinct forms and functions, analogous to worker and warrior ants. This cellular division of labor is crucial for organ-specific energy needs.
The term "hormone resistance" was misleading. Researchers discovered that even in a castrate state, prostate cancer tumors produce their own testosterone locally. This maintained androgen receptor signaling, proving the disease was still "androgen addicted" and opening the door for new targeted therapies.
Butyrate, a short-chain fatty acid from gut bacteria, functions similarly to HDAC inhibitor drugs used in cancer therapy. This provides a scientific mechanism for how diet impacts myeloma, revealing its role in anti-tumor and anti-inflammatory pathways.
Overeating acts like excessive voltage on a circuit, forcing too many electrons into mitochondria and creating high "energy resistance." This overwhelms the system, causing energy to dissipate as harmful reactive oxygen species, leading to molecular damage, disease, and accelerated aging.
Instead of just killing cancer cells, the primary mechanism is to insert a gene that forces the infected cell to produce and secrete a potent drug, like an anti-PD-L1 antibody. This creates a hyper-concentrated therapeutic effect directly in the tumor microenvironment, a concept termed "molecular surgery."
Instead of searching for elusive natural markers to target, EARLI's platform creates its own. It programs synthetic genetic "switches" that activate only inside cancer cells, turning them into factories that produce their own cancer-fighting therapies. This shifts the paradigm from biological discovery to biological engineering.
Cellcuity's drug is effective in breast cancer patients without PIK3CA mutations (wild type). This challenges the dominant precision medicine model that requires a specific genetic marker, showing that a pathway's aberrant activity can be a sufficient therapeutic target on its own.
