The Truth Behind News of a Treatment Completely Eliminating Cancer: Caspase-Independent Apoptosis!

Most cancer treatments aim to eliminate cells through apoptosis , or programmed cell death, which occurs when caspase proteins are activated. However, over time, resistance to cancer treatments can develop, leading to recurrence and worsening disease. Recently, cell-death mechanisms in cancer have been investigated in greater detail. Nature Cell Biologypublished a recent study showing that caspase-independent cell death (CCID) effectively eliminates cancer cellsin this research.

University of Glasgow researchers in Scotland investigated whether caspase-independent death would work in colorectal cancer cells.

Research Findings;

• Disrupting mitochondrial membrane structure activated the NF-κB protein, enabling caspase-independent death.
• In the Laboratory, CCID eliminated nearly all cancer cells. - Compared with conventional apoptosis, the method caused greater inflammation and thus greater immune activation.

What Does This Study Mean Clinically?

• A potentially more effective way of eliminating cancer cells was discovered. CCID activates immunity more than apoptosis. In other words, by activating the immune system , it may allow more effective attacks against cancer.
• The study could open the way to cancer treatments with very few side effects . Approaches activating this method only in tumor cells could produce tumor-specific medicines.
• It is important to emphasize that this study is not a definitive cure for cancer ! Its significance is discovering a new potentially effective elimination method. These are only initial laboratory findings, requiring animal models and further analyses.
• Cancer arises from numerous genetic and epigenetic abnormalities. Therefore, a single treatment for cancer is impossible! Cancer can be effectively managed with different treatment combinations.

The figure explains apoptosis mechanisms. Caspases activated by a molecule binding a death receptor activate one another and initiate apoptosis. Granzyme B can also activate caspases directly. Caspases increase mitochondrial membrane permeability, releasing apoptosis-related proteins such as cytochrome C, further activating caspases and apoptosis. Increased DNA damage activates the P53 gene . P53 likewise increases mitochondrial permeability and causes apoptosis.

What Is Apoptosis? — Further Reading

In normal processes and pathological conditions such as cancer, nuclear DNAcan issue instructions degrading intracellular proteins and causing death. Cells undergoing apoptosis, termed in English apoptosisand sometimes rendered in Turkish as apopitozis , retain intact membranes but change so that they and their fragments become attractive targets for immune phagocytes. Rapid removal before contents leak prevents an inflammatory response. Apoptosis differs from necrosis, in which membrane integrity breaks down, cells are digested, contents leak and inflammation often occurs.

Apoptosis in Pathological Conditions: Genetically altered or irreparably damaged cells are eliminated through apoptosis without severe inflammation, minimizing tissue injury.

For Example, DNA Damage: Harmful solar ultraviolet rays, tissue oxygen deficiency (hypoxia) and carcinogenssuch as smoking can damage DNA directly or through free radicals. If repair cannot cope, the cell activates apoptosis. Eliminating it may be preferable to damaged DNA generating cancer-promoting mutations. Mild injury may cause apoptosis, whereas much higher doses of the same agents may cause necrosis or cancerous transformation.

Apoptosis is the orderly elimination of unwanted, irreparably damaged cells with minimal inflammation, also called “programmed cell death.”

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