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Cancer Cells Have Become Habitual To Chemotherapy

A team of researchers at the Tulane University School of Medicine have found that some cancer cells endure chemotherapy by turning to cannibalism, i.e. by consuming neighboring tumor cells. The study, published in the scientific Journal of Cell Biology, proposes that this act of cannibalism provides these cancer cells with the energy they have to remain alive and initiate tumor relapse after the course of treatment is finished.

Chemotherapy medications, for example, doxorubicin kill cancer cells by harming their DNA, however, cells that endure initial treatment can soon give rise to relapsed tumors. This is a specific issue in breast cancers that retain a normal copy of a gene called TP53. Rather than dying in response to chemotherapy-induced DNA damage, these cancer cells simply quit multiplying and enter a dormant however metabolically dynamic state known as senescence. Notwithstanding enduring chemotherapy, these senescent cancer cells produce a lot of inflammatory molecules and other factors that can promote the tumor’s regrowth. Patients who treated breast cancer by getting a chemo, with normal TP53 genes are therefore inclined to backslide and have poor survival rates.

“Understanding the properties of these senescent cancer cells that permit their survival after chemotherapy treatment is extremely important,” says Crystal A. Tonnessen-Murray, a postdoctoral research fellow in James G. Jackson’s research lab at the Tulane University School of Medicine.

In the new study, Tonnessen-Murray and associates found that, after exposure to doxorubicin or other chemotherapy drugs, breast cancer cells that become senescent often inundate neighboring cancer cells. The researchers observed this astonishing behavior not just in cancer cells grown in the lab, yet in tumors growing in mice. Lung and bone cancer cells are additionally capable of inundating their neighbors in the wake of becoming senescent, the researchers found.

Tonnessen-Murray and his team found that senescent cancer cells trigger a group of genes that are normally dynamic in white platelets that immerse attacking microbes or cellular debris. After “eating” their neighbors, senescent cancer cells digested them by delivering them to lysosomes, acidic cellular structures that are likewise highly active in senescent cells.

Critically, the researchers verified that this process helps senescent malignant cancer cells to stay alive. Senescent cancer cells that ate a neighboring cell survived in culture for longer than senescent cancer cells that didn’t. The researchers speculate that engulfing their neighbors may give senescent cancer cells the energy and materials they need to endure and produce the factors that drive tumor relapse.

“Inhibiting this process may give new remedial chances, since we know that it is the breast cancer patients with tumors that undergo TP53-mediated senescence in response to chemotherapy that have a poor response and poor endurance rates,” Jackson says.

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